Alzheimer’s disease (AD) is currently the fifth leading cause of death for people older than 65 in the United States. Its exact underlying cause is far from a settled subject, but the features shared by the brains of people with AD may provide insights.
One of the main histopathological features of AD is the accumulation of amyloid plaques in the brain. These plaques, which are made up of a peptide called amyloid beta, have been proposed as a major driver of AD. This “amyloid hypothesis” has been challenged, however, notably because drugs targeting the amyloid pathway have not been found to improve cognition in AD. But maybe the drug trials were started too late in the course of the disease.
Another primary histopathological feature of AD is the presence of neurofibrillary tangles in the brain. These tangles are made up of tau proteins that, like amyloid beta, have misfolded and aggregated. According to the “tau hypothesis”, these tangles are a cause or contributor to AD. However, because tau proteins normally serve important functions in the brain, another possibility is that tau tangles are simply an indicator of a loss of tau function and are not themselves harmful.
Also common in AD is hypometabolism, a reduction in the brain’s ability to metabolize glucose for energy — which is why some researchers call AD “type 3 diabetes”. This reduction in the brain’s energy production may contribute to the cognitive impairments seen with AD and might contribute to the development of the disease itself.
Finally, AD is a neurodegenerative disease: it is characterized by neuronal death and subsequent cerebral atrophy. This process is widely believed to be central to the disease process and may be the result, at least in part, of some or all the previously mentioned factors.
No drugs have been shown to slow or prevent AD: nearly all of the existing drugs approved to treat AD (e.g., acetylcholinesterase inhibitors) merely improve symptoms, and these improvements are often fairly minor. Therefore, nonpharmaceutical strategies to prevent AD need to be explored.
One such strategy may be a Mediterranean diet, an eating pattern typically characterized by higher intakes of fish, fruit, vegetables, legumes, nuts, whole grains, and olive oil; a limited intake of meat and dairy; and a moderate intake of alcohol (often wine specifically). A 2021 systematic review and meta-analysis summarized here found observational evidence that adherence to a Mediterranean diet was associated with lower risks of both mild cognitive impairment and AD. (A “mild cognitive impairement” is a neurocognitive disorder involving memory problems that exceed what is expected based on a person’s age. It is often a precursor to AD.)
Another, compatible dietary strategy is to avoid consuming too much sugar, since a 1-year prospective cohort study summarized here found that a diet with a high glycemic index was associated with more amyloid-beta peptide accumulation in the precuneus, a pathological hallmark of Alzheimer’s disease. This association was stronger in participants with elevated amyloid at baseline.