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Wednesday, July 16, 2014

Biomarkers and Further Progress on a Blood Test for AD


Dear Readers,

Many of you have read or heard the term Biomarker. In this blog, I would like to review a recent discovery in AD biomarkers and provide the context for its meaning and potential value. A biomarker may be measured in a sample (as a blood, urine, or biopsy), it may be a recording obtained from a person (blood pressure, ECG), or it may be an imaging test (brain MRI or echocardiogram.

Biomarkers can indicate a variety of disease characteristics. For example, they can indicate the level of exposure to a toxic environmental factor, such as lead levels in the blood; or the presence of cancerous cells, such as in a pap smear looking for cervical cancer; or the genetic susceptibility for a disease, such as the BRCA1 DNA mutation for breast cancer. Thus, a simple way to think about and classify biomarkers is as 1) indicators of disease risk 2) indicators of disease state (is the disease present), or 3) indicators of disease rate (progression). One of the best known biomarkers is LDL cholesterol and the risk it imparts for heart disease.

A commonly used analogy when discussing biomarkers for Alzheimer’s disease is that of cancer. An individual may have a biomarker that indicates increased risk for breast cancer: positive BRCA1 gene mutation. Years later, that individual might have an abnormal mammogram showing a small tumor (disease state), and if left untreated she might develop metastatic disease with tumors in the lungs as seen by PET scan (disease progression.

In Alzheimer’s dementia, a genetic mutation, such as PSEN1 is a biomarker that indicates increased risk for developing AD. A positive amyloid PET scan can indicate presence of amyloid plaques (indicating increased risk and disease state). Finally, an MRI demonstrating brain atrophy, or shrinkage, can indicate neurodegeneration (which shows disease progression). A major effort in the field has been to find an accurate, reliable, practical and inexpensive biomarker for AD. The discovery of a blood test for AD would truly represent a watershed moment in the field, and likely be second in importance only to the discovery of a disease modifying drug.

In the most recent development, a paper published last week in the journal Alzheimer’s and Dementia, described a panel of 10 proteins in the blood. The researchers looked at blood samples from 1,148 subjects: 476 with AD dementia, 220 with MCI, and 452 elderly controls with no dementia. The researchers have identified a panel of plasma biomarkers that correlate closely with other biomarkers of AD, specifically, neuroimaging measures of disease and cognitive measures of memory functioning. Moreover, the 10 protein biomarkers can accurately predict disease conversion from MCI to AD dementia within a year of blood sampling. At the AAIC meeting in Copenhagen we have heard about a retinal measure of amyloid as a potential biomarker, as well as a simple smell test, which also seems to correlate with AD pathology in the brain.

As with other biomarker studies, we need to better understand if this protein panel, retinal scan and smell test will serve as an indicators of disease risk, disease state and disease progression. However, with this recent work, we are getting much closer to that possibility.



Thanks for reading,


Michael Rafii, MD, PhD
Director, Memory Disorders Clinic
Medical Core Director
Alzheimer’s Disease Cooperative Study
University of California San Diego
 
Author: Michael Rafii MD, PhD at 8:56 AM 0 Comments

Friday, May 30, 2014

New AD Mice Models


Dear Readers,

In a recent study published in Nature Neuroscience, researchers at the Riken Brain Science Institute in Japan have reported after a 12 year effort, the creation of two new mouse models of Alzheimer’s disease that may better mirror the disease in humans.

As readers will recall, many compounds that work in mice have not translated to new drugs in human studies. Some of the difficulty is the inadequacy of current mouse models to replicate the same conditions of Alzheimer's disease that would allow for an understanding of the underlying mechanisms that lead to dementia. Specifically, the current mouse models overproduce the protein amyloid precursor protein, or APP, which gives rise to the amyloid-beta (Abeta) peptides that accumulate in the brain, eventually leading to the neurodegeneration that characterizes Alzheimer's disease. However, in mice the overproduction of APP gives rise to additional effects which are not seen in human Alzheimer's disease.

The mouse model developed (NL-F/NL-F) was ‘knocked in’ with two mutations found in human familial Alzheimer's disease. These mice show early accumulation of beta-amyloid peptides, and importantly, were found to undergo cognitive dysfunction similar to the progression of AD seen in human patients. Inflammation accumulated around the amyloid plaques in the mouse brains as also seen in the brains of people with AD. And looking at the hippocampus, the knock-in mice also lose synapses in the same areas. Beginning at 18 months, NL-F mice also had trouble learning, which is seen in humans after plaques and tangles have developed. A second model, with the addition of a further mutation that had been discovered in a family in Sweden, showed even faster initiation of memory loss which occurs at six months.

These two mouse models represent a heroic effort to more closely model human AD and will undoubtedly help advance our search for early diagnostics and effective treatments.


Thanks for reading,


Michael Rafii, MD, PhD
Director, Memory Disorders Clinic
Medical Core Director
Alzheimer’s Disease Cooperative Study
University of California San Diego
 
Author: Michael Rafii MD, PhD at 8:46 AM 0 Comments

Friday, May 09, 2014

Young Blood and Old Brains


Dear Readers,
In a study published last week in the journal Nature Medicine, researchers at Stanford University School of Medicine looked at changes in the brains of old mice given the blood of young mice. They also compared how the old mice performed on standard tests of memory after they had received infusions of plasma – the cell-free part of blood – from young mice, versus no plasma at all. By transferring young plasma into an old mouse once every three days for three weeks, they found that old mice injected with plasma from young mice outperformed untreated old mice in two separate memory tests. Specifically, after a day of training, the mice treated with plasma from young mice averaged about 25 percent better than those of mice injected with aged plasma. Moreover, the treated mice also showed more neurogenesis (new brain cell production), synaptic density (brain cell communication) and less inflammation.

In a separate study published the same day in the prestigious journal Science, work from the Harvard Stem Cell Institute demonstrated that young blood reinvigorated blood vessels in the brains of old mice. In the treated old mice, the volume of blood vessels in the brain almost doubled. They formed new branches and allowed more blood to flow through them towards various brain regions. This, in turn, led to an increase in the number stem cells in the brain.

From the studies, it appears that young blood contains ‘pro-youthful’ factors that can reverse age related brain impairments while old blood may contain ‘pro-aging’ factors that lead to age-related brain impairment.

Surely, these findings are very exciting and could represent potential targets for intervention with regards to age-related brain disease. Still, much work is needed to understand the factors within plasma that are exerting such changes after transfusion and for how long. It is also important to keep in mind that the studies were conducted in mice, not humans, and that neither study looked at the type of cognitive impairment that is seen in Alzheimer’s disease or in animal models of Alzheimer’s disease. Only through well designed, placebo-controlled clinical trials in humans would the benefits of such treatments be fully understood.




Thanks for reading,


Michael Rafii, MD, PhD
Director, Memory Disorders Clinic
Medical Core Director
Alzheimer’s Disease Cooperative Study
University of California San Diego
 
Author: Michael Rafii MD, PhD at 8:58 AM 0 Comments

Thursday, March 27, 2014

What is Gender Medicine and why is it important to Alzheimer’s disease?



By Neelum Aggarwal, M.D.
Rush Alzheimer’s Disease Center

Prior to the mid-1900s, there was very little discussion about gender medicine. However, with the establishment of the Partnership for Gender Specific Medicine at Columbia University (1997), the Karolinska Institute (2002), and the Charité -Universitätsmedizin Berlin (2003), studies began to systematically examine comparisons between women and men. Over the last 20 years research has slowly but steadily begun to demonstrate the extent of these sex differences, but have also produced advancements in treatment, prevention and diagnosis. The result of this progress led to the 2010 Institute of Medicine declaration that being a woman or a man significantly affects disease course and should be considered in both diagnosis and therapy.

What is the difference between sex and gender and how is it related to medicine?
Gender medicine aims to improve treatment for women as well as for men, and differs from women’s health, because it also focuses on men’s health.

Gender medicine deals with the effects of sex, including biological differences between females and males. Examples of sex differences can include different concentrations of sex hormones, different expression of genes on X and Y chromosomes, or simply reporting a higher percentage and deposition of body fat in women.

Gender however, is the result of socio-cultural processes. Associated with behavior, stress, and lifestyle-related diseases, gender has been shown to determine access to health care, help-seeking behavior, and even individual use of the health care system. Recent studies have shown that gender largely determines one’s compliance with preventative measures, and whether one follows up on referrals or accepts invasive strategies like a pacemaker implant, heart transplant, or other surgeries.

Although the definitions of sex and gender appear straightforward, in medicine, it isn't always that easy to separate the influence of sex and gender on disease. For example, clinical manifestations of prevalent diseases have been shown to differ in women and men; with the question remaining, how much of these differences are due to sex differences in disease mechanisms? One area of medicine that has made great strides in this area is in cardiovascular diseases. Cardiovascular disease risk factors, disease and symptoms of atrial fibrillation, myocardial infarction, and heart failure all have been shown to have sex and gender differences, and have resulted in separately developed suggested treatment plans for men and women.

Alzheimer’s disease ( AD) is the latest medical condition to be put front and center in the sex and gender discussion. Data suggests that the risk for AD and memory decline appear to increase in women after menopause.

Reports have noted that a woman’s overall lifetime risk of developing AD is almost twice that of a man – a statistic not solely due to the fact that women live longer than men. Other areas of study are demonstrating notable sex and gender differences in basic brain structure and function between men and women. In addition, specific AD related risk factors that include cardiovascular disease, genetics (APOE 4 genotype) and depression all have shown to have sex and gender differences and could account for these observations.



Dr. Aggarwal is a cognitive neurologist at the Rush Alzheimer’s Disease Center in Chicago and a Steering Committee member of the Alzheimer’s Disease Cooperative Study.


 
Author: Neelum Aggarwal MD at 2:33 PM 0 Comments

Thursday, March 20, 2014

New Protein Implicated as Central to Alzheimer’s Disease


Dear Readers,

As many of you are aware, a major puzzle in the Alzheimer’s field has been the issue of how it is possible that some patients can have amyloid plaques and neurofibrillary tangles in the brain, but not show symptoms of dementia, while other patients are fully symptomatic. For years, researchers have explained that this observation is a result of ‘cognitive reserve,’ that is, some protective ability in certain individuals that provides resilience despite the presence of brain pathology.

Now, we have another possible explanation as to why some individuals are protected while others are not. Researchers at Harvard Medical School have published a monumental effort in the journal Nature, showing that a protein called RE1-Silencing Transcription factor (REST), that functions as a gene regulator during fetal brain development, switches back on later in life to protect aging neurons from various stressors, including the toxic effects of abnormally accumulating proteins such as beta-amyloid.

To understand REST's functions, the team genetically engineered mice that lacked REST only in their brains and watched what happened as they aged. Intriguingly, as the mice grew older, neurons in their brain started to die in the same places as in Alzheimer's patients. The research team also studied the REST protein in the worm C. elegans and found that it is necessary to protect against toxicity, thereby suggesting REST’s protective function in the aging brain is shared across species.

The team further showed that the REST protein was abundant in normal aging human brains. The brains of people who developed mild cognitive impairment, by contrast, showed an early decline in levels of REST. The affected brain regions of people with Alzheimer's were nearly devoid of the REST protein. The findings were also noted in the brains of patients with other neurodegenerative diseases that cause dementia, including frontotemporal dementia (FTD) and dementia with Lewy bodies (DLB). It appears that the toxic protein in each circumstance, beta-amyloid in AD, Tau in FTD and alpha-synuclein in DLB, bind to and inactivate REST, prohibiting its ability to perform its normal functions.

Getting back to the question about cognitive reserve and why some patients don’t exhibit dementia symptoms despite pathology, the researchers examined brain tissue gathered as part of the Religious Orders Study. Participants in the study were clergy who had detailed annual cognitive assessments performed and donated their brains for study after death. The team sorted the samples into two groups. One group had Alzheimer's pathology and experienced symptoms of dementia. The second group had the same amount of Alzheimer's pathology but did not have dementia. The researchers found that the group with no dementia had at least three times more REST protein within key brain areas. Furthermore, REST levels were highest in the brains of people who lived into their 90s and 100s and who remained cognitively intact. And, the levels were high specifically in the brain areas that are most vulnerable to Alzheimer's disease.

So what do all of these findings mean?

The human body has an incredible capacity for healing, and aging is, in essence a balance between damage and repair. In the liver, cells contain various proteins that process compounds and other molecules, including toxins to maintain health. And so it appears that the brain has its own detoxification system, one that involves the REST protein, a gene regulatory protein that turns on a host of other proteins to help protect neurons from age-related toxicities, including the accumulation of beta-amyloid.

The identification of REST as an endogenous neuroprotection system, so intimately involved in AD, identifies it as a prime target for intervention and drug development. One can imagine that by somehow increasing REST levels in the brain, we could increase resilience and reduce the occurrence of the brain dysfunction we call dementia that results from neurodegenerative disease. Undoubtedly, we will see more research following up on this important discovery.





Thanks for reading,


Michael Rafii, MD, PhD
Director, Memory Disorders Clinic
Medical Core Director
Alzheimer’s Disease Cooperative Study
University of California San Diego
 
Author: Michael Rafii MD, PhD at 12:18 PM 0 Comments

Thursday, March 13, 2014

A Possible New Blood Test for AD?


Dear Readers,

According to a study published last week in the journal, Nature Medicine, a team of researchers has identified 10 lipids in the blood that may be able to detect the early signs of Alzheimer’s disease (AD).

The study included 525 healthy participants aged 70 and older who gave blood samples upon enrolling at various points in the study. Over the course of the five-year study, 74 participants met the criteria for either mild AD or mild cognitive impairment (MCI). Of these, 46 were diagnosed upon enrollment and 28 developed MCI or mild AD during the study (the latter group called converters.

In the study's third year, the researchers selected 53 participants who developed aMCI/AD (including 18 converters) and 53 cognitively-normal matched controls for the lipid biomarker discovery phase of the study. The lipids were not targeted before the start of the study, but rather, were an outcome of the study.

They discovered a panel of 10 lipids, which researchers say appears to reveal the breakdown of neural cell membranes in participants who developed symptoms of cognitive impairment or AD. The panel was subsequently validated using the remaining 21 MCI/AD participants (including 10 converters), and 20 controls. The lipid panel was able to distinguish with 90 per cent accuracy these two distinct groups – cognitively normal participants who would progress to mild cognitive impairment or Alzheimer’s disease within two to three years, and those who would remain normal over the same time interval.

The study has garnered a significant amount of attention, as the need for an easy, inexpensive, and accurate test for AD cannot be found soon enough. However, it should be kept in mind that the findings of the paper are part of a long standing effort by researchers who have been working for at least a decade on a blood test for AD. For this finding to be truly stand apart from the rest, the lipid panel’s predictive power will need to be confirmed in a larger sample of participants.

As readers will recall, the accumulation of beta-amyloid seems to be the driving force behind brain cell injury in AD, leading to a cascade of events that further damage brain cells and compromise cognitive function. As the disease worsens and more neurons die off, atrophy or shrinkage of brain tissue occurs. Some of the most reliable tests in the field include measurements of brain atrophy with volumetric MRI, measures of beta-amyloid in the spinal fluid and detection of amyloid with amyloid PET scans. The premise behind a blood test would be to find a surrogate in the blood for these brain changes. Many have looked at beta-amyloid itself, as well as markers of inflammation. This most recent paper raises the possibility that we may be closer to finally having a blood-based test for AD.

Thanks for reading,


Michael Rafii, MD, PhD
Director, Memory Disorders Clinic
Medical Core Director
Alzheimer’s Disease Cooperative Study
University of California San Diego



 
Author: Michael Rafii MD, PhD at 11:09 AM 0 Comments

Thursday, February 20, 2014

Citalopram May Help Reduce Agitation in AD Patients


Dear Readers,

Data from the the Citalopram for Agitation in Alzheimer Disease(CitAD)study was recently published in the Journal of the American Medical Association. The study enrolled 186 patients with probable AD, with an average age of 78, and followed them for nine weeks. None of the participants had major depression or psychosis requiring treatment. Researchers randomly assigned the participants to citalopram or placebo. All participants also received psychosocial interventions that included education materials, crisis management, and individual counseling sessions. At the conclusion of the nine week study, researchers found a statistically significant improvement in the citalopram group compared with the placebo group on the Neurobehavioral Rating Scale-Agitation, which assesses symptoms such as agitation, hostility, and disinhibition, with higher scores indicating more severe symptoms.

Moreover, 40% of the patients receiving citalopram had moderate or marked improvement from baseline severity on the modified Alzheimer's Disease Cooperative Study–Clinical Global Impression of Change score, which assesses items specific to agitation in AD. This compared to 26% of the patients taking placebo. The fact that 26% of patients on placebo improved is important to note, and resulted from the benefits associated with the psychosocial interventions offered as part of the study.

Interestingly, the effect of citalopram on agitation is about the same as that reported for the atypical anti-psychotic drugs, such as olanzapine and risperidon.

What do the results of this study mean? Citalopram is one of many selective serotonin reuptake inhibitors, which are primarily used as anti-depressants. However, in patients with AD, where multiple neurotransmitter systems are becoming disrupted and leading to behavioral symptoms, the use of anti-depressants may provide some benefit. Additional studies should determine the duration of benefits beyond nine weeks of treatment. And, physicians should also continue to emphasize non-pharmacologic strategies to manage agitation. However, this study is a very important first step in looking at new therapies for a very challenging aspect of AD.


Thanks for reading,


Michael Rafii, MD, PhD
Director, Memory Disorders Clinic
Medical Core Director
Alzheimer’s Disease Cooperative Study
University of California San Diego

 
Author: Michael Rafii MD, PhD at 11:50 AM 0 Comments

Tuesday, February 11, 2014

Increasing Diversity in Clinical Trial Participation in Upcoming ADCS Trials


Over the last few years, increased attention has focused on disparities in health that exist between white Americans and other racial and ethnic minorities. Data from national health surveys has consistently shown that racial and ethnic minorities have higher rates and greater severity of disease than whites, for most, if not all leading causes of morbidity and mortality in the US. These include heart disease, cancer, stroke, diabetes and dementia. Yet, the majority of persons who continue to participate in medical research (including both prevention and treatment trials), often represent the well educated, middle class, married, white population.

Major reasons given for under-representation of minorities in clinical trials include mistrust of researchers and health insitutions, lack of awareness of clinical trials by minorities, inadequate involvement of minority investigators in the recruitment process, cultural differences, economic limitations, less access to both health care and to research facilities. Existing data has shown that minority participation in clinical trials is especially low among older persons.

The major barriers to recruitment and and participation in clinical trials, has traditionally centered around the physician’s concern for the patient, concerns about the conduct of studies, and concerns about the role as both physician care manager and trial researcher. In surveys conducted with physicians, they have often expressed that there a is intellectual and emotional tension between the role they have defined as a physician, which places the health interests of the individual patient first, and the role they define as a researcher, which places the benefit to humanity in general, second. As physicians have not received formal training in either medical school or residency regarding the roles and duties that are associated with that of a Principal Investigator/ Trial Researcher, many are unclear and uneasy about recommending participation in trials to their patients.

Since the ultimate goal of any clinical trial is to recruit and retain study participants, barriers to subject participation must also be understood and minimized. Patient concerns have often related to time commitments needed for participation, negative personal and family attitude regarding trials and their safety, and inadequate evidence of benefits from trial participation.

The challenge facing many large scale trials is to recruit diverse populations to participate in a wide range of prevention and treatment studies. In doing so one must carefully consider how we define diversity in trials. One set of guidelines put forth by the National Institute of Health, was developed to ensure that women and minorities are included in trials, and utilizes purely demographic categories. On the other end of the spectrum are the epidemiologists and social sciences researchers, who define diversity based on descriptors such as age, marital status, sex, race, ethnicity, religious affiliation, education level, socioeconomic status and other socio-cultural attributes. Despite all these efforts for characterization it is very important to recognize that diversity within ethnic and racial group will exist. No group is entirely homogeneous, and as such, many socio-cultural factors can converge and influence the individual’s behavior when a person considers participating in a trial.

Another area that has been shown to impact participation in trials in both minority and non-minority populations is the concept of health and disease. Health and illness concerns vary widely within and across ethnic populations. Chronic illness and disability are not always viewed as problems that are appropriate for intervention. For some groups, illness may be a burden that the individual or family is expected to bear. Such beliefs have shown to alter and affect the probability that people will participate in trials.

With the changes in the healthcare delivery underway, and the emergence of “population health” as a discipline within itself, it is becoming apparent that biomedical research and specifically, clinical trials, can have a prominent role in determining the most effective method of prevention and treatment of chronic conditions for all segments of the population. Encouraging and involving physicians and patients to consider participating in clinical trials should be viewed as opportunities to enhance our understanding of treatment and prevention outcomes.

Dr. Neelum Aggarwal is a cognitive neurologist at the Rush Alzheimer’s Disease Center and Rush University Medical Center, and serves on the clinical trial Steering Committee for the NIH-funded Alzheimer’s Disease Cooperative Study (ADCS).


 
Author: Neelum Aggarwal MD at 9:31 AM 0 Comments

Thursday, February 06, 2014

Watching Memories Form


Dear Readers,

In a technological tour de force, researchers at Albert Einstein College of Medicine of Yeshiva University have published two studies in the January 24 2014 issue of the journal, Science, that provide an unparalleled window into how the brain makes memories. Such insights into the molecular basis of memory formation have never before been achieved in animals.

Einstein researchers developed a mouse in which they fluorescently tagged all molecules of messenger RNA (mRNA) that code for the beta-actin protein – a key structural protein found in large amounts in neurons and considered a key player in making memories. mRNA is a family of RNA molecules that copy DNA's genetic information and translate it into the proteins that make life possible.

The researchers then stimulated neurons in the mouse's hippocampus, where memories are made and stored, and watched fluorescently glowing beta-actin mRNA molecules form in the nuclei of neurons and travel within dendrites, the neuron's branched projections. They discovered that mRNA in neurons is regulated through a novel process described as "masking" and "unmasking," which allows beta-actin protein to be synthesized from the mRNA.

As readers of this blog will recall, neurons communicate with each other at synapses. Studies over the past 30 years have demonstrated that repeated stimulation increases the strength of synaptic connections by changing the shape of synapses. Beta-actin protein plays an important role in physically strengthening these connections. Memories are thought to be encoded when stable, long-lasting synaptic connections form between neurons in contact with each other.

The relevance of such research in the field of AD cannot be overstated. By seeing the physical nature of memory formation, we can now look at this process in various disease states, including memory robbing diseases such as AD. Further, we can better understand how beta-amyloid may perhaps interfere with the brain’s memory machinery.

Thanks for reading,


Michael Rafii, MD, PhD
Director, Memory Disorders Clinic
Medical Core Director
Alzheimer’s Disease Cooperative Study
University of California San Diego


 
Author: Michael Rafii MD, PhD at 2:12 PM 0 Comments

Wednesday, January 22, 2014

More Data on DHA and AD


Dear Readers,

As many of you are aware, there is growing evidence that dietary changes can affect the brain’s structure and even functioning. For example, higher adherence to a Mediterranean-type diet has been shown to be associated with decreased cognitive decline. The typical dietary pattern of the Mediterranean-type diet is characterized by a high intake of vegetables, fruits and nuts, legumes, ?sh and monounsaturated fatty acids; relatively low intakes of meat and dairy products; and moderate consumption of alcohol. In fact, higher consumption of olive oil, very rich in monounsaturated fatty, is considered the hallmark of the traditional Mediterranean-type diet.

One particular form of omega-3 fatty acid, called DHA, which is the most abundant fatty acid in the brain, has been of particular interest in regards to AD. In 2006, researchers at the USDA Human Nutrition Research Center on Aging at Tufts University found individuals with the highest DHA levels had a 47% reduction in all-cause dementia and a 39% lower risk of developing AD. In that study, which was a nine-year prospective, follow-up cohort study researchers analyzed completed dietary questionnaires and measured DHA blood levels of 899 study subjects who were participating in the Framingham Heart Study.

Neuropsychological testing revealed that all study participants were dementia-free at baseline. Thereafter, subjects had their cognitive function tested every two years using the Mini-Mental State Examination (MMSE). Those who experienced a decline of three or more points on the MMSE from the most recent exam were called back for a neurological and neuropsychological examination. The study population was 36.5% male and had an average age of 76 years. Plasma samples were measured for plasma DHA. In addition, a subgroup of 488 patients completed dietary questionnaires.

During the study period, 99 of 899 subjects developed dementia, including 71 cases of AD. Researchers divided individuals into quartiles according to their blood DHA levels. Those in the upper quartile experienced a significantly lower risk of all-cause dementia and AD compared with participants with levels in the lower three quartiles.

However, there are two ways to measure blood DHA: to directly measure it in the plasma fraction of blood, or to measure it within the red blood cells. It turns out that red blood cell DHA reflects dietary DHA intake up to 120 days, whereas plasma concentrations reflect intake over only the last few days.

Last year, researchers looked at red blood cell DHA levels and found that lower red blood cell DHA levels are associated with smaller brain volumes even in persons free of clinical dementia. The MRI finding of lower brain volume represents a change equivalent to approximately two years of structural brain aging.

For the latest study, Pottala and colleagues looked at the omega-3 fatty acids levels in the red blood cells of 1,111 women who participated in the Women's Health Initiative Memory Study. The women had MRI scans eight years after the study began to measure their brain volume. They were an average of 78 years old. Those with the highest levels of omega-3 fatty acids in their red blood cells had a 2.7% larger volume in the hippocampus portion of the brain compared with those with the lowest levels of omega-3 fatty acid and those with the highest levels of omega-3 fatty acids in their blood had 0.7% larger overall brain volume compared with those with the lowest levels.

What do these results mean? More data is accumulating that high dietary omega-3 acid levels may reduce the risk of AD in healthy individuals and also reduce the atrophy or shrinkage rate of the brain, including that of the hippocampus. Of course, one must consult with their doctor or pharmacist before purchasing or taking any supplement, as they can interact with medications. But we remain excited about the possibility that diet may influence AD risk.


Thanks for reading,


Michael Rafii, MD, PhD
Director, Memory Disorders Clinic
Medical Core Director
Alzheimer’s Disease Cooperative Study
University of California San Diego
 
Author: Michael Rafii MD, PhD at 4:17 PM 0 Comments

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About Us

The Alzheimer's Disease Cooperative Study (ADCS) was formed in 1991 as a cooperative agreement between the National Institute on Aging (NIA) and the University of California, San Diego. The ADCS is a major initiative for Alzheimer's disease (AD) clinical studies in the Federal government, addressing treatments for both cognitive and behavioral symptoms. This is part of the NIA Division of Neuroscience's effort to facilitate the discovery, development and testing of new drugs for the treatment of AD and also is part of the Alzheimer's Disease Prevention Initiative.

The ADCS was developed in response to a perceived need to advance research in the development of drugs that might be useful for treating patients with Alzheimer's disease (AD), particularly drugs that might not be developed by industry.