Blood test predicts progression of Alzheimer's

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Medical Xpress

A new study from Tel Aviv University suggests that early clues about the progression of the disease can be found in the metabolism of the brain, making it possible to detect and diagnose Alzheimer's at an early stage with a simple blood test.

When it comes to Alzheimer's disease, scientists usually—and understandably—look to the brain as their first center of attention. Now researchers at Tel Aviv University say that early clues regarding the progression of the disease can be found in the brain's metabolism. In very early stages of the disease, before any symptoms appear, metabolic processes are already beginning to change in the brain, says PhD candidate Shiri Stempler of TAU's Sackler Faculty of Medicine. Working with Profs. Eytan Ruppin and Lior Wolf of TAU's Blavatnik School of Computer Science, Stempler has developed predictor models that use metabolic information to pinpoint the progression of Alzheimer's. These models were 90 percent accurate in predicting the stage of the disease. Published in the journal Neurobiology of Aging, the research is the first step towards identifying biomarkers that may ensure better detection and analysis of the disease at an early stage, all with a simple blood test. It could also lead to novel therapies. "We hope that by studying metabolism, and the alterations to metabolism that occur in the very early stages of the disease, we can find new therapeutic strategies," adds Stempler. Interrupting a regulated process Metabolism describes a set of chemical reactions in cells which sustain life by controlling processes such as growth and reproduction. It is also responsible for providing energy to the body. To delve deeper into the connection between metabolism, brain functioning, and Alzheimer's disease, the researchers used data collected from the hippocampus region of the brain. Controlling memory and learning, this region of the brain is damaged as Alzheimer's progresses. Based on the number of metabolic genes found in the neurons and surrounding tissue, they built a predictive model which relates abnormalities in these genes to the progression of the disease. Out of almost 1500 genes, the researchers were able to select 50 genes that were the most predictive of Alzheimer's, says Stempler, noting that in Alzheimer's patients these genes are either over or under expressed, meaning that there are either too many or too few. Ads by Google 3 Early Signs of Dementia - Doctor: Know These 3 Warning Signs You're About to Suffer Dementia - www.newsmax.com Alzheimer's Directory - Alzheimer's Care for Every Need. Free Consult with Local Advisors. - Find.APlaceForMom.com When they compared the findings from these 50 genes among Alzheimer's patients, healthy patients, and primates (including chimpanzees and rhesus monkeys), the researchers discovered that in all but the Alzheimer's group, the number of the specific genes was tightly limited, with little difference in their number between individuals among each of the species, she explains. This implies that these genes are significant to normal brain functioning, and their strict regulation in healthy patients is compromised by Alzheimer's disease. Exploring new pathways Whether metabolic changes are a cause of the disease or merely a symptom remains a topic for future study. But the discovery of this connection is encouraging. "The correlation between metabolic gene expression and cognitive score in Alzheimer's patients is even higher than the correlation we see in medical literature between beta amyloid plaques – found in deposits in the brains of Alzheimer's patients – and cognitive score, pointing to a strong association between cognitive decline and an altered metabolism," Stempler says. Next the researchers will try to identify biomarkers in the blood that are associated with these metabolic changes. They may lead to detection and information about the disease's progression with an easy and non-invasive blood test. And as their work advances, Stempler hopes to develop therapeutic strategies that are based around these alterations in the metabolic network to help Alzheimer's patients, such as medications that can re-introduce strict regulation over gene expression. They believe that the research is a promising direction for Alzheimer's research. 

Journal reference: Neurobiology of Aging Provided by Tel Aviv University 

Sophisticated scan may spot seeds of Alzheimer's risk

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Steve Reinberg HealthDay news

Using an advanced MRI scan, researchers believe they have found changes in the chemistry of the brains of people with no cognitive problems that signal who is at future risk for Alzheimer's disease and other dementias.

And although there is no good treatment or cure for the disease, experts say finding ways to identify those at risk is essential when treatments and possibly a cure become available.

"We found biochemical changes that correlated with cognitive performance," said lead researcher Dr. Kejal Kantarci, a radiologist at Mayo Clinic in Rochester, Minn. "The better people did on tests that measure cognitive abilities, the fewer changes there were."

These biochemical changes were also associated with other changes in the brain that are markers for Alzheimer's disease, Kantarci said.

Kantarci said that people should not be looking at getting scans to detect these changes. "We are just at the early stages of identifying markers," she stressed.

However, finding these biomarkers is important, Kantarci added. "When possibilities for preventive intervention come about, then we will have a marker which will help us identify those individuals who would benefit from these preventive interventions," she said.

The report was published in the Aug. 24 online edition of Neurology.

For the study, Kantarci's group used a technique called proton magnetic resonance spectroscopy to see if they could identify changes in brain chemistry in 311 men and women in their 70s and 80s who had no apparent cognitive problems.

The participants also underwent PET scans to see if there were any amyloid-beta deposits, or plaques, in the brain. These plaques are the first signs of Alzheimer's disease, the researchers noted.

In addition, participants took tests that evaluated memory, language and other skills.

Kantarci's team found that 33 percent of the people had significantly high levels of amyloid-beta deposits in their brains. These people also had high levels of two chemicals: myoinositol/creatine and choline/creatine.

Those with high levels of these so-called brain metabolites also were more likely to have lower scores on several of the cognitive tests, regardless of the amount of amyloid-beta deposits in their brains, the researchers added.

Kantarci said these biochemical changes start years before people show signs of cognitive problems. Whether these markers are a cause of dementia or only a signal for other changes isn't known, she said. "What we are seeing is a marker of a pathological process rather than a cause," she explained.

Heather M. Snyder, senior associate director of medical & scientific relations at the Alzheimer's Association, said "there is a growing body of evidence that biological changes associated with Alzheimer's disease are occurring maybe even 20 years prior to any individual having any cognitive issues."

"The goal is that we would like people to live a healthy life as long as possible, so if we can diagnose people with these changes as early as possible, when a treatment is available we can intervene -- that's really our ultimate goal," she said.

That's why finding ways to identify people at risk early is important while the search for treatments and cures continues, Snyder said.

Identifying people at risk for dementia is also important for research, said Dr. Marc L. Gordon, a neurologist and Alzheimer's researcher at The Feinstein Institute for Medical Research in Manhasset, N.Y.

"It is important to identify people at risk of dementia, particularly if we want to test therapies that have the potential to alter the process to try to prevent people from converting to dementia," he said.

Greg M. Cole, a neuroscientist at the Greater Los Angeles VA Healthcare System and associate director of the Alzheimer's Disease Research Center at the University of California Los Angeles David Geffen School of Medicine, said that "these results show that more and more specific biochemical changes that presage Alzheimer's disease can be detected in our normal aging population using sophisticated imaging technology."

But, Cole added, "The question now is whether we can find a way to intervene in people where these very early steps in the disease process are measurable by suppressing the pathological process until we normalize the disease indices and show that they don't go on to develop dementia."

ICAD: Biomarkers Take Center Stage in Alzheimer's Field

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By John Gever, Senior Editor, MedPage Today

PARIS – Although disease-modifying treatments for Alzheimer's disease are still years away, research on biomarkers and imaging techniques for identifying individuals most likely to benefit from them is making great strides.

That's the view of William Thies, PhD, chief medical and scientific officer of the Alzheimer's Association, sponsor of the International Conference on Alzheimer's Disease (ICAD) that starts here today.

In an exclusive interview with MedPage Today senior editor John Gever, Thies said that new results on diagnostic and prognostic markers would be among the major highlights of this year's meeting.

A major trend in the field, he said, has been "increasing interest in biomarkers and increased understanding of biomarkers – they're not created equal, there may be different biomarkers that are going to be useful in different parts of the disease."

"It's certainly true that the progress in biomarkers and the progress in new treatments almost has to go hand in hand," Thies added.

Indeed, another trend receiving significant attention at this year's ICAD is early treatment of Alzheimer's disease, before dementia becomes severe.

The recently updated diagnostic criteria for the disease are facilitating early intervention, he said, because they better describe what he called "the continuum of Alzheimer's disease."

These trends are interrelated and will become more so when disease-modifying therapies finally become available, Thies predicted.

"As new medications are developed and [approved], they'll probably receive labeling with some careful instructions about biomarkers used during the diagnostic procedure," he suggested.

Whether those medications will be directed against beta-amyloid protein is still unclear, he conceded.

But Thies said the recent negative results with anti-amyloid drugs did not yet mean the approach was a dead end.

"There are several anti-amyloid therapies that are still in phase III testing. These are the monoclonal antibodies that bind to beta-amyloid," he said.

"I think we're going to see very important data coming out of those trials. I think it's too early to declare the amyloid hypothesis dead."

Those data will not be reported here, but the ICAD agenda does feature results from other studies that will shed light on other aspects of the disease, including:

•Modifiable risk factors
•Traumatic brain injury as a cause of Alzheimer's disease
•Safety of anti-amyloid therapies
•Cerebrospinal fluid proteins and imaging results early in the disease

Thies also mentioned that a critical need for future research is recruitment of potential research participants.

The Alzheimer's Association has launched a service called TrialMatch to place volunteers into research studies – including cognitively healthy and mildly impaired individuals as well as those with overt Alzheimer's disease.

"The hope is to increase the number of people in trials," he said, noting that about 10,000 people are now available in the pool.

"We hope that eventually this will drastically speed the recruitment of people in trials," alleviating a major obstacle to progress.

"Currently, to recruit a full cohort for a phase III clinical trial in Alzheimer's disease, it takes somewhere between a year and a year and a half. That's just wasted time," Thies declared.