Omega-3s In Fish, Seafood May Protect Seniors' Eyes

December 6, 2010

Adapted from the American Academy of Ophthalmology

Seniors interested in lifestyle choices that help protect vision will be encouraged by a Johns Hopkins School of Medicine study, and people concerned about glaucoma can take heart from work on early detection by the University of Miami Miller School of Medicine. Both studies are published in the December issue of Ophthalmology, the journal of the American Academy of Ophthalmology.

Researchers at Wilmer Eye Institute, Johns Hopkins School of Medicine, wanted to know how the risk of age-related macular degeneration (AMD) would be affected in a population of older people who regularly ate fish and seafood, since some varieties are good sources of omega-3 fatty acids. A diet rich in omega-3s probably protects against advanced AMD, the leading cause of blindness in whites in the United States, according to the Age-Related Eye Disease Study (AREDS) and other recent studies. High concentrations of omega-3s have been found in the eye's retina, and evidence is mounting that the nutrient may be essential to eye health. The new research, led by Sheila K. West, Ph.D., was part of the Salisbury Eye Evaluation (SEE) study.

Food intake information with details on fish and shellfish consumed was collected over one year using a validated questionnaire for 2,391 participants aged 65 to 84 years who lived along Maryland's Eastern Shore. After dietary assessment was complete, participants were evaluated for AMD. Those with no AMD were classified as controls (1,942 persons), 227 had early AMD, 153 had intermediate-stage disease, and 68 had advanced AMD. In the advanced AMD group, the macular area of the retina exhibited either neovascularization (abnormal blood vessel growth and bleeding) or a condition called geographic atrophy. Both conditions can result in blindness or severe vision loss.

"Our study corroborates earlier findings that eating omega-3-rich fish and shellfish may protect against advanced AMD." Dr. West said. "While participants in all groups, including controls, averaged at least one serving of fish or shellfish per week, those who had advanced AMD were significantly less likely to consume high omega-3 fish and seafood," she said.

The study also looked at whether dietary zinc from crab and oyster consumption impacted advanced AMD risk, but no significant relationship was found. Zinc is also considered protective against AMD and is included in an AMD-vitamin/nutrient supplement developed from the AREDS study. Dr. West speculated that her study found no effect because the levels of zinc obtained from seafood/fish were low compared to supplement levels.

A side note: fish and shellfish were part of the normal diet of the study population, rather than added with the intention of improving health. The links between fish consumption, omega-3s and healthy lifestyles were not widely known in the early 1990s when the dietary survey was conducted. In fact, some of the study participants who consumed the most seafood were also smokers and/or overweight, two factors usually associated with AMD and other health risks.

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Tau Disrupts Neural Communication Prior To Neurodegeneration

December 22, 2010

On behalf of our donors, Alzheimer's Disease Research (ADR), a program of the American Health Assistance Foundation (AHAF), recognizes Dr. Liao, an AHAF grantee, for his work on this important study.

Dr. Dezhi Liao and co]authors discovered that part of the memory loss from Alzheimerfs disease is not due to cell death, but caused by a buildup of tau protein in the parts of the nerve cell, called the gdendritic spines,h that are used to store memories. Specifically, tau is forced to go where it shouldnft by a change called phosphorylation. In a laboratory study, when the researchers used genetically-modified tau proteins that couldnft be phosphorylated, they also blocked the damaging tau protein buildup in rat nerve cells. In the future, a new drug could be developed to prevent this phosphorylation and stop tau from entering the dendritic spines, potentially halting the loss of memories in early stages of Alzheimerfs disease.

Adapted from Cell Press

A new study is unraveling the earliest events associated with neurodegenerative diseases characterized by abnormal accumulation of tau protein.  The research, published by Cell Press in the December 22 issue of the journal Neuron, reveals how tau disrupts neuronal communication at synapses and may help to guide development of therapeutic strategies that precede irreversible neuronal degeneration.

Tau normally contributes to the supportive framework of proteins in the cell. It is well established that abnormal tau sometimes clumps into neuron-damaging filamentous deposits and that aggregates of tau with multiple phosphate groups attached are a defining feature of neurodegenerative disorders called gtauopathiesh, which include Alzheimerfs disease and other dementias.

gResearch has shown that healthy neurons have more tau in the axon and less in the cell body and dendrites, and that this gradient is reversed in neurodegenerative disorders like Alzheimerfs,h explains study author, Dr. Karen H. Ashe from the University of Minnesota. gAlthough studies have shown that accumulation of tau in dendrites induced neurodegeneration, they do not address how tau diminished brain function at preclinical disease stages preceding neurodegeneration.h   

Dr. Ashe, co-author Dr. Dezhi Liao, and their colleagues investigated how tau induces early memory deficits and disrupts neuronal communication, prior to obvious neuron damage. The researchers found that early accumulation of hyperphosphorylated tau in dendrites and dendritic spines disrupted communication coming in from other neurons.  Dendritic spines are sites where there is a synapse between two neurons. The phosphorylation state of tau played a critical role in mediating tau mislocalization and subsequent impairment of synaptic communication.

gThese findings capture what is likely the earliest synaptic dysfunction that precedes synapse loss in tauopathies and provide an important mechanistic link between tau phosphorylation and the mislocalization of tau to dendritic spines,h concludes Dr. Liao. gUnderstanding the  key interactions that occur  prior to neuronal loss will become increasingly important as preventative strategies shift the timing of interventions to pre-degenerative phases of disease,h adds Dr. Ashe. gThe aberrant mislocalization of tau proteins in dendritic spines might be a novel target in these strategies.h

Preliminary Results Show That Walking May Slow The Progression Of Alzheimer's Disease

December 3, 2010

Adapted from the Radiological Society of North America

Walking may slow cognitive decline in adults with mild cognitive impairment (MCI) and Alzheimer's disease, as well as in healthy adults, according to a study presented today at the annual meeting of the Radiological Society of North America (RSNA).

"We found that walking five miles per week protects the brain structure over 10 years in people with Alzheimer's and MCI, especially in areas of the brain's key memory and learning centers," said Cyrus Raji, Ph.D., from the Department of Radiology at the University of Pittsburgh in Pennsylvania. "We also found that these people had a slower decline in memory loss over five years."

Alzheimer's disease is an irreversible, progressive brain disease that slowly destroys memory and cognitive skills. According to the National Institute on Aging, between 2.4 million and 5.1 million Americans have Alzheimer's disease. Based on current population trends, that number is expected to increase significantly over the next decade.

In cases of MCI, a person has cognitive or memory problems exceeding typical age-related memory loss, but not yet as severe as those found in Alzheimer's disease. About half of the people with MCI progress to Alzheimer's disease. "Because a cure for Alzheimer's is not yet a reality, we hope to find ways of alleviating disease progression or symptoms in people who are already cognitively impaired," Dr. Raji said.

For the ongoing 20-year study, Dr. Raji and colleagues analyzed the relationship between physical activity and brain structure in 426 people, including 299 healthy adults (mean age 78), and 127 cognitively impaired adults (mean age 81), including 83 adults with MCI and 44 adults with Alzheimer's dementia.

Patients were recruited from the Cardiovascular Health Study. The researchers monitored how far each of the patients walked in a week. After 10 years, all patients underwent 3-D MRI exams to identify changes in brain volume. "Volume is a vital sign for the brain," Dr. Raji said. "When it decreases, that means brain cells are dying. But when it remains higher, brain health is being maintained."

In addition, patients were given the mini-mental state exam (MMSE) to track cognitive decline over five years. Physical activity levels were correlated with MRI and MMSE results. The analysis adjusted for age, gender, body fat composition, head size, education and other factors.

The findings showed across the board that greater amounts of physical activity were associated with greater brain volume. Cognitively impaired people needed to walk at least 58 city blocks, or approximately five miles, per week to maintain brain volume and slow cognitive decline. The healthy adults needed to walk at least 72 city blocks, or six miles, per week to maintain brain volume and significantly reduce their risk for cognitive decline.

Over five years, MMSE scores decreased by an average of five points in cognitively impaired patients who did not engage in a sufficient level of physical activity, compared with a decrease of only one point in patients who met the physical activity requirement.

"Alzheimer's is a devastating illness, and unfortunately, walking is not a cure," Dr. Raji said. "But walking can improve your brain's resistance to the disease and reduce memory loss over time