Food and Alzheimer’s Disease

Alzheimer’s disease is a dreaded and cruel condition that devastates more than 5 million Americans, a number that the Alzheimer’s Association expects to rise to 16 million by 2050. The most common form of dementia, it affects nearly 50% of those 85 years of age and older.

Simple, familiar mental tasks become arduous as those affected with Alzheimer’s lose their memory and intellectual abilities and experience personality changes and mood swings. Subjective awareness in patients’ cognitive loss results in depression and huge tangible and intangible costs to society.

The extensive neuronal network of more than 100 billion bundled nerve cells that assimilate nutrients, generate energy, and process and store information communicates and coordinates numerous activities, including thinking, learning, remembering, and reasoning.

Alzheimer’s is a progressive disease characterized by two types of abnormal lesions—beta-amyloid plaques and neurofibrillary tangles. The apparent increased production of the insoluble β-amyloid peptides and their subsequent aggregation is one of many targets in clinical investigations. Tangles consist of hyperphosphorylated twisted protein fibers called tau that form within dying cells. Mutation of transmembrane proteins called presenilins contributes to early onset of the disease.

Studies indicate that dietary factors, such as caffeine, β-glucan, docosahexaenoic acid (DHA), docosapentaenoic acid (DPA), folic acid, pomegranate, and blueberries may have neuroprotective effects.

A prospective study among 7,300 French men and women age 65 years and older and a population-based cohort suggested that caffeine from three or more cups of coffee, or its caffeine equivalent in tea, per day over a 4-year period may reduce age-related cognitive decline in women without dementia. This effect was not observed in men, suggesting hormonal and specific neuro-architectural influences related to gender (Ritchie et al., 2007). Animal studies and evidence from neuronal cultures indicate that caffeine may decrease β-amyloid production in specific regions of the brain (Arendash et al., 2006).

β-1,3- and 1,6-glucans from fungi and yeast have numerous biological effects, including immunostimulation against infectious diseases and some forms of cancer. In-vivo and in-vitro studies indicate that β-glucans may augment the effects of some anti-tumor monoclonal antibodies and independently promote tumor regression (Hong et al., 2004; Allendorph et al., 2005), suggesting that that these β-glucans or their fragments could function to modulate β-amyloid production through similar cytotoxic mechanisms.

Brain tissue is composed of an outer convoluted gray and deep white matter, collectively consisting of 10–12% lipids. Some studies indicate a low level of brain DHA among Alzheimer’s patients, compared to age-matched, non-demented controls. Oral administration of a DHA-rich diet (1.3% DHA) to a transgenic Alzheimer’s disease mouse model reduced β-amyloid accumulation, diminished presenilin steady-state levels, and decreased accretion of tau after 3 months. The addition of DPA presented a short-term tau buildup and subsequent pathogenesis via reduced phosphorylation of this protein (Green et al., 2007).

A longitudinal cohort study among Medicare 965 subjects revealed that those consuming the higher quartile of folic acid (≥488 μg) had a lower risk of Alzheimer’s disease. This observation was independent of several other nutrients, including vitamins B-6 and B-12. Folic acid continues to be a dynamic area for clinical nutrition investigations.

Pomegranate juice delayed the onset or progression of Alzheimer’s disease in transgenic mice, yielding a 50% reduction in β-amyloid accumulation and deposition in the hippocampus (Hartman et al., 2006). And a similar study with homogenized blueberries suggested that behavioral deficits may be conquered even among a genetically predisposed Alzheimer’s model (Joseph et al., 2003).

These kinds of rodent, culture, and human studies indicate that selected dietary components may affect cognitive function and the development of Alzheimer’s disease. Future studies may enhance our understanding of the potentially exciting role of other dietary components that protect the brain from age-related degeneration and behavioral disorders.

References for the studies mentioned above are available from the authors.

by Roger Clemens, Dr.P.H.,
Contributing Editor
Special Projects Advisor,
ETHorn, La Mirada, Calif.
[email protected]

by Peter Pressman, M.D.,
Contributing Editor 
Attending Staff, Internal Medicine,
Cedars-Sinai Medical Center, Los Angeles, Calif.
[email protected]