Vascular System Changes May Trigger Alzheimer’s disease

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Neuroscience News

Summary: Researchers report a plasma component that is usually involved in blood clotting and inflammation may also play a role in the development of Alzheimer’s disease.

Source: Rockefeller University.

As the average age of Americans increases, so too does the problem of Alzheimer’s, one of the world’s most common neurological diseases. In recent years, scientists have explored many new approaches to clear the plaques and tangles in the brain that characterize the condition, but the new drugs have largely turned out to be disappointing.

A team of Rockefeller scientists is now using a fresh approach to look at biological processes that occur in the development of Alzheimer’s disease (AD). Somewhat unexpectedly, they have found that a plasma component normally involved in blood clotting and inflammation may also be part of the problem in some patients.

This isn’t the first time the condition has been linked to the vascular system. “There’s a lot of evidence that exercise, which helps keep your blood vessels healthy and blood flow consistent, can be protective against AD,” says Sidney Strickland, head of the Patricia and John Rosenwald Laboratory of Neurobiology and Genetics. “In addition, we know that diseases that compromise the vascular system, like diabetes, put people at higher risk.”

Yet it’s still not clear precisely how changes in the blood might spur Alzheimer’s. The latest study from Strickland’s lab, published recently in the journal Blood, offers a clue and a possible path to early diagnosis and new drugs.

Exploring the link

The plasma protein, called Factor XII, is part of a cascade of enzymes that induces blood coagulation and inflammation. Previous studies from Strickland’s lab had shown that this cascade can be activated by beta-amyloid, a molecule that forms sticky plaques in the brains of Alzheimer’s patients. Other research had demonstrated that the process might be overly active in the disease.

Because people with AD don’t show cognitive problems until their disease is quite advanced, it’s been difficult to study what’s transpiring in the brain at the earlier stages. But in recent years, genes linked to an early-onset hereditary form of the disease have been found, and researchers have been able to study what’s happening in the brains of people genetically predetermined to develop Alzheimer’s, even before they show any symptoms.

“It’s a devastating disease to have,” Strickland says about this inherited form of AD, “but it’s given us new research opportunities. The first changes observed in these patients are in beta-amyloid levels. The second changes are brain abnormalities related to the vascular system, which can occur 20 years before overt cognitive symptoms appear.”

“We speculated that activation of Factor XII by beta-amyloid could play a role in initiating Alzheimer’s,” says Zu-Lin Chen, a senior research associate in the Strickland lab. “That’s not something you can study in humans, so we looked at mouse models of disease to see what happens when Factor XII is knocked down.”

Exploring results in mice

To take out Factor XII, the team used a molecule that prevented the gene from making the protein. Normally, AD mice show much greater brain inflammation than healthy mice. However, AD mice whose Factor XII had been knocked down had much less inflammation than untreated AD mice and had brains that were more similar to those of healthy mice.

The brain of a mouse with Alzheimer’s disease is infiltrated with inflammatory cells, which light up in red when activated (left). These cells become less active when Factor XII is removed (right). NeuroscienceNews.com image is credited to Laboratory of Neurobiology and Genetics at The Rockefeller University/Blood.

In addition, behavioral studies of AD mice with reduced Factor XII showed that their cognitive function improved. In one test, the mice were introduced to a maze with an escape hole. The animals learn the location of the hole by remembering visual cues around the maze, allowing them to escape through the hole on subsequent visits. Unlike normal mice, AD mice are unable to remember where the hole was located.

Knocking down Factor XII helped: AD mice lacking the protein learned to find their way quicker than the untreated AD mice, although their memory wasn’t as good as that of normal mice.

These and other findings in the study point to one potential factor in initiating AD, though the researchers caution they may not lead to new drugs anytime soon. “We need to further define what’s going on, so we can identify patients with vascular problems and develop a targeted therapy to help that aspect,” Chen says. “We had great improvements in our mice but we didn’t fully correct the problem. Alzheimer’s is a complex disease, and there are multiple elements involved.”

“Our work contributes to the increasing evidence that vascular abnormalities are playing an important role in cognitive decline and inflammation in some AD patients,” Strickland concludes. “The hope is that defining the vascular mechanisms involved will allow for better diagnosis and eventually new treatments. Each step forward is a step closer to understanding this terrible disease.”

ABOUT THIS ALZHEIMER’S DISEASE RESEARCH ARTICLE

Source: Katherine Fenz – Rockefeller University 

New hope for dementia sufferers

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The Dementia Caregiver's Little Book of Hope [Kindle Edition

Medical Xpress

Researchers are investigating new ways to treat Alzheimer's disease by targeting the blood-brain barrier 

—Research that aims to rid dementia sufferers' brains of toxins could lead to a new treatment that reverses the symptoms of Alzheimer's disease in the future.

Researchers are investigating new ways to treat Alzheimer's by targeting the blood-brain barrier, which acts as a door to the brain, and is responsible for pumping toxins in the blood away from the brain. Dr Joseph Nicolazzo, from the Monash Institute of Pharmaceutical Sciences, in collaboration with the University of Washington, is examining pumps at the blood-brain barrier that are known to become dysfunctional in Alzheimer's patients. This diminished pumping action is believed to result in a build-up of the toxin amyloid in the brain, killing nerve cells and leading to memory loss associated with Alzheimer's. The researchers are investigating how to get the pumps working again, to safely filter toxins out of the brain. 

"Alzheimer's is the most common form of dementia affecting 300,000 Australians and 5.4 million Americans," Dr Nicolazzo said. "While there are medications that can assist with memory, there is currently no cure that can reverse the disease. "We hope that unravelling how to get the pumps working again to decrease amyloid build-up in the brain will lead to new drugs that may cure Alzheimer's disease."

Atypical psychotics may hasten dementia decline (part 2)

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Medscape Today
Deborah Brauser

great deal of care," said Dr. Schneider.

He added that the meta-analysis showing a link between atypical antipsychotics and increased mortality risk in an elderly population with dementia helped support the Food and Drug Administration's (FDA's) subsequent black box warning in 2005.

A recent study published in the Archives of General Psychiatry and reported by Medscape Medical News at that timeshowed use of atypicals to treat behavioral symptoms has decreased significantly since the FDA warning was issued. However, other studies have shown that the overall prescription rate has not decreased ( Arch Intern Med. 2010;170:89-95 and CMAJ. 2008;179:438-446).

In the current study, investigators evaluated data on the 421 outpatients with AD and psychosis or aggressive behavior from CATIE-AD, which was conducted at 45 sites in the United States between April 2001 and November 2004.

Significant Decline

During the first phase of the trial all participants were randomized to receive flexible doses of either olanzapine (n = 100; mean dose, 5.5 mg/day), quetiapine (n = 94; mean dose, 56.5 mg/day), risperidone (n = 85; mean dose, 1.0 mg/day), or placebo (n = 142).

After 2 weeks, they could discontinue their allocated treatment and switch to another randomly assigned medication, on their clinicians' request. If they discontinued use of that medication, patients could move into phase 3 of the study, which consisted of open-label treatment with one of the other randomly assigned study drugs.

"At any time, the clinician could choose to enter the patient into phase 4, where data collection continued but the physician prescribed medication," explain the researchers.

The subjects were followed up for 9 months and scheduled to undergo cognitive assessments at the 12-, 24-, and 36-week timepoints. This new analysis assessed the 357 patients (54% male; mean age, 77.6 years) who participated in at least 1 baseline and 1 follow-up cognitive measure.

Measurements included the Mini-Mental State Examination (MMSE), the cognitive subscales of the AD Assessment Scale (ADAS-Cog) and of the Brief Psychiatric Rating Scale (BPRS), a cognitive summary score that combined changes on 18 cognitive tests, and the Clinical Global Impression of Change (CGIC).

Results showed that at 36-week follow-up all of the patients had declined significantly in most cognitive areas, including worsening scores on the MMSE (−2.4 points) and ADAS-Cog (−4.4 points).

The only statistically significant difference between individual antipsychotic groups and the placebo group were greater cognitive decline in the following:

•the cognition summary for those taking olanzapine or risperidone (P = .04 and P = .001, respectively);
•the MMSE for those taking olanzapine (P = .05); and
•BPRS for those taking quetiapine (P = .05).
When all 3 atypical groups were combined, participants' cognitive function decreased significantly more than their counterparts who were taking placebo on the MMSE (P = .004), BPRS (P = .05), and cognitive summary (P = .004).

"Over the 36-week trial period, patients receiving any antipsychotic had an average decline 2.46 points greater on the MMSE than placebo patients, a difference both statistically significant and clinically relevant," write the researchers.

The average CGIC scores for all 4 groups indicated minimal improvement and did not differ significantly (placebo, 3.13; olanzapine, 3.11; quetiapine, 2.83; risperidone, 2.81).

Permanent Effect?

"Because we did not measure differences in the rates of cognitive decline over longer exposure periods, we cannot address the question of whether these drugs would accelerate [the] decline permanently or merely impair cognition during acute administration," the investigators write.

They note that they also do not know whether the decrease in cognition was due to a worsening of Alzheimer's pathology or if it was an independent effect.

Much of medication use is due to the lack of interest, willingness, funding, or ability to provide psychosocial or environmental interventions to patients with agitation, aggression, and psychosis who have dementia.
Although the investigators write that the declines found in this study reached "at least as great a magnitude as the effect of cholinesterase inhibitors but in the negative direction," they add that use of atypicals may still be warranted in individual cases.

"The relative adverse effects on cognitive function within the class of medication need to be addressed in further studies that include assessment of attention, psychomotor function, and executive function," they write.

Dr. Schneider noted that nonpharmacologic treatments should also be investigated.

"Much of medication use is due to the lack of interest, willingness, funding, or ability to provide psychosocial or environmental interventions to patients with agitation, aggression, and psychosis who have dementia."

He explained that much agitation can be redirected and that aggression often comes about due to cognitive impairment — and can be mitigated by the way caregivers react to or communicate with patients.

"These approaches have limits too, but certainly they are not applied enough because they involve significant amounts of time and training," said Dr. Schneider.

Few Alternative Treatments

"Risk-benefit analysis is always part of the decision to use psychotropic medication. The aged are a particularly vulnerable group, and this study strongly underscores that vulnerability," write D. P. Devanand, MD, from the Division of Geriatric Psychiatry at the College of Physicians and Surgeons at Columbia University in New York City, and Susan K. Schultz, MD, from the Department of Psychiatry at the University of Iowa College of Medicine in Iowa City, in an accompanying editorial.

"Neuropsychological testing across a range of domains in this study offers a powerful look at the progression of AD in the context of treating neuropsychiatric symptoms," they add.

However, they caution that several caveats should be considered "when interpreting the findings and their potential impact on clinical practice," including that the investigators had to combine the 3 treatment groups to find statistical differences from placebo on the MMSE and the summary scores.

"It is likely that individual vulnerabilities to specific antipsychotics are mediated by a variety of factors, including concomitant medications, medical comorbidity, and underlying frailty, that are beyond the scope of this analysis."

Despite the widespread awareness of adverse consequences, we can only infer that atypical antipsychotics continue to be prescribed for dementia treatment because there is a lack of alternatives and there is a perceived clinical benefit by care providers.
In addition, the editorialists note that "while dose effects were not addressed in this analysis, adverse events in this population are dose related, and treatment dropouts occur more frequently with risperidone doses above 2 mg and olanzapine doses above 5 mg."

Other concerns cited include that data for any patient receiving an antipsychotic for at least 2 weeks was included, whether they had switched medications or not, which may result in short-term harmful effects that may not continue with longer treatment exposure.

Dr. Devanand and Dr. Schultz note that alternative pharmacologic treatments, such as benzodiazepines, also provide risky cognitive liabilities.

"Despite the widespread awareness of adverse consequences, we can only infer that atypical antipsychotics continue to be prescribed for dementia treatment because there is a lack of alternatives and there is a perceived clinical benefit by care providers," they write.

"These complex issues will require a thoughtful and balanced evaluation with an appreciation of the care setting, individual patient vulnerabilities, and goals of care."

The study was supported by the National Institute of Mental Health, the USC Alzheimer's Disease Research Center, and the Department of Veterans Affairs. Medications were provided by AstraZeneca, Forest, Janssen, and Eli Lilly. The study authors report several disclosures, which are listed in the original article. The editorialists report having received research support from Eli Lilly and Novartis and are currently consultants for Bristol-Myers Squibb and Sanofi-Aventis.

Alzheimer's disease research advances

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ScienceDaily Advances in research into Alzheimer's disease: transporter proteins at the blood CSF barrier and vitamin D may help prevent amyloid β build up in the brain.

Advancing age is a major risk factor for Alzheimer's disease and is associated with build- up of the peptide amyloid β in the brain. New research published in BioMed Central's open access journal Fluids and Barriers of the CNS shows that removal of amyloid β from the brain depends on vitamin D and also on an age-related alteration in the production of transporter proteins which move amyloid β in and out of the brain.

Low levels of vitamin D are thought to be involved in age-related decline in memory and cognition and are also associated with Alzheimer's disease. Researchers from Tohoku University, Japan, looked at the mechanism behind this and found that vitamin D injections improved the removal of amyloid β from the brain of mice.

Prof Tetsuya Terasaki said, "Vitamin D appears increase transport of amyloid β across the blood brain barrier (BBB) by regulating protein expression, via the vitamin D receptor, and also by regulating cell signaling via the MEK pathway. These results lead the way towards new therapeutic targets in the search for prevention of Alzheimer's disease."

The transport of amyloid β across the BBB is known to be orchestrated by transporter proteins such as LRP-1 and P-gp, which move amyloid β out of the brain, and RAGE, which controls influx. Looking at the transport of amyloid β from blood to cerebrospinal fluid (CSF), and from CSF to blood, researchers from Rhode Island Hospital and The Warren Alpert Medical School, found that , and P-gp at the blood-cerebrospinal fluid barrier (BCSFB), increased with age so increasing removal of amyloid β from the CSF and brain.

Prof Gerald Silverberg said, "While increased production of transporter proteins at the blood CSF barrier may help amyloid β removal from the older brain, production of these proteins eventually fails. This failure may be an important event in brain function as we age and for people with Alzheimer's disease."

Alzheimer's disease may start in youth

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By Shari Roan, Los Angeles Times

Alzheimer's disease research has shifted to looking for the earliest signs and symptoms of the disease process. A new study has found evidence of early brain damage in some young people at increased risk for the disease.

Researchers led by Dr. Paul Thompson, a UCLA professor of neurology, conducted brain scans on 398 young, healthy people ages 20 to 30. Those participants who carried a particular gene mutation that is known to raise the risk of Alzheimer's -- linked to the CLU gene -- had unique characteristics in white matter (the bundles of nerve cells) in multiple brain regions, including in some areas known to become damaged in Alzheimer's disease. The findings suggest that changes in myelin, the substance that protects nerve cells, may be a sign of increased risk of developing the disease later in life.

"Alzheimer's has traditionally been considered a disease marked by neuronal cell loss and widespread gray matter atrophy," Thompson said in a news release. "But degeneration of myelin in white matter fiber pathways is more and more being considered a key disease component and another possible pathway to the disease, and this discovery supports that."

People who have this particular mutation in the CLU -- which is common -- aren't doomed to develop Alzheimer's disease, the authors noted. And young people who have these changes in white matter are not cognitively impaired. But knowledge about this genetic risk could be used to help prevent the disease later in life, the authors said.

The study was published online last week in the Journal of Neuroscience.

Latest Research Shows Alzheimer's Protein Disrupts Normal Brain Cell Function

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AC Content

Scientists at the University of South Florida said that it was determined that a protein associated with Alzheimer's disease clogs some of the motors needed for cell transport. The experiments were conducted using human cell cultures and frog egg extracts. This finding was part of a new study at Byrd Alzheimer's Institute which is Florida's Alzheimer's Disease Research Center. This finding was also reported at Indiana University. This information was published in the journal Cell Cycle online.

This protein called beta amyloid seems to interfere with the normal division of the cells in the brain. The build up of beta amyloid leads to defective neurons (nerve cells in the brain). The defective neurons contribute directly to the memory loss that is found in Alzheimer's disease. As more beta amyloid builds up more neurons are affected and this most likely causes the memory loss seen in Alzheimer's disease to progress. The scientists conducting the study feel that by identifying a new and important target of the beta amyloid protein, drugs can be developed to protect the motors from destruction and allow the brain to regenerate.

This latest study adds to earlier research done by Dr. Huntington Potter, professor of Molecular Medicine, lead investigator and those working with him. Their earlier research showed that the beta amyloid protein was the culprit that damages the transport system responsible for moving nutrients in the brain cells. The microtubules are important in separating newly duplicated chromosomes as cells divide. When the duplicated chromosomes do not segregate properly, they can create cells with the incorrect number and incorrect mixture of genes.

Over 20 years ago, Potter stated the idea that read all of Latest Research Shows Alzheimer's Protein Disrupts Normal Brain Cell Function

Is your brain shrinking

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Reuters

If your brain is shrinking, you are probably three times as likely to develop Alzheimer's disease in the mext ten years.

This finding was published in the journal Neurology. Also this discovery may offer a new way to detect the disease early. This advance could help in the development of effective treatments for Alzheimer's disease which affects at least 26 million people world wide.

"The magnetic resonance measurements could be very important indicators to help identify who may be at risk of developing Alzheimer's dementia," Leyla deToledo-Morrell of Rush University Medical Center in Chicago, who worked on the study, said in a statement.

"If a drug therapy or treatment is developed in the future, those who are still without symptoms but at great risk would benefit the most from treatment," deToledo-Morrell said.

The study involved two groups of healthy people in their 70s who had brain scans at Rush University in Chicago and at Massachusetts General Hospital/Harvard Medical School in Boston and were followed for an average of nine years.

During the study, 50 participants remained cognitively normal and 15 developed Alzheimer's disease.

At the end of the study, people who had the highest amount of shrinkage in specific areas of the cerebral cortex were three times more likely to develop the disease.

"We also found that those who express this MRI marker of the Alzheimer's disease in the brain were three times more likely to develop dementia over the following 10 years than those with higher measurements," Dr. Brad Dickerson of Massachusetts General, who led the study, said in a statement.

"These are preliminary results that are not ready to be applied outside of research studies right now, but we are optimistic that this marker will be useful in the future," he said.

Researchers in the study used magnetic resonance imaging or MRI, equipment that is already in wide use in most hospitals.

Eli Lilly and Co, General Electric and other companies are developing special imaging agents that can detect proteins in the brain that signal the presence of Alzheimer's disease-related proteins.

But these tests read all of Is your brain shrinking

Could Alzheimer's Disease Start in the Liver

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AC Content

Up until this point, it was thought that beta amyloid was made in the brain

A new study lead by research professor, Greg Sutcliffe, suggests that beta amyloid might... read all of Could Alzheimer's Disease Start in the Liver

Researchers Discover How Alzheimer's Disease Kills Brain Cells

EMaxHealth

Submitted by Kathleen Blanchard RN
Posted under: Alzheimer's Disease
Until now, scientists have been uncertain exactly how Alzheimer’s disease kills brain cells, causing debate among researchers. The results of a new study show how amyloid plaques, found in the brain of Alzheimer’s patients, cause brain cells to die.

Researchers from University of Michigan and the University of California, San Diego were able to observe spikes in electrical currents across artificial cell membranes and in the membranes of live human cancer cells in the presence of the amyloid-beta peptide. What that told the scientists is that amyloid peptides poke holes in the cell membranes, allowing influx of calcium. Prior to the current research, it was believed that amyloid peptides thinned the cell membranes, producing calcium ion fluctuations. When ions become imbalanced, cell death results.

The researchers say that controversy about how Alzheimer’s disease kills brain cells has been a hindrance to developing new drugs. Michael Mayer, an assistant professor in the U-M departments of Biomedical Engineering and Chemical Engineering says, “It is our hope that putting this disagreement to rest by showing that amyloid beta peptides do not thin membranes but instead form discrete pores in membrane can help the field move forward at a more rapid pace."

Mayer explains how his team was able to........read the whole article

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Alzheimer's gene 'linked to Vitamin D'

Telegraph.com
Scientists have found a new Alzheimer's gene they believe could affect how our bodies use a vital vitamin.

By Kate Devlin, Medical Correspondent
Researchers hope that the breakthrough could one day lead to new treatments for the devastating neurological condition.

They believe that the gene could be connected to how the brain uses vitamin D, a lack of which has been linked to memory problems.

Scientists have previously found that the onset of the devastating condition was linked to the apolipoprotein E gene.

However, this is a "weak" gene, whose influence would not be enough to cause the illness.

The study looked at the genes of 492 patients who suffered from Alzheimer's disease and compared these to genes from 498 people who did not have the condition.

The analysis was detailed enough to identify single variants within DNA cells which are more common in patients with Alzheimer's.

The variation is close to the gene which uses vitamin D in the brain and has previously been linked to memory, the findings, published in the American Journal of Human Genetics, show.

"It is possible that (this variation) is in a region that may play some sort of regulatory role (with......read the whole story

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Scientist uses reprogrammed cells to study Alzheimer’s

JS ONLINE: NEWS: WISCONSIN:
By MARK JOHNSON
Madison - Ten months after scientists in Madison and Japan reprogrammed human skin cells back to an embryonic state, Lawrence Goldstein of the University of California-San Diego is collecting skin samples from patients with Alzheimer's disease and hoping the new technique will offer a unique window into the disease.

Previously, scientists often had to rely on animal models to research a disease such as Alzheimer’s.

“We have worn out what we can do with animal models,” Goldstein told the World Stem Cell Summit on Monday.

Goldstein’s work is part of a surge of stem cell research in the past year. But the new work has been accompanied by mounting expectations almost 10 years after James Thomson isolated the first human embryonic stem cells.

Now scientists can...read the whole article

Expression of CD74 is increased in neurofibrillary tangles in Alzheimer's disease

7thSpaceInteractive

Alzheimer disease (AD) is a chronic neurodegenerative disease that is characterized by progressive memory loss. Pathological markers of AD include neurofibrillary tangles, accumulation of amyloid-beta plaques, neuronal loss, and inflammation.

The exact events that lead to the neuronal dysfunction and loss are not completely understood. However, pro-inflammatory cytokines, such as interleukin-1beta, interleukin-6, and tumor necrosis factor alpha, are increased in AD, along with gene expression of major histocompatibility complex (MHC) class II molecules and macrophage migration inhibitory factor (MIF).

MHC class II molecules are found in microglia of the brain, while MIF is found in both microglia and neurons of the hypothalamus, hippocampus, and cortex. MIF is not only a lymphocyte mediator but also a pituitary factor with endocrine properties and can mediate phosphorylation of the extracellular signal-regulated kinase-1/2 MAP kinases pathway.

In this study, we looked at CD74, an integral membrane protein that acts....read the whole article
I realize it is a little technical. Perhaps it will give you some idea of what we are dealing with

New project uses nanoparticles to tackle Alzheimer's disease

CordisNews
A new EU-funded project is exploring the use of nanoparticles in the diagnosis and treatment of Alzheimer's disease. The five-year NAD ('Nanoparticles for the therapy and diagnosis of Alzheimer's disease') initiative has a budget of €14.6 million and is financed by the EU's Seventh Framework Programme (FP7). It brings together researchers from a variety of disciplines working in 19 organisations in 13 countries.

Alzheimer's disease is the most common form of dementia: of Europe's five million dementia sufferers, over half have a diagnosis of Alzheimer's. These figures are likely to rise dramatically as the population ages. The condition is caused by the accumulation in the brain of plaques made up of beta-amyloid peptide molecules. These plaques cause the nerve cells to degenerate.

Symptoms of Alzheimer's include confusion, memory loss and mood swings. As yet, there is no cure for the condition, although some drugs exist that are able to slow the progression of the disease in some patients.

'Somewhere in the world there is a new case of dementia diagnosed every seven seconds. The majority of these people are suffering from Alzheimer's disease,' said Professor David Allsop of Lancaster University in the UK, one of the project partners. 'But despite great progress in the scientific field, which has made interpretation of the molecular bases of the disease possible, so far there has been little progress in improved diagnosis and therapy.'

The NAD project will design a range of nanoparticles that are...Read the whole article

Blood Marker Predicts Alzheimer's

By Daniel J. DeNoon
WebMD Health News
Reviewed by Louise Chang, MD
High blood levels of a plaque peptide may predict Alzheimer's disease in elderly people.

The finding comes from a study of 1,125 people who were in their late 70s when their blood was first tested. Four and a half years later, 104 of them had Alzheimer's disease.

Those with the highest blood levels of A-beta 42, a major component of the plaque that clogs the brains of Alzheimer's patients, were far more likely to get Alzheimer's than were those with the lowest A-beta 42 levels.

"Compared with individuals with low [blood] A-beta 42 levels at baseline, those with high A-beta 42 levels had more than a threefold increased risk of developing Alzheimer's disease over an average of...read the whole article

Fatal Protein Interactions May Explain Neurological Diseases

ScienceDaily (Sep. 3, 2008) — In a collaborative study at the University of California, San Diego, investigators from neurosciences, chemistry and medicine, as well as the San Diego Supercomputer Center (SDSC) have investigated how proteins involved in neurodegenerative diseases such as Alzheimer's and Parkinson's disease interact to form unique complexes. Their findings explain why Alzheimer's patients might develop Parkinson's, and vice versa.

The new and unique molecular structures they discovered can now be used to model and develop new drugs for these devastating neurological diseases. Their findings will be published in the September 3 issue of Public....

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Brain injury study adds to Alzheimer's enigma

CHICAGO (Reuters) – Levels of a protein linked with Alzheimer's disease rise as people recover from brain injuries – a surprising finding that may help explain why injuries boost the risk of developing the disease, U.S. and Italian researchers said on Thursday. Researchers at Washington University in St. Louis and the University of Milan did hour-by-hour measurements of the protein amyloid beta in 18 patients with severe brain injury as they were coming out of a coma

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Einstein researchers find a way to get rid of damaged proteins of Alzheimer's and other dementias

BRONX, NY)
As people age, their cells become less efficient at getting rid of damaged protein — resulting in a buildup of toxic material that is especially pronounced in Alzheimer's, other dementias, Parkinson's disease, and other neurodegenerative disorders.

Now, for the first time, scientists at the Albert Einstein College of Medicine of Yeshiva University have prevented this age-related decline in an entire organ — the liver — and shown that, as a result, the livers of older animals functioned as well as they did when the animals were much younger. Published in the online edition of Nature Medicine....

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When it comes to Alzheimer's, brain size does matter

WMAQ NBC5 TV Chicago

Alzheimer's disease and related dementias usually shows up late in life, but researchers said that signs may appear decades in advance.

One of the signs could be poor school performance, University of South Florida researchers said.
The researchers based their conclusion on a study of nuns. Those who had a smaller head size were more likely to have had dementia or showed signs of Alzheimer's during an autopsy.

The people with smaller heads -- and, thus, it was assumed, smaller brains -- also were more likely to have done poorly in school.

A news release said that previous studies have found that Alzheimer’s disease is related to head size, with people having smaller heads more likely to show symptoms...
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Still no cure for Alzheimer's

August 7, 2008 - 9:54AM
Joy Slagowski
Daily News-Sun
Clinical trial results and presentations were the highlights of the Alzheimer's Association International Conference on Alzheimer's Disease last week in Chicago.
About eight key researchers with the Sun Health Research Institute in Sun City joined approximately 5,000 other scientists at the annual convention.
Dr. Joe Rogers, president and senior scientist at SHRI, said he contributed to a presentation with members of the Arizona Alzheimer's Consortium, and also was there to learn about other important clinical trial results.
"We presented new results from the Arizona investigators concerning the genetic risk factor for developing Alzheimer's disease," Rogers said. "From this we may be able to determine some day who will get Alzheimer's and who will not."
Rogers said the two clinical trial presentations produced mixed results.
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Oxidative Stress - An Emerging Approach to Fighting Alzheimer's and Related Dementias

Week of July 27 - August 2, 2008
Alzheimer's Weekly

Anavex is enthusiastic about its experimental medication that fights Alzheimer's andother dementias by battling oxidative stress.

A growing number of publications have supported the idea that oxidative stress may be the real cause of Alzheimer's. For example, in "Involvement of Oxidative Stress in Alzheimer's Disease," published in the Journal of Neuropathology and Experimental Neurology in 2006, study leader Dr. Akihiko Nunomura pointed to extensive evidence of mechanistic and chronological links between oxidative stress and a number of key characteristics of the disease.

Interestingly, this research also suggests that amyloid beta, which can act as an anti-oxidant, could in fact be initially produced by the body as it tries to combat the disease, only later turning toxic as the substance accumulates in large amounts. In other words, amyloid-beta could be the body's early protective reaction to the disease - suggesting that its removal from the brain during the early stages of Alzheimer's could in fact do more harm than good.

This theory is consistent with a number of factors for which the amyloid-beta hypothesis has been unable to account. There are reports, for instance, of individuals with amyloid-beta loads equivalent to Alzheimer's patients who do not suffer from the disease, as noted by R. J. Castellani et al in a 2006 article in the American Journal of Alzheimer's Disease and Other Dementias.

In addition, scientists have found a weak correlation between the amount of amyloid beta present in the brains of Alzheimer's sufferers and the severity of the illness. Furthermore, even though some test drugs reduce the amount of amyloid-beta in the brain, this is not correlated with substantial improvements in cognitive functioning.

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