Epigenetic Diet May Prevent Alzheimer's Disease
Neuroprotective nutrients appear to enhance cognition, memory, and other impaired functions seen in patients with Alzheimer's disease.
With no available cure for Alzheimer's disease (AD)—and none on the immediate horizon—researchers are searching for potential causes and contributors to the most common neurodegenerative disorder.
An article published ahead of print in Neurochemistry International this week discussed epigenetic mechanisms that have been linked to AD. These mechanisms modulate gene expression patterns using DNA methylation, histone post-translational modifications, or microRNAs, but they leave the overall DNA sequence unaltered.
Every cell in an individual has the same DNA sequence, but epigenetic regulation occurs at specific gene loci in certain cells to create precise cellular phenotypes. Humans acquire these mutations as they become exposed to environmental factors such as diet and toxins throughout their lives. When epigenetic alterations occur, genetic transcriptional activity may change and create risk for specific diseases, especially neurodegenerative disorders like AD.
The present article detailed the current understanding of how neuroprotective nutrients appear to enhance cognition, memory, and other impaired functions seen in patients with AD, including:
- Folic acid and vitamin B12 are critical to DNA methylation as they work to replenish cellular S-adenosyl-L-methionine (SAM), an essential cosubstrate involved in methyl group transfers. Post-mortem studies have shown that AD patients have decreased SAM levels.
- Choline, which is usually found in milk, eggs, and meat, also plays a role in methylation. Animal studies have shown that choline deficiency reduces histone methylation in the central nervous system.
- Researchers suspect—and are in the process of confirming—that deficiencies in zinc, selenium, and magnesium promote AD pathogenesis.
- Resveratrol, curcumin, and other dietary polyphenolsfound in fruits and vegetables seem to influence epigenetic mechanisms and, ultimately, gene expression.
Since diet is a key epigenetic influence, its modification may decrease neuronal vulnerability. Many associated vitamins and minerals are either abundant in foods or can be obtained through supplementation. In the future, an epigenetic diet may be prescribed as preventive therapy for AD.