Alzheimer’s Updates: Why It’s Important to Eat Healthy and Other Findings

In the past six months, several interesting and promising studies have been published on Alzheimer’s disease. They’ve ranged from how what we eat might affect our odds of developing it, to discovering the underlying mechanisms. Taken together, researchers are definitely making progress in developing treatments — and preventative measures — for Alzheimer’s. For those of us who have watched older family members mentally decline due to the devastating effects of this genetic disease, these studies may help give some hope that the same fate does not await us.

The studies that will be explored here are specifically on: how eating fruits, vegetables, and other components of a healthy diet may decrease the risk of developing Alzheimer’s; the effects of other risk factors; and how some chemicals affect the formation of amyloid plaques or dementia (but not both). Read on for the details.

In March, a doctoral thesis reported that a person’s diet in midlife (when they’re around 50-years-old) can significantly affect their chances of getting Alzheimer’s later (by their mid-60s). Specifically, a healthier midlife diet — one with “vegetables, berries and fruits, fish, and unsaturated fats” — led to a nearly 90% decreased risk compared to having an unhealthy midlife diet — one with “sausages, eggs, sweets, sugary drinks, salty fish and saturated fats.” This interestingly correlates with a study published in December of last year showing that a chemical commonly found in fruits and vegetables may help prevent memory loss associated with Alzheimer’s. The chemical, called fisetin, was fed daily to lab mice that typically develop Alzheimer’s disease within a year of being born. The memory and learning skills of the mice that ate fisetin was just as good as normal mice when they were all tested at nine months, and one year, after birth. However, fascinating, the mice still developed amyloid plaques, which are associated with Alzheimer’s disease.

It’s definitely still unclear whether amyloid plaques are a cause of, or an effect of, having Alzheimer’s; some people have amyloid plaques but no signs of dementia. Related to this is a study that was published in March — it found that such inconsistencies could be due to the amounts of REST a person has. REST is a transcription factor (it helps control which genes get made into protein) and in people who are middle aged and elderly it’s been shown to help protect neurons (from stress and potentially dangerous, misfolded proteins). People with plaques, but no dementia, had three times as much REST as people with plaques and dementia. In mouse cells, REST was also found to help rescue and fix damaged cells somehow. It’s unclear how important REST ultimately is in people — there’s correlative data, but not casual data, and there could be many other similar factors at play.

Speaking of amyloid plaques — in May, an anti-depressant drug, specifically citalopram (a selective serotonin reuptake inhibitor [SSRI]), was found to help stop amyloid plaques from growing (and reduce the size of new plaques by about 78%) in mouse models of Alzheimer’s. But while SSRIs may decrease plaque formation, these drugs do not look like they effectively treat Alzheimer’s symptoms in patients; it hasn’t been shown that reducing plaques will reduce chances of getting Alzheimer’s. (Once again, it’s still unclear whether plaques are a cause or an effect.)

Lastly, a study in April explored why women may be at a greater risk of having Alzheimer’s; in people who have a variant of a specific gene (APOE4) that makes them predisposed to getting Alzheimer’s, women are much more likely than men to actually get the disease. (For example, in one study men with the APOE4 variant were at a 27% increased risk for coming down with Alzheimer’s, while women had an 80% greater risk). Some theorize that there could be “an interaction between APOE4 and estrogen” that causes this varied response.

For some previous Biology Bytes posts that explore Alzheimer’s, try checking these two out:

• “Blood Test for Alzheimer’s:” This post is on how a recently-developed blood test predicts with >90% accuracy if a person 70-years-old or older would develop Alzheimer’s disease in the next 2-3 years.
• “Sleep on the Brain:” This post hints at the possibility of there being a correlation between sleep deprivation and occurrence of Alzheimer’s disease in patients.

So while diseases like Alzheimer’s are clearly complex and seem daunting to tackle, it’s only with continued research and funding that we can continue to put together the pieces to solve this puzzle and make more effective treatments available.

For further reading:

• ScienceDaily’s article “Healthy midlife diet may prevent dementia later”
• Antonio Currais et al.’s article “Modulation of p25 and inflammatory pathways by fisetin maintains cognitive function in Alzheimer’s disease transgenic mice”
• ScienceDaily’s article “Natural plant compound prevents Alzheimer’s disease in mice”
• Tao Lu et al.’s article “REST and stress resistance in ageing and Alzheimer’s disease”
• Anna Azvolinsky’s article “Protein Protects Aging Brain”
• Yvette I. Sheline et al.’s article “An Antidepressant Decreases CSF A-Beta Production in Healthy Individuals and in Transgenic AD Mice”
• Rina Shaikh-Lesko’s article “Antidepressant Could Be Prophylactic for Alzheimer’s“
• Andre Altmann et al.’s article “Sex modifies the APOE-related risk of developing Alzheimer disease“
• Kerry Grens’s article “Sex-Biased Alzheimer’s Variant”
• Teisha J. Rowland’s book Biology Bytes: Digestible Essays on Stem Cells and Modern Medicine