Thursday, February 2, 2012

Study adds piece to the Alzheimer's puzzle

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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

Tuesday, January 31, 2012

Framework of the National Alzheimer's Plan is only the beginning

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Alzheimer's Association

The efforts and input of the Alzheimer's Association and our advocates were crucial to the passage of the National Alzheimer's Project Act (NAPA) and its upcoming implementation as the National Alzheimer's Plan. We still have much work ahead to ensure we build on the momentum to lead our country toward overcoming the Alzheimer's crisis. Lend your VOICE in the fight against Alzheimer's disease and attend the 2012 Alzheimer's Association Advocacy Forum, April 23-25, in Washington, D.C.

2012 Alzheimer's Association Advocacy Forum
Make your VOICE heard! Every story matters, every story counts.

Amplify your VOICE by joining us this year as we convene in our nation's capital on April 23-25, 2012 for the Alzheimer's Association Advocacy Forum.

Help build the national movement to end Alzheimer's by being educated about legislative issues; networking with advocates from across the nation to make our case loud and clear as we demonstrate the commitment to advancing our legislative agenda and a world without Alzheimer's disease.

Register Now

Sunday, January 29, 2012

Hope for dementia patients after Alzheimer's cells created in lab for first time Read more: http://www.dailymail.co.uk/health/article-2091716/Hope-dementia-patients-Alzheimers-cells-created-lab-time.html#ixzz1kWG64NIL

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Mail Online

Cells damaged by Alzheimer's created for first time
Hoped discovery will enable better understanding of dementia

By SADIE WHITELOCKS

Brain cells damaged by Alzheimer's have been created for the first time, offering hope to dementia patients.
It is believe that the breakthrough could help scientists better understand how the degenerative condition affects the the nervous system, prompting more effective treatment.
Alzheimer's is characterised by loss of neurons and synapses, leading to gradual memory loss and difficulties with language and emotions.

And until now investigations have been limited to 'non-neuronal human cells' or 'animal models'.
However a team from the University of California have developed a way of growing human cells.
Currently there is no cure for Alzheimer’s disease, but medication is available that can slow down its development.

More...
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The grandma who's a mum again at 53... despite the fact she was still taking the Pill just in case
During the research skin cells from two patients with a rare inherited form of Alzheimer's were taken and used to create neurons displaying biochemical hallmarks of the disease.
Lead researcher Professor Lawrence Goldstein, said: 'Creating highly purified and functional human Alzheimer's neurons in a dish - this has never been done before.
'It's a first step. These aren't perfect models. They're proof of concept. But now we know how to make them.
'It requires extraordinary care and diligence, really rigorous quality controls to induce consistent behaviour, but we can do it.'
Professsor Goldstein highlighted in the paper, published in the journal Nature, that differences between a healthy neuron and an Alzheimer's neuron are subtle.
But being able to grow Alzheimer's neurons will help scientists to better understand how the nervous system is impacted and which drugs would be most effective.
He added: 'We need to do everything we can because the cost of this disease is just too heavy and horrible to contemplate.
'Without solutions, it will bankrupt us - emotionally and financially.'
Further research is now underway.
He said: 'We're dealing with the human brain. You can't just do a biopsy on living patients.
'Instead, researchers have had to work around, mimicking some aspects of the disease in . Neither approach is really satisfactory.'
Alzheimer's disease is the most common form of dementia, which is a group of symptoms associated with a decline in mental abilities, such as memory and reasoning and is most common in people aged over 65.
It attacks nerves, brain cells and neurotransmitters (chemicals that carry messages to and from the brain).
Dementia affects around 5.4 million people in the US, with Alzheimer’s disease responsible for around 60 per cent of all cases.

Friday, January 27, 2012

More promising news on the Alzheimer's research front

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Follow Alzheimers1 on twitterVancover Sun

BY EVA FERGUSON, POSTMEDIA NEWS

CALGARY — A new study by researchers at the University of Calgary's Hotchkiss Brain Institute is challenging the conventional thinking about how brain cells die in Alzheimer's disease, and may one day lead to effective treatment for the memory-ravaging condition.

Researchers Peter Stys and Gerald Zamponi have shown that brain cells of Alzheimer's patients are dying because of malfunctions in key receptors known as NMDA receptors, which are critical for memory and learning.

"We've shown that the NMDA receptor functions improperly when there is too much alpha beta (a protein) around the ,NMDA receptor" says Zamponi, head of the university's department of physiology and pharmacology.

"So the key now is to find out how to reverse this, and find the right drug that regulates the NMDA receptor."

And by reversing that malfunction, scientists may one day be able to reverse the effects of Alzheimer's.

Zamponi says the University of Calgary is now working with the Centre for Drug Discovery Research and Development in Vancouver, screening hundreds of thousands of drugs to find one that is safe and successfully regulates NMDA.

It may take about two to three years to get to clinical trials, then another four to five years to complete them.

Gaudette says in all his years of working with Alzheimer's patients and their families, this is the most exciting discovery yet, calling it a potential "game changer" for everyone involved in dementia research and care.

"This offers hope. It's a ray of light for people who suffer from this terrible disease."

Alzheimer's disease destroys brain cells and results in memory loss, changes in mood and behaviour, and difficulty with day-to-day tasks.

While it is most commonly diagnosed in adults over the age of 65, more and more cases are being diagnosed in people in their 50s and sometimes even in their 40s.

"Ten years ago, that was unheard of. But we have better diagnoses, better awareness, and people feel more comfortable now getting a diagnosis."

Gaudette encourages anyone who may suspect they are showing symptoms of early onset to go to see their doctor because early diagnoses can lead to early intervention and drug therapy which can significantly slow down progression on the disease.

Zamponi and Stys' research was funded by Alberta Innovates-Health Solutions.

Wednesday, January 25, 2012

New strategies for treatment of disease of protein unfolding

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RxPG News


By Northwestern University, [RxPG] Two related studies from Northwestern University offer new strategies for tackling the challenges of preventing and treating diseases of protein folding, such as Alzheimer's, Parkinson's and Huntington's diseases, amyotrophic lateral sclerosis (ALS), cancer, cystic fibrosis and type 2 diabetes.

To do its job properly within the cell, a protein first must fold itself into the proper shape. If it doesn't, trouble can result. More than 300 diseases have at their root proteins that misfold, aggregate and eventually cause cellular dysfunction and death.

The new Northwestern research identifies new genes and pathways that prevent protein misfolding and toxic aggregation, keeping cells healthy, and also identifies small molecules with therapeutic potential that restore health to damaged cells, providing new targets for drug development.

The genetic screening study is published by the journal PLoS Genetics. The small molecule study is published by the journal Nature Chemical Biology.

"These discoveries are exciting because we have identified genes that keep us healthy and small molecules that keep us healthy," said Richard I. Morimoto, who led the research. "Future research should explain how these two important areas interact."

Morimoto is the Bill and Gayle Cook Professor of Biology in the department of molecular biosciences and the Rice Institute for Biomedical Research in Northwestern's Weinberg College of Arts and Sciences. He also is a scientific director of the Chicago Biomedical Consortium.

The genetic study reported in PLoS Genetics was conducted in the transparent roundworm C. elegans, which shares much of the same biology with humans. The small animal is a valued research tool because of this and also because its genome, or complete genetic sequence, is known.

In the work, Morimoto and his team tested all of the approximately 19,000 genes in C. elegans. They reduced expression of each gene one at a time and looked to see if the gene suppressed protein aggregation in the cell. Did the gene increase aggregation or lessen it or have no effect at all?

The researchers found 150 genes that did have an effect. They then conducted a series of tests and zeroed in on nine genes that made all proteins in the cell healthier. (These genes had a positive effect on a number of different proteins associated with different diseases.)

These nine genes define a core homeostastis network that protects the animal's proteome (the entire set of proteins expressed by the organism) from protein damage. "These are the most important genes," Morimoto said. "Figuring out how nine genes -- as opposed to 150 -- work is a manageable task."

In the Nature Chemical Biology study, Morimoto and his colleagues screened nearly one million small molecules in human tissue culture cells to identify those that restore the cell's ability to protect itself from protein damage.

They identified seven classes of compounds (based on chemical structure) that all enhance the cell's ability to make more protective molecular chaperones, which restore proper protein folding. The researchers call these compounds proteostasis regulators. They found that the compounds restored the health of the cell and resulted in reduction of protein aggregation and protection against misfolding. Consequently, health was restored when diseased animals were treated with the small molecules.

Morimoto and his team then conducted detailed molecular analyses of 30 promising small molecules, representing all seven classes. They discovered some compounds were much more effective than others.

"We don't yet know the detailed mechanisms of these small molecules, but we have identified some good drug targets for further development," Morimoto said.

Monday, January 23, 2012

Bingo! Boost thinking skills and keep your mind healthy

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Examiner

Florence McGinn

Lifelong learning’s active mantra of “Use it or lose it” is boosted by new, perception research done by researchers from Case Western Reserve University, Boston University, and Bridgewater State University. Those university-based perception researchers found high-contrast, large bingo cards boosted thinking and playing skills for people with cognitive difficulties and visual perception problems produced by Alzheimer’s disease and Parkinson’s disease.

Active interventions

With research-based knowledge, productive interventions unfold. The university researchers indicate interventions connected to their studies work to allow individuals with mild dementia and others with visual perception deficits to achieve benefits that facilitate their basic abilities to live independently longer, perform daily tasks, and enjoy life’s simple pleasures.
The research findings were reported in the article, “Bingo! Externally supported performance intervention for deficit visual search in normal aging, Parkinson’s disease, and Alzheimer’s disease,” in the journal Aging, Neuropsychology, and Cognition. Concerning beneficial interventions, the researchers wrote, “The general finding of improved performance across healthy and afflicted groups suggests the value of visual support as an easy-to-apply intervention to enhance cognitive performance.”

Exploration needed in understanding connections

As people age, they begin to lose sensitivity to perceive contrasts. The perception problem is exacerbated in people with dementia, according to Grover C. Gilmore, a psychologist and dean of the Mandel School of Applied Social Sciences at Case Western Reserve University.

But, Gilmore, who has done extensive testing in his Perception Lab at Case Western Reserve, indicates, “Little is known about how visual perception problems—common in aging players—affect the way these people think and play.” Gilmore and the study’s lead investigator, Alice Cronin-Golomb from Boston University, have collaborated for two decades on projects that look at visual sensory deficits and cognition among people with dementia. For example, in individuals with Parkinson’s disease, driving is affected by low contrasts as demonstrated in simulated fog situations.

Bingo becomes a research tool

Bingo is often used in nursing homes and senior centers as a social activity, and being socially engaged helps keep the mind healthy. However, Bingo, a popular activity in nursing homes, senior centers and assisted-living facilities, has benefits that extend well beyond socializing.

Perception researchers tested Bingo cards of different sizes, contrasts and visual complexities to find out how visual perception problems impact cognitive functions among the study’s participants: 19 younger adults, 14 individuals with probable Alzheimer’s Disease, 13 Alzheimer’s Disease matched healthy adults, 17 non-demented individuals with Parkinson’s disease and 20 Parkinson’s disease-matched healthy adults.

When study participants played Bingo on computer-generated cards that were manipulated for brightness, size and contrast, the researchers could compare the performance among the different age and health groups.

Benefits in those with mild dementia

With some contrast and size changes to the cards, researchers reported improvement in performances. For those with mild dementia, they could perform at levels of their healthy peers. However, little change was reported for people with more severe dementia.

Living environment interventions

Boosting contrast is among interventions known as Externally Supported Performance Interventions (ESPI). Gilmore and Alice Cronin-Golomb found that boosting contrast in the living environment and also at the table enables people with dementia—who have lost the ability to distinguish between similar-contrast objects—to move safely around their homes and improve their eating.

For example, putting a black sofa in a white room would improve the contrast of the room and make it easier for individuals to move about. Additionally, they found that individuals with dementia actually eat more if they use a white plate and tableware on a dark tablecloth or are served food that contrasts the color of the plate.

Critical research

As more of the world’s population ages and experience age-related issues and diseases, understanding of interventions that can maintain or build mental capacities are critical. Cognitive difficulties can prove to be the silent epidemic that robs an aging population of final years that are active, productive, and meaningful. All of society benefits when systemic, cognitive process insights work to help keep brains active and healthy.

Saturday, January 21, 2012

Alzheimer’s Disease: Managing Behavior Symptoms without Medication (part 2)

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EmpowHER

In the late stages of Alzheimer’s, patients often spend about half of their time at night awake and a significant part of their daylight hours sleeping.

In extreme cases, people may have a complete reversal of the typical nighttime sleep pattern.

Non-drug treatments seek to create a regular sleep routine, improve the sleeping environment and reduce daytime napping. Non-drug sleep strategies include eliminating alcohol, caffeine and/or nicotine, increasing morning sunlight exposure and encouraging regular exercise (more than four hours before bedtime).

In addition, regular mealtime, bedtime and waking time schedule creates a pattern for the body to emulate. Moreover, it’s suggested that the bed be used only for sleep. Therefore, if the person awakens, discourage him/her from staying in the bed while awake.

In addition, for some reason, television is associated with sleep irregularities for Alzheimer’s patients. Therefore, consider discouraging the person with Alzheimer’s from watching television while awake.

Sources:

Treatments for Sleep Changes. Web. www.alz.org. Accessed 09 Jan. 2012.

Treatments for Alzheimer’s Disease. Web. www. Alz.org. Accessed 09 Jan. 2012.

For Edge on Alzheimer’s, Testing Early Treatments. Web. www.nytimes.com. Accessed 09 Jan. 2012.

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