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Fox News
by Rachel Rether
When we come down with the flu, we might think the worst is over after a week of a sore throat and body aches. But such viral infections may have lasting, unseen effects on the brain, emerging research suggests.
Viruses such as influenza and herpes may leave brain cells vulnerable to degeneration later in life, and increase the risk of developing diseases such as Alzheimer's and Parkinson's, research suggests. That's because these the viruses can enter the brain and trigger an immune response — inflammation — which can damage brain cells.
Viruses and other sources of inflammation "may be initiating factors in some of the most common neurological diseases," said Dr. Ole Isacson, professor of neurology at Harvard Medical School, who discussed the topic in an article published today (Feb. 15) in the journal Science Translational Medicine.
It's unlikely one bout of the flu will cause significant damage. But over a lifetime, injuries to cells accumulate, Isacson said, and along with environmental stresses, this can kill cells and the development of brain diseases. Variations in the number of infections we get may be the difference between a person developing Parkinson's disease at age 65 or at age 95, Isacson said.
It's possible that toning down the inflammation that occurs shortly after viral infection could reduce cell damage and the risk of subsequent brain disease, Isacson said. Isacson pointed to a 2011 study of 135,000 men and women found that those who took ibuprofen (a medication that can reduce inflammation) were 30 percent less likely to develop Parkinson's over a six year period compared to those who did not take the medication.
Brain infection
One of the earliest pieces of evidence for the virus-brain disease link comes from the 1918 influenza pandemic, according to Isacson's article. After that outbreak, there was a dramatic increase in cases of a disease called postencephalitic parkinsonism, which has many of the same symptoms as Parkinson's.
In a more rigorous test of the link, a 2009 study showed that mice injected with the H5N1 flu virus developed infections in cells in a brain region known to be significantly impacted by Parkinson's disease, Isacson said.
Research has also shown that infection with certain herpes viruses can increase the risk of Alzheimer's disease. And very rarely,encephalitis, or brain inflammation caused by viruses, can lead directly to an acute, but transient, form of Parkinson's disease.
But more often, viral infections in our brain are silent, Isacson said. We don't see the full impact of these infections until brain degeneration is substantial, he said.
Preventing disease
Several weeks after infection, inflammatory molecules known as cytokines reach a peak concentration, Isacson said. It's this "cytokine storm" that Isacson and his colleagues suspect is responsible for the brain cell damage associated with viral infections.
If researchers could find a way to block this peak from occurring, they might reduce the risk of certain neurological diseases, Isacson said.
In addition, researchers could also try to identify viruses that cause particularly severe cytokine storms, to better understand which infections pose the greatest risk to the brain, Isacson said.
The idea that immune system inflammation may influence the development of Alzheimer's disease and other neurological disorders is just one hypothesis out of many that are being investigated today, said Heather Snyder, senior associate director of medical and scientific relations at the Alzheimer's Association. More research is needed to understand what, if any, effect the immune system has on brain diseases, Snyder said.
Tuesday, February 28, 2012
Sunday, February 26, 2012
Guide dogs for the mind: The retrievers being trained to give dementia sufferers a new life Read more: http://www.dailymail.co.uk/news/article-2103137/Guide-dogs-mind-The-retrievers-trained-dementia-sufferers-new-life.
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Mail online
By GEORGE ARBUTHNOTT
First there were guide dogs for the blind, then hearing dogs for the deaf. Now man’s best friend could help to care for people suffering from dementia.
Golden retrievers and labradors are being taught to remind people to take their tablets, raise the alarm in an emergency, assist with undressing and help out around the home.
Under the ‘Dementia Dog’ project the animals are trained to respond to an alarm that goes off whenever a person who is struggling with memory loss needs to take medication.
The dog then clenches its mouth around the medicine, stored in a bite-proof bag, and carries it to the sufferer.
Animals can also be taught to recognise a specific movement that their owner would make when in distress.
The dog would then either press an emergency button on a telephone or bark loudly to raise the alarm.
And dogs can learn to open cupboards, drawers, fridges and washing machines, flick light switches, and even help people suffering from dementia to undress.
Experts say the animals can be trained to carry out any task that requires a pulling motion. So if a short rope is attached to a cupboard door, the dog can open it.
When it comes to helping with undressing, the dogs are trained to pull at the sleeve of a coat or tug off socks.
So far the project has been given £52,000 of Government funding, but needs to raise a further £130,000 to launch a pilot scheme later this year.
Eventually, it is hoped the initiative will allow many more of the 750,000 Britons who suffer from dementia to retain their independence for longer.
The dogs will undergo a six-month training programme using ‘positive reinforcement’, which means that whenever they complete a task correctly, they get a treat.
If the scheme, developed by voluntary organisation Alzheimer Scotland, gains funding, it will be the first time that dogs have been used to assist those with dementia.
The organisation’s deputy director, Joyce Gray, said: ‘We are really hopeful the dogs will not only be a huge practical help but also provide great emotional support.
‘People with the condition can easily become isolated and the dog will be a constant companion, which will help them to keep social.’
Sufferers of early-stage dementia are now being urged to suggest other ways the dogs could improve their lives.
The feedback will be incorporated into the pilot scheme once the funding is raised.
Four students at Glasgow School of Art came up with the idea after Alzheimer Scotland challenged the college to suggest an innovative way to improve the lives of dementia sufferers.
The concept was pitched to the Design Council, which in partnership with the Department of Health was offering funding for projects that helped those with early-stage dementia.
The Dementia Dogs scheme has now gained the backing of charities Dogs For The Disabled and Guide Dogs, which already provide dogs with similar skills to help those with physical disabilities.
The number of people with dementia is set to hit one million by 2021 and 1.7 million by 2050. It is believed that six out of ten of those with the condition are undiagnosed.
Sufferers of dementia and their relatives are urged to suggest ways that dogs could help them via the website dementiadog.org.
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Mail online
By GEORGE ARBUTHNOTT
First there were guide dogs for the blind, then hearing dogs for the deaf. Now man’s best friend could help to care for people suffering from dementia.
Golden retrievers and labradors are being taught to remind people to take their tablets, raise the alarm in an emergency, assist with undressing and help out around the home.
Under the ‘Dementia Dog’ project the animals are trained to respond to an alarm that goes off whenever a person who is struggling with memory loss needs to take medication.
The dog then clenches its mouth around the medicine, stored in a bite-proof bag, and carries it to the sufferer.
Animals can also be taught to recognise a specific movement that their owner would make when in distress.
The dog would then either press an emergency button on a telephone or bark loudly to raise the alarm.
And dogs can learn to open cupboards, drawers, fridges and washing machines, flick light switches, and even help people suffering from dementia to undress.
Experts say the animals can be trained to carry out any task that requires a pulling motion. So if a short rope is attached to a cupboard door, the dog can open it.
When it comes to helping with undressing, the dogs are trained to pull at the sleeve of a coat or tug off socks.
So far the project has been given £52,000 of Government funding, but needs to raise a further £130,000 to launch a pilot scheme later this year.
Eventually, it is hoped the initiative will allow many more of the 750,000 Britons who suffer from dementia to retain their independence for longer.
The dogs will undergo a six-month training programme using ‘positive reinforcement’, which means that whenever they complete a task correctly, they get a treat.
If the scheme, developed by voluntary organisation Alzheimer Scotland, gains funding, it will be the first time that dogs have been used to assist those with dementia.
The organisation’s deputy director, Joyce Gray, said: ‘We are really hopeful the dogs will not only be a huge practical help but also provide great emotional support.
‘People with the condition can easily become isolated and the dog will be a constant companion, which will help them to keep social.’
Sufferers of early-stage dementia are now being urged to suggest other ways the dogs could improve their lives.
The feedback will be incorporated into the pilot scheme once the funding is raised.
Four students at Glasgow School of Art came up with the idea after Alzheimer Scotland challenged the college to suggest an innovative way to improve the lives of dementia sufferers.
The concept was pitched to the Design Council, which in partnership with the Department of Health was offering funding for projects that helped those with early-stage dementia.
The Dementia Dogs scheme has now gained the backing of charities Dogs For The Disabled and Guide Dogs, which already provide dogs with similar skills to help those with physical disabilities.
The number of people with dementia is set to hit one million by 2021 and 1.7 million by 2050. It is believed that six out of ten of those with the condition are undiagnosed.
Sufferers of dementia and their relatives are urged to suggest ways that dogs could help them via the website dementiadog.org.
Friday, February 24, 2012
Alzheimer's Drug May Impair Memory
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Sciencecodex
CHICAGO --- Alzheimer's disease drugs now being tested in clinical trials may have potentially adverse side effects, according to new Northwestern Medicine research. A study with mice suggests the drugs could act like a bad electrician, causing neurons to be miswired and interfering with their ability to send messages to the brain.
The findings, from the scientist whose original research led to the drug development, are published in the journal Molecular Neurodegeneration and will be presented Saturday, Feb. 18, at the 2012 annual meeting for the American Association for the Advancement of Science in Vancouver.
"Let's proceed with caution," said Robert Vassar, professor of cell and molecular biology at Northwestern University Feinberg School of Medicine. "We have to keep our eyes open for potential side effects of these drugs." Ironically, he says, the drugs could impair memory.
The drugs are designed to inhibit BACE1, the enzyme Vassar originally discovered that promotes the development of the clumps of plaque that are a hallmark of Alzheimer's. BACE1 acts as a molecular scissors, cutting up and releasing proteins that form the plaques. Thus, drug developers believed blocking the enzyme might slow the disease.
But in Vassar's new study, he found BACE1 also has a critical role as the brain's electrician. In that role, the enzyme maps out the location of axons, the wires that connect neurons to the brain and the rest of the nervous system. This mapping is called axonal guidance.
Working with mice from which BACE1 was genetically removed, Vassar discovered the animals' olfactory system – used for the sense of smell -- was incorrectly wired. The axons of the olfactory neurons were not wired properly to the olfactory bulb of the brain. The findings show the key role of BACE1 in axonal guidance.
"It's like a badly wired house," Vassar said. "If the electrician doesn't get the wiring pattern correct, your lights won't turn on and the outlets won't work."
The olfactory system is a good model for axonal guidance or wiring. If the axons aren't being properly connected in the olfactory system, Vassar said, the problem likely exists elsewhere in the brain and nervous system. The hippocampus could be particularly vulnerable to BACE1 blockers, he noted, because its population of neurons is continually being reborn, which may play a role in forming new memories. The neurons need to grow new axons that in turn must connect them with new targets. Axonal guidance is a continuous need.
"It's not all bad news," Vassar noted. "These BACE1 blockers might be useful at a specific dose that will reduce the amyloid plaques but not high enough to interfere with the wiring. Understanding the normal function of BACE1 may help us avoid potential drug side effects."
Source: Northwestern University
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Here is a way for nurses administrators, social workers and other health care professionals to get an easyceu or two
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Sciencecodex
CHICAGO --- Alzheimer's disease drugs now being tested in clinical trials may have potentially adverse side effects, according to new Northwestern Medicine research. A study with mice suggests the drugs could act like a bad electrician, causing neurons to be miswired and interfering with their ability to send messages to the brain.
The findings, from the scientist whose original research led to the drug development, are published in the journal Molecular Neurodegeneration and will be presented Saturday, Feb. 18, at the 2012 annual meeting for the American Association for the Advancement of Science in Vancouver.
"Let's proceed with caution," said Robert Vassar, professor of cell and molecular biology at Northwestern University Feinberg School of Medicine. "We have to keep our eyes open for potential side effects of these drugs." Ironically, he says, the drugs could impair memory.
The drugs are designed to inhibit BACE1, the enzyme Vassar originally discovered that promotes the development of the clumps of plaque that are a hallmark of Alzheimer's. BACE1 acts as a molecular scissors, cutting up and releasing proteins that form the plaques. Thus, drug developers believed blocking the enzyme might slow the disease.
But in Vassar's new study, he found BACE1 also has a critical role as the brain's electrician. In that role, the enzyme maps out the location of axons, the wires that connect neurons to the brain and the rest of the nervous system. This mapping is called axonal guidance.
Working with mice from which BACE1 was genetically removed, Vassar discovered the animals' olfactory system – used for the sense of smell -- was incorrectly wired. The axons of the olfactory neurons were not wired properly to the olfactory bulb of the brain. The findings show the key role of BACE1 in axonal guidance.
"It's like a badly wired house," Vassar said. "If the electrician doesn't get the wiring pattern correct, your lights won't turn on and the outlets won't work."
The olfactory system is a good model for axonal guidance or wiring. If the axons aren't being properly connected in the olfactory system, Vassar said, the problem likely exists elsewhere in the brain and nervous system. The hippocampus could be particularly vulnerable to BACE1 blockers, he noted, because its population of neurons is continually being reborn, which may play a role in forming new memories. The neurons need to grow new axons that in turn must connect them with new targets. Axonal guidance is a continuous need.
"It's not all bad news," Vassar noted. "These BACE1 blockers might be useful at a specific dose that will reduce the amyloid plaques but not high enough to interfere with the wiring. Understanding the normal function of BACE1 may help us avoid potential drug side effects."
Source: Northwestern University
Wednesday, February 22, 2012
UCLA scientists boost memory by stimulating key site in brain
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UCLA Newsroom
Mechanism holds potential for improving recall in dementia patients
By Elaine Schmidt
Have you ever gone to the movies and forgotten where you parked the car? New UCLA research may one day help you improve your memory.
UCLA neuroscientists have demonstrated that they can strengthen memory in human patients by stimulating a critical junction in the brain. Published in the Feb. 9 edition of the New England Journal of Medicine, the finding could lead to a new method for boosting memory in patients with early Alzheimer's disease.
The UCLA team focused on a brain site called the entorhinal cortex. Considered the doorway to the hippocampus, which helps form and store memories, the entorhinal cortex plays a crucial role in transforming daily experience into lasting memories.
"The entorhinal cortex is the golden gate to the brain's memory mainframe," said senior author Dr. Itzhak Fried, a professor of neurosurgery at the David Geffen School of Medicine at UCLA. "Every visual and sensory experience that we eventually commit to memory funnels through that doorway to the hippocampus. Our brain cells must send signals through this hub in order to form memories that we can later consciously recall."
Fried and his colleagues followed seven epilepsy patients who already had electrodes implanted in their brains to pinpoint the origin of their seizures. The researchers monitored the electrodes to record neuron activity as memories were being formed.
Using a video game featuring a taxi cab, virtual passengers and a cyber-city, the researchers tested whether deep-brain stimulation of the entorhinal cortex or the hippocampus altered recall. Patients played the role of cab drivers who picked up passengers and traveled across town to deliver them to one of six requested shops.
"When we stimulated the nerve fibers in the patients' entorhinal cortex during learning, they later recognized landmarks and navigated the routes more quickly," Fried said. "They even learned to take shortcuts, reflecting improved spatial memory.
"Critically, it was the stimulation at the gateway into the hippocampus — and not the hippocampus itself — that proved effective," he added.
The use of stimulation only during the learning phase suggests that patients need not undergo continuous stimulation to boost their memory, but only when they are trying to learn important information, Fried noted. This may lead the way to neuro-prosthetic devices that can switch on during specific stages of information processing or daily tasks.
Six million Americans and 30 million people worldwide are diagnosed with Alzheimer's disease each year. The progressive disorder is the sixth leading cause of death in the United States and the fifth leading cause of death for those aged 65 and older.
"Losing our ability to remember recent events and form new memories is one of the most dreaded afflictions of the human condition," Fried said. "Our preliminary results provide evidence supporting a possible mechanism for enhancing memory, particularly as people age or suffer from early dementia. At the same time, we studied a small sample of patients, so our results should be interpreted with caution."
Future studies will determine whether deep-brain stimulation can enhance other types of recall, such as verbal and autobiographical memories. No adverse effects of the stimulation were reported by the seven patients.
Fried's co-authors included first author Nanthia Suthana, Dr. Zulfi Haneef, Dr. John Stern, Roy Mukamel, Eric Behnke and Barbara Knowlton, all of UCLA. The research was supported by grants from the National Institute of Neurological Disorders and Stroke and the Dana Foundation.
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UCLA Newsroom
Mechanism holds potential for improving recall in dementia patients
By Elaine Schmidt
Have you ever gone to the movies and forgotten where you parked the car? New UCLA research may one day help you improve your memory.
UCLA neuroscientists have demonstrated that they can strengthen memory in human patients by stimulating a critical junction in the brain. Published in the Feb. 9 edition of the New England Journal of Medicine, the finding could lead to a new method for boosting memory in patients with early Alzheimer's disease.
The UCLA team focused on a brain site called the entorhinal cortex. Considered the doorway to the hippocampus, which helps form and store memories, the entorhinal cortex plays a crucial role in transforming daily experience into lasting memories.
"The entorhinal cortex is the golden gate to the brain's memory mainframe," said senior author Dr. Itzhak Fried, a professor of neurosurgery at the David Geffen School of Medicine at UCLA. "Every visual and sensory experience that we eventually commit to memory funnels through that doorway to the hippocampus. Our brain cells must send signals through this hub in order to form memories that we can later consciously recall."
Fried and his colleagues followed seven epilepsy patients who already had electrodes implanted in their brains to pinpoint the origin of their seizures. The researchers monitored the electrodes to record neuron activity as memories were being formed.
Using a video game featuring a taxi cab, virtual passengers and a cyber-city, the researchers tested whether deep-brain stimulation of the entorhinal cortex or the hippocampus altered recall. Patients played the role of cab drivers who picked up passengers and traveled across town to deliver them to one of six requested shops.
"When we stimulated the nerve fibers in the patients' entorhinal cortex during learning, they later recognized landmarks and navigated the routes more quickly," Fried said. "They even learned to take shortcuts, reflecting improved spatial memory.
"Critically, it was the stimulation at the gateway into the hippocampus — and not the hippocampus itself — that proved effective," he added.
The use of stimulation only during the learning phase suggests that patients need not undergo continuous stimulation to boost their memory, but only when they are trying to learn important information, Fried noted. This may lead the way to neuro-prosthetic devices that can switch on during specific stages of information processing or daily tasks.
Six million Americans and 30 million people worldwide are diagnosed with Alzheimer's disease each year. The progressive disorder is the sixth leading cause of death in the United States and the fifth leading cause of death for those aged 65 and older.
"Losing our ability to remember recent events and form new memories is one of the most dreaded afflictions of the human condition," Fried said. "Our preliminary results provide evidence supporting a possible mechanism for enhancing memory, particularly as people age or suffer from early dementia. At the same time, we studied a small sample of patients, so our results should be interpreted with caution."
Future studies will determine whether deep-brain stimulation can enhance other types of recall, such as verbal and autobiographical memories. No adverse effects of the stimulation were reported by the seven patients.
Fried's co-authors included first author Nanthia Suthana, Dr. Zulfi Haneef, Dr. John Stern, Roy Mukamel, Eric Behnke and Barbara Knowlton, all of UCLA. The research was supported by grants from the National Institute of Neurological Disorders and Stroke and the Dana Foundation.
Monday, February 20, 2012
FDA-Approved Bexarotene Improves Memory, Reversing Alzheimer's in Mice
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CBS) A new study of a promising Alzheimer's treatment has doctors buzzing that the drug may reverse the deadly neurodegenerative disease. But the new treatment isn't a new drug at all, rather a skin cancer pill that's been FDA-approved for more than a decade.
The drug, bexarotene, reversed signs of Alzheimer's in mice brains and also improved their memory in as little as 72 hours, according to the study.
"This is an unprecedented finding," study author Paige Cramer, a PhD candidate at Case Western Reserve School of Medicine, said in a university written statement. "Previously, the best existing treatment for Alzheimer's disease in mice required several months to reduce plaque in the brain."
Bexarotene - sold under the brand name Targretin - was approved by the FDA in 1999 for treating cutaneous T-cell lymphoma, a cancer of the white blood cells that primarily affects the skin. But the drug also happens to switch on a gene that makes a naturally occurring protein in the brain called Apolipoprotein E, or ApoE.
Previous research by study co-author Dr. Gary Landreth, a professor of neurosciences at Case Western Reserve, showed that ApoE could help facilitate the removal of amyloid beta proteins, which are a toxic substance in the brain that causes plaque buildup that's a marker for Alzheimer's.
Dr. Landreth and his grad student, Cramer, thought if they could use this drug to increase ApoE, then maybe they could reduce some of the plaques in mice that were genetically bred to have Alzheimer's. The researchers found that the drug caused a 50 percent reduction in the amount of amyloid plaques within only three days, and after 14 days, they saw a 75 percent reduction. The drug essentially "reprogrammed" the brain's immune cells to "eat" the amyloid plaques.
The brain plaque reduction was also associated with improvements in the rat's behavior. Mice instinctively make nests out of materials around them, but mice with Alzheimer's typically fail this task. But after 72 hours of bexarotene treatment, the Alzheimer's mice could build nests from tissue paper, and also performed better on other tests, which suggest a "clearer thought process," Cramer said in a university video.
The study is published in the Feb. 9 issue of the journal, Science.
One caveat to the study - mice aren't people. Despite how promising the findings may seem, the researchers tempered expectations.
"I want to say as loudly and clearly as possible that this was a study in mice, not in humans," Landreth told CNN. "We've fixed Alzheimer's in mice lots of times, so we need to move forward expeditiously but cautiously."
Dr. Maria C. Carrillo, director of scientific relations at the Alzheimer's Association agreed and told the Washington Post, "We need to be cautiously optimistic and pursue this lead as we would any other." But she added, "This an exciting study is that it involves a repurposed drug."
The researchers hope to get approval to study bexarotene in humans as soon as possible, and Landreth told the Post there's an urgency since he's heard from other doctors that patients are already asking about bexarotene.
"We've got to work fast, and we have got to be right," Landreth said. "We can't screw this up."
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CBS) A new study of a promising Alzheimer's treatment has doctors buzzing that the drug may reverse the deadly neurodegenerative disease. But the new treatment isn't a new drug at all, rather a skin cancer pill that's been FDA-approved for more than a decade.
The drug, bexarotene, reversed signs of Alzheimer's in mice brains and also improved their memory in as little as 72 hours, according to the study.
"This is an unprecedented finding," study author Paige Cramer, a PhD candidate at Case Western Reserve School of Medicine, said in a university written statement. "Previously, the best existing treatment for Alzheimer's disease in mice required several months to reduce plaque in the brain."
Bexarotene - sold under the brand name Targretin - was approved by the FDA in 1999 for treating cutaneous T-cell lymphoma, a cancer of the white blood cells that primarily affects the skin. But the drug also happens to switch on a gene that makes a naturally occurring protein in the brain called Apolipoprotein E, or ApoE.
Previous research by study co-author Dr. Gary Landreth, a professor of neurosciences at Case Western Reserve, showed that ApoE could help facilitate the removal of amyloid beta proteins, which are a toxic substance in the brain that causes plaque buildup that's a marker for Alzheimer's.
Dr. Landreth and his grad student, Cramer, thought if they could use this drug to increase ApoE, then maybe they could reduce some of the plaques in mice that were genetically bred to have Alzheimer's. The researchers found that the drug caused a 50 percent reduction in the amount of amyloid plaques within only three days, and after 14 days, they saw a 75 percent reduction. The drug essentially "reprogrammed" the brain's immune cells to "eat" the amyloid plaques.
The brain plaque reduction was also associated with improvements in the rat's behavior. Mice instinctively make nests out of materials around them, but mice with Alzheimer's typically fail this task. But after 72 hours of bexarotene treatment, the Alzheimer's mice could build nests from tissue paper, and also performed better on other tests, which suggest a "clearer thought process," Cramer said in a university video.
The study is published in the Feb. 9 issue of the journal, Science.
One caveat to the study - mice aren't people. Despite how promising the findings may seem, the researchers tempered expectations.
"I want to say as loudly and clearly as possible that this was a study in mice, not in humans," Landreth told CNN. "We've fixed Alzheimer's in mice lots of times, so we need to move forward expeditiously but cautiously."
Dr. Maria C. Carrillo, director of scientific relations at the Alzheimer's Association agreed and told the Washington Post, "We need to be cautiously optimistic and pursue this lead as we would any other." But she added, "This an exciting study is that it involves a repurposed drug."
The researchers hope to get approval to study bexarotene in humans as soon as possible, and Landreth told the Post there's an urgency since he's heard from other doctors that patients are already asking about bexarotene.
"We've got to work fast, and we have got to be right," Landreth said. "We can't screw this up."
Saturday, February 18, 2012
Study Shows Alzheimer's Disease May Spread by 'Jumping' from One Brain Region to Another
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PRWeb
Findings open new opportunities for studying Alzheimer's and testing potential therapies.
For decades, researchers have debated whether Alzheimer's disease starts independently in vulnerable brain regions at different times, or if it begins in one region and then spreads to neuroanatomically connected areas. A new study by Columbia University Medical Center (CUMC) researchers strongly supports the latter, demonstrating that abnormal tau protein, a key feature of the neurofibrillary tangles seen in the brains of those with Alzheimer's, propagates along linked brain circuits, ''jumping'' from neuron to neuron.
The findings, published today in the online journal PloS One, open new opportunities for gaining a greater understanding of Alzheimer's disease and other neurological diseases and for developing therapies to halt its progression, according to senior author Karen E. Duff, PhD, professor of pathology (in psychiatry and in the Taub Institute for Research on Alzheimer's Disease and the Aging Brain) at CUMC and at the New York State Psychiatric Institute.
Alzheimer's disease, the most common form of dementia, is characterised by the accumulation of plaques (composed of amyloid-beta protein) and fibrous tangles (composed of abnormal tau) in brain cells called neurons.
Post mortem studies of human brains and neuroimaging studies have suggested that the disease, especially the neurofibrillary tangle pathology, begins in the entorhinal cortex, which plays a key role in memory. Then as Alzheimer's progresses, the disease appears in anatomically linked higher brain regions.
''Earlier research, including functional MRI studies in humans, have also supported this pattern of spread,'' said study coauthor Scott A. Small, MD, professor of neurology in the Sergievsky Center and in the Taub Institute for Research on Alzheimer's Disease and the Aging Brain at CUMC. ''But these various findings do not definitively show that Alzheimer's spreads directly from one brain region to another.''
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PRWeb
Findings open new opportunities for studying Alzheimer's and testing potential therapies.
For decades, researchers have debated whether Alzheimer's disease starts independently in vulnerable brain regions at different times, or if it begins in one region and then spreads to neuroanatomically connected areas. A new study by Columbia University Medical Center (CUMC) researchers strongly supports the latter, demonstrating that abnormal tau protein, a key feature of the neurofibrillary tangles seen in the brains of those with Alzheimer's, propagates along linked brain circuits, ''jumping'' from neuron to neuron.
The findings, published today in the online journal PloS One, open new opportunities for gaining a greater understanding of Alzheimer's disease and other neurological diseases and for developing therapies to halt its progression, according to senior author Karen E. Duff, PhD, professor of pathology (in psychiatry and in the Taub Institute for Research on Alzheimer's Disease and the Aging Brain) at CUMC and at the New York State Psychiatric Institute.
Alzheimer's disease, the most common form of dementia, is characterised by the accumulation of plaques (composed of amyloid-beta protein) and fibrous tangles (composed of abnormal tau) in brain cells called neurons.
Post mortem studies of human brains and neuroimaging studies have suggested that the disease, especially the neurofibrillary tangle pathology, begins in the entorhinal cortex, which plays a key role in memory. Then as Alzheimer's progresses, the disease appears in anatomically linked higher brain regions.
''Earlier research, including functional MRI studies in humans, have also supported this pattern of spread,'' said study coauthor Scott A. Small, MD, professor of neurology in the Sergievsky Center and in the Taub Institute for Research on Alzheimer's Disease and the Aging Brain at CUMC. ''But these various findings do not definitively show that Alzheimer's spreads directly from one brain region to another.''
Thursday, February 16, 2012
Research finds potential for Alzheimer’s therapy
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cavalierdaily.com
by Amanda Gellet, Senior Writer
Clinical trial results, published in The Journal of Neuroscienceby Eli Lilly & Co., suggest a promising new therapy for Alzheimer’s disease.
The BACE1 inhibitor drug called LY2811376 prevents beta-secretase 1 from producing amyloid-beta, a protein fragment commonly associated with Alzheimer’s.
Researchers considered BACE1 inhibition to be a potential therapy for more than a decade, but Eli Lilly & Co.’s findings marked the first successful pharmaceutical reduction of amyloid-beta levels in humans.
In Alzheimer’s patients, amyloid-beta collects in the brain and becomes pathogenic. This excess leads to extreme memory loss, severe problems with daily activities and eventually death, said Matt Seward, a University Ph.D. student who studies Alzheimer’s disease.
During Phase I, Eli Lilly & Co. found LY2811376 lowered the levels of amyloid-beta in blood plasma and cerebrospinal fluid — the fluid surrounding the brain. The inhibitor proved more successful than other current drugs at lowering amyloid-beta levels in healthy volunteers.
This drug does not reverse the damage already caused to the brains of Alzheimer patients. Since the brain is not able to regenerate itself, Seward said a drug must be found which alters amyloid-beta levels in seemingly healthy individuals to successfully delay or prevent disease progression. The success of LY2811376 in Phase I studies suggests this drug could offer a viable solution.
Testing on pre-clinical animals demonstrated the potential side effects of long-term exposure to LY2811376, including the collection of granules in the eyes and some parts of the brain. The retina cells of the animals’ eyes became enlarged because of the number of granules which had collected in the cells. Moreover, there was evidence of degeneration in the eye. Phase I participants did not experience significant side effects.
Alzheimer’s disease accounts for 60 to 80 percent of all dementia and is the sixth-leading cause of death in the United States, according to the Alzheimer’s Association.
The number of Alzheimer’s-related deaths rose 66 percent between 2000 and 2008, reflecting the aging of the United States’ baby-boomer generation. This number is expected to continue to increase as the population becomes even older. Experts predict that by 2050 Alzheimer’s care will cost Medicare and Medicaid $800 billion annually, surpassing the country’s current military budget.
Of the top-10 causes of death in the United States, Alzheimer’s is the only disease without a treatment which prevents, cures or slows its progression.
Current therapies for Alzheimer’s only treat the symptoms of the disease. A drug such as LY2811376, which is directed at the disease itself, may represent a huge leap forward for Alzheimer’s treatment, Seward said.
Eli Lilly & Co.’s research also helped the medical community understand the principles directing the disease, he added.
“The success of LY2811376 is that it shows proof of principle,” Seward said
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cavalierdaily.com
by Amanda Gellet, Senior Writer
Clinical trial results, published in The Journal of Neuroscienceby Eli Lilly & Co., suggest a promising new therapy for Alzheimer’s disease.
The BACE1 inhibitor drug called LY2811376 prevents beta-secretase 1 from producing amyloid-beta, a protein fragment commonly associated with Alzheimer’s.
Researchers considered BACE1 inhibition to be a potential therapy for more than a decade, but Eli Lilly & Co.’s findings marked the first successful pharmaceutical reduction of amyloid-beta levels in humans.
In Alzheimer’s patients, amyloid-beta collects in the brain and becomes pathogenic. This excess leads to extreme memory loss, severe problems with daily activities and eventually death, said Matt Seward, a University Ph.D. student who studies Alzheimer’s disease.
During Phase I, Eli Lilly & Co. found LY2811376 lowered the levels of amyloid-beta in blood plasma and cerebrospinal fluid — the fluid surrounding the brain. The inhibitor proved more successful than other current drugs at lowering amyloid-beta levels in healthy volunteers.
This drug does not reverse the damage already caused to the brains of Alzheimer patients. Since the brain is not able to regenerate itself, Seward said a drug must be found which alters amyloid-beta levels in seemingly healthy individuals to successfully delay or prevent disease progression. The success of LY2811376 in Phase I studies suggests this drug could offer a viable solution.
Testing on pre-clinical animals demonstrated the potential side effects of long-term exposure to LY2811376, including the collection of granules in the eyes and some parts of the brain. The retina cells of the animals’ eyes became enlarged because of the number of granules which had collected in the cells. Moreover, there was evidence of degeneration in the eye. Phase I participants did not experience significant side effects.
Alzheimer’s disease accounts for 60 to 80 percent of all dementia and is the sixth-leading cause of death in the United States, according to the Alzheimer’s Association.
The number of Alzheimer’s-related deaths rose 66 percent between 2000 and 2008, reflecting the aging of the United States’ baby-boomer generation. This number is expected to continue to increase as the population becomes even older. Experts predict that by 2050 Alzheimer’s care will cost Medicare and Medicaid $800 billion annually, surpassing the country’s current military budget.
Of the top-10 causes of death in the United States, Alzheimer’s is the only disease without a treatment which prevents, cures or slows its progression.
Current therapies for Alzheimer’s only treat the symptoms of the disease. A drug such as LY2811376, which is directed at the disease itself, may represent a huge leap forward for Alzheimer’s treatment, Seward said.
Eli Lilly & Co.’s research also helped the medical community understand the principles directing the disease, he added.
“The success of LY2811376 is that it shows proof of principle,” Seward said
Tuesday, February 14, 2012
Cracks in the Plaques: Mysteries of Alzheimer's Slowly Yielding to New Research
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Scientific American
Science is bringing some understanding of the heritability, prevalence and inner workings of one of the most devastating diseases
By Daisy Yuhas
This has been a big week in Alzheimer's news as scientists put together a clearer picture than ever before of how the disease affects the brain. Three recently published studies have detected the disease with new technologies, hinted at its prevalence, and described at last how it makes its lethal progress through the brain.
The existence of two forms of Alzheimer's—early- and late-onset—has long baffled scientists. Of the estimated five million Americans who suffer from Alzheimer's, only a few thousand are diagnosed with an early-onset form of the affliction, which affects people before the age of 65. This rare early-onset form is thought to be hereditary and scientists have associated multiple genetic mutations contributing to its occurrence. Late-onset Alzheimer's, although more common, has been the bigger mystery. One variant of the APOE gene-—sometimes known as the Alzheimer's gene—is linked to the late-onset disease. But the APOE gene, unlike dominant early-onset genes, does not determine whether a person will ultimately have dementia.
Now there's evidence that late-onset Alzheimer's has a genetic basis similar to that of early-onset Alzheimer's. By sequencing select genes associated with the latter, along with frontotemporal dementia, researchers at Washington University in Saint Louis and other institutions found that patients with late-onset Alzheimer's carry some of the same genetic mutations as those with the early-onset form. The evidence, published on Wednesday in PLoS ONE, bolsters the argument that the forms of Alzheimer's that appear at different life stages should be classified as the same disease. As to why the disease appears earlier in some cases, the scientists speculated that those patients diagnosed relatively early in life carry more genetic risk factors for the disease.
This study's use of rapid genetic sequencing, the authors noted, may provide a model for more precise identification of dementias. Within the study, the researchers identified patients who may have been misdiagnosed as having Alzheimer's; the genes of these patients suggested that they had another type of dementia. Given the heritable component, patients with a family history could be screened to detect and diagnose Alzheimer's early.
Other genetic research unveiled in the past week or so has shed light on the biological processes that underlie how Alzheimer's affects the brain. Certain mutations may lead to an increased production of a protein called amyloid beta in the region of the brain that creates memory. This excess amyloid beta, naturally secreted by brain cells, then becomes a complex called an oligomer. These oligomers may interrupt the signals transmitted between neurons. As in other neurodegenerative diseases like Parkinson's or Huntington's, the spread of oligomers appears to be driving the disease process.
Oligomer-linked diseases are relatively common, in part because oligomers can also play an essential biological role in the brain. A recent investigation using fruit flies reveals that the presence of a specific oligomer is actually required for the flies to form long-term memories.
In an early stage of Alzheimer's, the naturally secreted amyloid beta protein builds up as oligomers in the brain, which then go on to form larger aggregates called plaques. Later in the disease, another aberrant form of a protein called tau starts to build up, in the entorhinal cortex. Normally, tau helps provide structure crucial to neuron functioning. The buildup of tau, however, causes the protein to tangle and eventually kill brain cells. What was unknown until recently, however, was how the tau protein spreads through different brain regions.
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Scientific American
Science is bringing some understanding of the heritability, prevalence and inner workings of one of the most devastating diseases
By Daisy Yuhas
This has been a big week in Alzheimer's news as scientists put together a clearer picture than ever before of how the disease affects the brain. Three recently published studies have detected the disease with new technologies, hinted at its prevalence, and described at last how it makes its lethal progress through the brain.
The existence of two forms of Alzheimer's—early- and late-onset—has long baffled scientists. Of the estimated five million Americans who suffer from Alzheimer's, only a few thousand are diagnosed with an early-onset form of the affliction, which affects people before the age of 65. This rare early-onset form is thought to be hereditary and scientists have associated multiple genetic mutations contributing to its occurrence. Late-onset Alzheimer's, although more common, has been the bigger mystery. One variant of the APOE gene-—sometimes known as the Alzheimer's gene—is linked to the late-onset disease. But the APOE gene, unlike dominant early-onset genes, does not determine whether a person will ultimately have dementia.
Now there's evidence that late-onset Alzheimer's has a genetic basis similar to that of early-onset Alzheimer's. By sequencing select genes associated with the latter, along with frontotemporal dementia, researchers at Washington University in Saint Louis and other institutions found that patients with late-onset Alzheimer's carry some of the same genetic mutations as those with the early-onset form. The evidence, published on Wednesday in PLoS ONE, bolsters the argument that the forms of Alzheimer's that appear at different life stages should be classified as the same disease. As to why the disease appears earlier in some cases, the scientists speculated that those patients diagnosed relatively early in life carry more genetic risk factors for the disease.
This study's use of rapid genetic sequencing, the authors noted, may provide a model for more precise identification of dementias. Within the study, the researchers identified patients who may have been misdiagnosed as having Alzheimer's; the genes of these patients suggested that they had another type of dementia. Given the heritable component, patients with a family history could be screened to detect and diagnose Alzheimer's early.
Other genetic research unveiled in the past week or so has shed light on the biological processes that underlie how Alzheimer's affects the brain. Certain mutations may lead to an increased production of a protein called amyloid beta in the region of the brain that creates memory. This excess amyloid beta, naturally secreted by brain cells, then becomes a complex called an oligomer. These oligomers may interrupt the signals transmitted between neurons. As in other neurodegenerative diseases like Parkinson's or Huntington's, the spread of oligomers appears to be driving the disease process.
Oligomer-linked diseases are relatively common, in part because oligomers can also play an essential biological role in the brain. A recent investigation using fruit flies reveals that the presence of a specific oligomer is actually required for the flies to form long-term memories.
In an early stage of Alzheimer's, the naturally secreted amyloid beta protein builds up as oligomers in the brain, which then go on to form larger aggregates called plaques. Later in the disease, another aberrant form of a protein called tau starts to build up, in the entorhinal cortex. Normally, tau helps provide structure crucial to neuron functioning. The buildup of tau, however, causes the protein to tangle and eventually kill brain cells. What was unknown until recently, however, was how the tau protein spreads through different brain regions.
Sunday, February 12, 2012
Obama administration proposes raise for Alzheimer’s research, some now and some next year
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Washington Post
WASHINGTON — The Obama administration is increasing spending on Alzheimer’s research — planning to surpass half a billion dollars next year — as part of a quest to find effective treatments for the brain-destroying disease by 2025.
In a two-part plan announced Tuesday, the National Institutes of Health immediately will devote an extra $50 million dementia research, on top of the $450 million a year it currently spends. The boost opens the possibility that at least one stalled study of a possible therapy might get to start soon.
Next week, President Barack Obama will ask Congress for $80 million in new money to spend for Alzheimer’s research in 2013.
“The science of Alzheimer’s disease has reached a very interesting juncture,” with promising new findings to pursue after years of false starts, NIH Director Dr. Francis Collins told The Associated Press. “We would love to be able to come up with a way of bringing forward an even larger amount of support.”
Patient advocates have long said the nation’s spending on Alzheimer’s research is far too little considering the disease’s current and coming toll. More than 5 million people already have Alzheimer’s or related dementias, a number that, barring a medical breakthrough, is expected to more than double by 2050 because of the aging population. By then, the medical and nursing home bills are projected to cost $1 trillion annually.
At a meeting last month, some of the government’s own Alzheimer’s advisers said it could take a research investment of as much as $2 billion a year to make a real impact. “Our country cannot afford not to make these commitments,” Alzheimer’s Association President Harry Johns told that meeting.
For comparison, the government spends nearly $3 billion on AIDS research; about 1.1 million Americans are living with the AIDS virus.
But Tuesday, advocates praised the administration for making a needed down payment in tough economic times.
“This is a positive step forward. It’s going to take additional steps on the journey that’s going to get us to the end of this,” Johns said.
“There is no doubt that there is commitment that needs to be applauded here,” added Eric J. Hall, president of the Alzheimer’s Foundation of America.
The move is part of the administration’s development of the first National Alzheimer’s Plan, to combine research toward better treatments — the goal is to have some by 2025 — along with steps to help overwhelmed families better cope today. In addition to the biomedical research, the administration said it will propose spending $26 million for other goals of the still-to-be-finalized plan, including caregiver support.
“Reducing the burden of Alzheimer’s disease on patients and their families is an urgent national priority,” Health and Human Services Secretary Kathleen Sebelius said.
Given the nation’s fiscal problems, it’s not clear what the chances are in Congress for a boost in next year’s Alzheimer’s funding.
But for this year, Collins said Alzheimer’s is such a priority that the NIH will shift some of its budget from other research areas to eke out an extra $50 million right away.
Among his examples: Some cutting-edge gene-mapping will be directed to concentrate on uncovering the genetics of Alzheimer’s, including what protects the brains of some people in dementia-prone families. Collins also said he will determine whether the extra money is enough to start some clinical trials that otherwise would have to wait, including one to test whether an intranasal form of insulin might reach and protect the brain cells of people with early dementia symptom
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Washington Post
WASHINGTON — The Obama administration is increasing spending on Alzheimer’s research — planning to surpass half a billion dollars next year — as part of a quest to find effective treatments for the brain-destroying disease by 2025.
In a two-part plan announced Tuesday, the National Institutes of Health immediately will devote an extra $50 million dementia research, on top of the $450 million a year it currently spends. The boost opens the possibility that at least one stalled study of a possible therapy might get to start soon.
Next week, President Barack Obama will ask Congress for $80 million in new money to spend for Alzheimer’s research in 2013.
“The science of Alzheimer’s disease has reached a very interesting juncture,” with promising new findings to pursue after years of false starts, NIH Director Dr. Francis Collins told The Associated Press. “We would love to be able to come up with a way of bringing forward an even larger amount of support.”
Patient advocates have long said the nation’s spending on Alzheimer’s research is far too little considering the disease’s current and coming toll. More than 5 million people already have Alzheimer’s or related dementias, a number that, barring a medical breakthrough, is expected to more than double by 2050 because of the aging population. By then, the medical and nursing home bills are projected to cost $1 trillion annually.
At a meeting last month, some of the government’s own Alzheimer’s advisers said it could take a research investment of as much as $2 billion a year to make a real impact. “Our country cannot afford not to make these commitments,” Alzheimer’s Association President Harry Johns told that meeting.
For comparison, the government spends nearly $3 billion on AIDS research; about 1.1 million Americans are living with the AIDS virus.
But Tuesday, advocates praised the administration for making a needed down payment in tough economic times.
“This is a positive step forward. It’s going to take additional steps on the journey that’s going to get us to the end of this,” Johns said.
“There is no doubt that there is commitment that needs to be applauded here,” added Eric J. Hall, president of the Alzheimer’s Foundation of America.
The move is part of the administration’s development of the first National Alzheimer’s Plan, to combine research toward better treatments — the goal is to have some by 2025 — along with steps to help overwhelmed families better cope today. In addition to the biomedical research, the administration said it will propose spending $26 million for other goals of the still-to-be-finalized plan, including caregiver support.
“Reducing the burden of Alzheimer’s disease on patients and their families is an urgent national priority,” Health and Human Services Secretary Kathleen Sebelius said.
Given the nation’s fiscal problems, it’s not clear what the chances are in Congress for a boost in next year’s Alzheimer’s funding.
But for this year, Collins said Alzheimer’s is such a priority that the NIH will shift some of its budget from other research areas to eke out an extra $50 million right away.
Among his examples: Some cutting-edge gene-mapping will be directed to concentrate on uncovering the genetics of Alzheimer’s, including what protects the brains of some people in dementia-prone families. Collins also said he will determine whether the extra money is enough to start some clinical trials that otherwise would have to wait, including one to test whether an intranasal form of insulin might reach and protect the brain cells of people with early dementia symptom
Wednesday, February 8, 2012
UT researchers use worms in Alzheimer's study
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abs Texas
AUSTIN, TX -- University of Texas researchers Adela Ben-Yakar and Jon Pierce-Shimomura are on a mission. It's professional, personal and not conducive to patience.
Armed with a five-year, $3 million grant from the National Institutes of Health for "exceptionally innovative" research projects that can shift science in new directions, the two colleagues are devoting a large part of their professional lives to collaborating on new drug therapies for Alzheimer's disease that might also slow down the aging process. It's personal because Ben-Yakar's mother has Alzheimer's disease and is deteriorating. Pierce-Shimomura's 10-year-old son has Down syndrome, which causes premature aging and a high risk of developing memory-stealing Alzheimer's.
"I got into this because of him," said Pierce-Shimomura, an assistant professor in neurobiology.
Ben-Yakar, an associate professor of mechanical engineering, echoes that sentiment. "I'm losing her every day," she said of her 78-year-old mother.
Neither has the time to be patient. Perhaps that is why they have turned to roundworms, rather than the traditional lab mice, for their drug studies.
The two are testing chemicals on minuscule worms, called C. elegans, because of the worms' brief life span -- about 15 days -- and the quick results that can be gathered when testing drugs on them.
The primitive worms share essential biological characteristics with humans, making them an effective tool for researchers.
"If we give the worm an extra copy of a gene, it contributes to the protein that makes up Alzheimer plaques," Pierce-Shimomura said. "When worms get that gene, they develop the disease in middle age."
The worms reach middle age in about five days; mice would take two years, Pierce-Shimomura said.
The researchers can peer at the transparent worms with a fluorescent microscope -- an area of Ben-Yakar's expertise -- and see the nerve cells dying.
They also can test to see whether any chemicals delay the degeneration of the neurons, Ben-Yakar said.
She has pioneered a device using microtechnologies to manipulate a large group of worms at once, making the process more efficient and faster than manipulating the worms manually, one at a time.
As a result, she and Pierce-Shimomura can use the nation's vast drug library to test a million drugs a year, rather than just a thousand.
Without the ability to manipulate the worms and treat with chemical compounds in this manner, "it would take 1,000 years to test 1 million drugs," Ben-Yakar said.
In addition to testing drugs that might delay or even prevent Alzheimer's disease, "the goal is to discover drugs we don't even know about," Ben-Yakar said.
One drug they are experimenting with has been working well in the worms and also has shown promise in rodent and human trials, the researchers said. They declined to name the drug, saying they first need to publish the results.
Their work has just begun, and so far, they have tested only about a dozen compounds, Pierce-Shimomura said.
Understanding how neurons degenerate -- as they do during Alzheimer's -- can also provide important clues to aging, they said.
When humans and animals age, neurons degenerate and die. "The question is," Pierce-Shimomura said, "are there different kinds of neurons that degenerate and can something be done about it."
By working together, he and Ben-Yakar hope to get answers.
Collaborations involving biologists and engineers are producing medical devices, advances in delivering drugs and new treatments.
"It's encouraged by the grant-making agencies," Ben-Yakar said. "We know we cannot confront the future challenges by sitting alone by ourselves in our offices and labs."
Nor do she and her colleague have that kind of time.
(Copyright ©2012 by The Associated Press. All Rights Reserved.)
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Here is information on being the best caregiver you can be
Here is a way for nurses administrators, social workers and other health care professionals to get an easyceu or two
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abs Texas
AUSTIN, TX -- University of Texas researchers Adela Ben-Yakar and Jon Pierce-Shimomura are on a mission. It's professional, personal and not conducive to patience.
Armed with a five-year, $3 million grant from the National Institutes of Health for "exceptionally innovative" research projects that can shift science in new directions, the two colleagues are devoting a large part of their professional lives to collaborating on new drug therapies for Alzheimer's disease that might also slow down the aging process. It's personal because Ben-Yakar's mother has Alzheimer's disease and is deteriorating. Pierce-Shimomura's 10-year-old son has Down syndrome, which causes premature aging and a high risk of developing memory-stealing Alzheimer's.
"I got into this because of him," said Pierce-Shimomura, an assistant professor in neurobiology.
Ben-Yakar, an associate professor of mechanical engineering, echoes that sentiment. "I'm losing her every day," she said of her 78-year-old mother.
Neither has the time to be patient. Perhaps that is why they have turned to roundworms, rather than the traditional lab mice, for their drug studies.
The two are testing chemicals on minuscule worms, called C. elegans, because of the worms' brief life span -- about 15 days -- and the quick results that can be gathered when testing drugs on them.
The primitive worms share essential biological characteristics with humans, making them an effective tool for researchers.
"If we give the worm an extra copy of a gene, it contributes to the protein that makes up Alzheimer plaques," Pierce-Shimomura said. "When worms get that gene, they develop the disease in middle age."
The worms reach middle age in about five days; mice would take two years, Pierce-Shimomura said.
The researchers can peer at the transparent worms with a fluorescent microscope -- an area of Ben-Yakar's expertise -- and see the nerve cells dying.
They also can test to see whether any chemicals delay the degeneration of the neurons, Ben-Yakar said.
She has pioneered a device using microtechnologies to manipulate a large group of worms at once, making the process more efficient and faster than manipulating the worms manually, one at a time.
As a result, she and Pierce-Shimomura can use the nation's vast drug library to test a million drugs a year, rather than just a thousand.
Without the ability to manipulate the worms and treat with chemical compounds in this manner, "it would take 1,000 years to test 1 million drugs," Ben-Yakar said.
In addition to testing drugs that might delay or even prevent Alzheimer's disease, "the goal is to discover drugs we don't even know about," Ben-Yakar said.
One drug they are experimenting with has been working well in the worms and also has shown promise in rodent and human trials, the researchers said. They declined to name the drug, saying they first need to publish the results.
Their work has just begun, and so far, they have tested only about a dozen compounds, Pierce-Shimomura said.
Understanding how neurons degenerate -- as they do during Alzheimer's -- can also provide important clues to aging, they said.
When humans and animals age, neurons degenerate and die. "The question is," Pierce-Shimomura said, "are there different kinds of neurons that degenerate and can something be done about it."
By working together, he and Ben-Yakar hope to get answers.
Collaborations involving biologists and engineers are producing medical devices, advances in delivering drugs and new treatments.
"It's encouraged by the grant-making agencies," Ben-Yakar said. "We know we cannot confront the future challenges by sitting alone by ourselves in our offices and labs."
Nor do she and her colleague have that kind of time.
(Copyright ©2012 by The Associated Press. All Rights Reserved.)
Monday, February 6, 2012
Agent Lights Up Alzheimer's Tangles
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By MedPage Today Staff2
Lighting Up the Tangles
Several contrast agents are in development for imaging beta-amyloid plaques in patients with incipient Alzheimer's disease, but what about the disorder's other major pathology, neurofibrillary tangles? Nothing suitable has yet come along for measuring these abnormalities in live patients.
That may now be changing, thanks to efforts by Masahiro Ono, PhD, and colleagues at Japan's Kyoto University. In ACS Medicinal Chemistry Letters, they say they have identified a new agent that binds both to beta-amyloid plaques and to neurofibratory tangles made of rogue tau proteins.
Studies in mice showed that the compound, based on fluorine-18, is stable enough in vivo to serve as a useful contrast agent. And, when applied to brain sections from deceased Alzheimer's disease patients, tangles as well as plaques lit up brightly in PET and SPECT scans.
-- J.G.
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By MedPage Today Staff2
Lighting Up the Tangles
Several contrast agents are in development for imaging beta-amyloid plaques in patients with incipient Alzheimer's disease, but what about the disorder's other major pathology, neurofibrillary tangles? Nothing suitable has yet come along for measuring these abnormalities in live patients.
That may now be changing, thanks to efforts by Masahiro Ono, PhD, and colleagues at Japan's Kyoto University. In ACS Medicinal Chemistry Letters, they say they have identified a new agent that binds both to beta-amyloid plaques and to neurofibratory tangles made of rogue tau proteins.
Studies in mice showed that the compound, based on fluorine-18, is stable enough in vivo to serve as a useful contrast agent. And, when applied to brain sections from deceased Alzheimer's disease patients, tangles as well as plaques lit up brightly in PET and SPECT scans.
-- J.G.
Saturday, February 4, 2012
Health Discovery of new active compounds against Alzheimer''s disease
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ENEVA,(KUNA) -- Based on computer simulations, biochemists from the University of Zurich in Switzerland have shown on Tuesday shown how the active compounds and fragments of the peptide, that causes Alzheimer disease, interact with each other and found that it is the disordered structure of the peptide that determines the interactions with active compounds.
"Various molecules have been synthesized that inhibit self-assembly of the amyloid beta peptide in vitro. This peptide is strongly linked to Alzheimer's disease," said Dr. Andreas Vitalis to KUNA.
Dr. Vitalis said that more than half of all cases of dementia in the elderly can be attributed to Alzheimer's disease, adding that despite vast research efforts; an effective therapy has not been developed, and treatment consists of dealing with the symptoms.
He noted that changes in brain tissues are a hallmark of Alzheimer's. In affected individuals, small protein fragments known as amyloid beta peptides accumulate and are deposited in the gray brain matter, said Dr.Vitalis.
Researchers recently identified a series of synthetic compounds (inhibitors) that interfere with the self-assembly of the amyloid beta peptide in vitro; they influence both early stages and the transition to the characteristic amyloid fibrils.
On a theoretical level, these compounds thus satisfy an initial condition for the development of an Alzheimer drug.
In order to understand the interactions between the amyloid beta peptide and active compounds at a structural level, Marino Convertino, Andreas Vitalis, and Amedeo Caflisch from the University of Zurich's Department of Biochemistry simulated these interactions on the computer.
"In doing so, we focused on a fragment of the peptide that is thought to control both interactions with inhibitors and progression of disease," Dr.
Vitalis explained to KUNA.
Based on these simulations, the biochemists were able to identify a hierarchy of interaction patterns between the peptide and various active compounds. To their surprise, they discovered that the disordered structure of the peptide controls the interactions.
"The peptide's disorder and flexibility enable it to adapt to many basic structural frameworks," Dr.Vitalis explained.
Often it is only subparts of the molecules that mediate interactions on the compound side. However, even minimal changes to a compound may induce measurable changes to the peptide-compound interactions.
"Design of active compounds that influence the amyloid beta peptide structurally in a specific manner will only be possible with the aid of high-resolution methods that are limited to one or a few molecules," concludes Vitalis.
In the next step, the researchers from the University of Zurich want to identify new classes of active substances with controllable properties that interact with the amyloid beta peptide
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ENEVA,(KUNA) -- Based on computer simulations, biochemists from the University of Zurich in Switzerland have shown on Tuesday shown how the active compounds and fragments of the peptide, that causes Alzheimer disease, interact with each other and found that it is the disordered structure of the peptide that determines the interactions with active compounds.
"Various molecules have been synthesized that inhibit self-assembly of the amyloid beta peptide in vitro. This peptide is strongly linked to Alzheimer's disease," said Dr. Andreas Vitalis to KUNA.
Dr. Vitalis said that more than half of all cases of dementia in the elderly can be attributed to Alzheimer's disease, adding that despite vast research efforts; an effective therapy has not been developed, and treatment consists of dealing with the symptoms.
He noted that changes in brain tissues are a hallmark of Alzheimer's. In affected individuals, small protein fragments known as amyloid beta peptides accumulate and are deposited in the gray brain matter, said Dr.Vitalis.
Researchers recently identified a series of synthetic compounds (inhibitors) that interfere with the self-assembly of the amyloid beta peptide in vitro; they influence both early stages and the transition to the characteristic amyloid fibrils.
On a theoretical level, these compounds thus satisfy an initial condition for the development of an Alzheimer drug.
In order to understand the interactions between the amyloid beta peptide and active compounds at a structural level, Marino Convertino, Andreas Vitalis, and Amedeo Caflisch from the University of Zurich's Department of Biochemistry simulated these interactions on the computer.
"In doing so, we focused on a fragment of the peptide that is thought to control both interactions with inhibitors and progression of disease," Dr.
Vitalis explained to KUNA.
Based on these simulations, the biochemists were able to identify a hierarchy of interaction patterns between the peptide and various active compounds. To their surprise, they discovered that the disordered structure of the peptide controls the interactions.
"The peptide's disorder and flexibility enable it to adapt to many basic structural frameworks," Dr.Vitalis explained.
Often it is only subparts of the molecules that mediate interactions on the compound side. However, even minimal changes to a compound may induce measurable changes to the peptide-compound interactions.
"Design of active compounds that influence the amyloid beta peptide structurally in a specific manner will only be possible with the aid of high-resolution methods that are limited to one or a few molecules," concludes Vitalis.
In the next step, the researchers from the University of Zurich want to identify new classes of active substances with controllable properties that interact with the amyloid beta peptide
Thursday, February 2, 2012
Study adds piece to the Alzheimer's puzzle
Here is a great dementia resource for caregivers and healthcare professionals,
You will love the Amazon Kindle Fire
Here is information on being the best caregiver you can be
Here is a way for nurses administrators, social workers and other health care professionals to get an easyceu or two
Follow Alzheimers1 on twitter
Toronto Sun
CALGARY - Research out of the University of Calgary has endeavoured to further explain why brain cells in Alzheimer's disease patients die.
The study by scientists at the U of C's Hotchkiss Brain Institute shows the cells are being killed off as the result of a malfunctioning neurotransmitter receptor called NMDA, which is responsible for memory and learning.
It had previously been shown a malformed protein exists in Alzheimer's disease patients' brains. The recent study used animal models to show a new mechanism of how the protein kills cells.
Dr. Gerald Zamponi and Dr. Peter Stys found the NMDA receptor is strongly regulated by copper, and if copper is prevented from regulating it — as it is in Alzheimer's disease— the cells are over-stimulated and eventually die.
The malformed protein is believed to steal copper from the NMDA receptor, causing the cell deaths.
Zamponi said the discovery may open doors for the development of treatments for the neurodegenerative disease.
"We think we can design drugs that restore the normal function of the receptor, therefore protecting brain cells," he said. "It really gives you a new insight into a mechanism and really lays out a road map for developing new therapeutics."
"Ultimately, we are seeing an underlying deficiency in copper, but at a sub-cellular level,” added Stys. "Unfortunately, because of the way that the body regulates copper, we can't simply eat more of a certain kind of food or take a copper supplement to compensate.
"What we are looking at now is the development of a drug that acts on the NMDA receptor to mimic the effect of copper in the brain."
Bill Gaudette, CEO of the Alzheimer Society of Alberta and the Northwest Territories, said the results of the study are very promising.
"Finding a cure for Alzheimer's disease and dementia is really like a puzzle and this is one of the pieces in that jigsaw puzzle," he said.
There are over 5.4 million Americans with Alzheimer’s disease or related dementia, according to the Alzheimer's Association.
jenna.mcmurray@sunmedia.ca
You will love the Amazon Kindle Fire
Here is information on being the best caregiver you can be
Here is a way for nurses administrators, social workers and other health care professionals to get an easyceu or two
Follow Alzheimers1 on twitter
Toronto Sun
CALGARY - Research out of the University of Calgary has endeavoured to further explain why brain cells in Alzheimer's disease patients die.
The study by scientists at the U of C's Hotchkiss Brain Institute shows the cells are being killed off as the result of a malfunctioning neurotransmitter receptor called NMDA, which is responsible for memory and learning.
It had previously been shown a malformed protein exists in Alzheimer's disease patients' brains. The recent study used animal models to show a new mechanism of how the protein kills cells.
Dr. Gerald Zamponi and Dr. Peter Stys found the NMDA receptor is strongly regulated by copper, and if copper is prevented from regulating it — as it is in Alzheimer's disease— the cells are over-stimulated and eventually die.
The malformed protein is believed to steal copper from the NMDA receptor, causing the cell deaths.
Zamponi said the discovery may open doors for the development of treatments for the neurodegenerative disease.
"We think we can design drugs that restore the normal function of the receptor, therefore protecting brain cells," he said. "It really gives you a new insight into a mechanism and really lays out a road map for developing new therapeutics."
"Ultimately, we are seeing an underlying deficiency in copper, but at a sub-cellular level,” added Stys. "Unfortunately, because of the way that the body regulates copper, we can't simply eat more of a certain kind of food or take a copper supplement to compensate.
"What we are looking at now is the development of a drug that acts on the NMDA receptor to mimic the effect of copper in the brain."
Bill Gaudette, CEO of the Alzheimer Society of Alberta and the Northwest Territories, said the results of the study are very promising.
"Finding a cure for Alzheimer's disease and dementia is really like a puzzle and this is one of the pieces in that jigsaw puzzle," he said.
There are over 5.4 million Americans with Alzheimer’s disease or related dementia, according to the Alzheimer's Association.
jenna.mcmurray@sunmedia.ca
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