After all these years, have scientists finally discovered the cause of Alzheimer's disease? This has been suggested by a number of news stories about some findings by researchers at UC Riverside. They propose that we have focused too much on the beta amyloid plaques and not enough on tau protein. The secret to Alzheimer's disease, then, lies in understanding the dysfunction of tau protein.
If you read Beating the Dementia Monster you will recall that we discussed amyloid and tau as two possible pathways by which the disease might develop, but certainly not the only two. You may recall our sub-chapter in the appendix, "Either? Both? Neither?" Much of the recent focus on treating the disease has focused on the use of monoclonal antibodies (like aducanumab/Aduhelm) to remove amyloid from the brain. But that hasn't led to the dramatic disease cure we had hoped for.
We further explained that tau protein is involved in the structure of microtubules in brain cells. With the exception of red blood cells, microtubules are an important organelle in most cells in the body. They act like a sort of skeleton in the cell, but also like a conveyor belt moving nutrients and other material around within the cell. The tau proteins stabilize them. (If you were in my 10th grade biology class, you would have been required to draw the microtubules in a cell.) But if the tau proteins fail, the microtubules collapse into a "tangle." So at autopsy, the pathologist will be looking for both amyloid plaques and tau tangles for evidence of Alzheimer's disease.
An aside: Physicist Sir Roger Penrose has suggested that microtubules, influenced by quantum mechanics, may hold the key to the "hard problem" of consciousness. His thinking goes against the notion that the brain is just a very powerful computer, and human made computers might someday achieve consciousness. Penrose shared the Nobel Prize in physics in 2020.
As a skeptic of the amyloid hypothesis, I was encouraged by one thing the UC Riverside researchers said, and that was that we have spent too much time looking at amyloid, and not enough study has gone into tau. The research was led by Professor Ryan Julian. Julian explained to reporters that most proteins remain in the body for a limited time. If they remain too long, they may change in a way that causes them to become dysfunctional. The body has systems for removing aging proteins, but these lose effectiveness with age. Autophagy is the primary process for this. And this process weakens in people over age 65. So Julian's takeaway is that the progressive weakening of the process of autophagy may be the primary driver of Alzheimer's disease.
Enter intermittent fasting. Intermittent fasting has been shown to be helpful with weight loss, metabolic syndrome, and other maladies. Including Alzheimer's disease. It works through a variety of mechanisms, such as inducing ketosis. But it also induces autophagy. At least if you do it aggressively enough. From what I've been able to find out, a 20 hour/day fast is the minimum required to spark enough autophagy to help with Alzheimer's disease. I don't know if the people saying that know what they're talking about, but I can't find anything to suggest differently.
I began intermittent fasting in January 2019, and I've held to a consistent 20 hour fast for nearly all of the time since then. Especially in older people, an aggressive intermittent fast may have negative consequences, such as excessive weight loss. My neurologist wonders if aggressive fasting has caused a recent escalation in the visual migraines that I have experienced since 2012. My sister tells me that it impairs the uptake of calcium in the elderly, which is not good. So don't do anything radical without talking with your doctor.
But I also wonder if my fasting contributed to my improved test scores this year and the improved standing of my hippocampus volume in my recent MRI.
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