Fatty brain

I have a friend who works in an elderly care facility, and she often laments that patients with Alzheimer’s and other forms of dementia have no status or honor. The behavior of these patients seems unimaginable. They eat bug spray, they eat feces and play with it. My mother’s close, childhood friend is also an Alzheimer’s patient. She lost all of her memories of her political and royal family connections. My heart aches every time I visit her to see how she is doing.

Over the past decade, the number of Alzheimer’s patients in the U.S. has increased significantly, and it is estimated that by 2025, approximately 7.2 million Americans over the age of 65 will have Alzheimer’s disease.

According to Wikipedia, Alzheimer’s disease is “believed to occur when abnormal amounts of amyloid beta (Aβ), accumulating extracellularly as amyloid plaques and tau proteins, or intracellularly as neurofibrillary tangles, form in the brain, affecting neuronal functioning and connectivity, resulting in a progressive loss of brain function.” However, new research published in the medical journal, “Immunity”, has uncovered another major culprit: an overload of fat.

A study published this September by Purdue University researchers found that excess fat in the brain’s immune cells weakens its defense against Alzheimer’s disease. When overloaded, immune cells stop removing toxic proteins like amyloid beta, accelerating the damage they are supposed to prevent.

Most Alzheimer’s drugs in development target the main hallmarks of the disease, amyloid beta protein plaques and tau protein tangles, but they were not the underlying cause.

The study, led by Purdue University professor Gaurav Chopra, found that in Alzheimer’s disease brains, microglia, the brain’s immune cells located near the plaque, contain twice as many fat droplets as microglia located farther away. These “fat suffocated” immune cells removed 40% less amyloid beta protein. Professor Chopra’s team focused on the cause of this problem, an enzyme called DGAT2, which converts free fatty acids into stored fat (= triglycerides). And in Alzheimer’s disease brains, this enzyme is not broken down and accumulates, resulting in an excess of stored fat in the microglia. When researchers inhibited or degraded DGAT2 in their experimental model, microglia regained their strength, removed the plaque, and restored brain balance.

Chopra said, “In our view, directly targeting plaques or tangles will not solve the problem; we need to restore function of immune cells in the brain. We’re finding that reducing accumulation of fat in the diseased brain is the key, as accumulated fat makes it harder for the immune system to do its job and maintain balance. By targeting these pathways, we can restore the ability of immune cells like microglia to fight disease and keep the brain in balance, which is what they’re meant to do.”

A Spanish study published February 2024 stated that a high-fat diet alters levels of key miRNAs in the brain and body and may accelerate or worsen symptoms of Alzheimer’s disease. miRNAs are small molecules that regulate gene expression, the epigenetic (gene expression) I explained about before, small molecular switches that turn genes on and off.

The high-fat diet not only leads to lifestyle-related diseases such as type 2 diabetes, heart disease, and obesity, but also affects the brain and causes dementia. Anthony William, author of Medical Medium, says, “Just as the liver becomes unhealthy and fatty, resulting in a fatty liver, the brain becomes equally unhealthy and fatty, resulting in a fatty brain.”

I highly recommend that limiting processed oils (canola, soy, corn) that disrupt the lipid balance of the brain and cell membranes, take CoQ10, PQQ, and alpha-lipoic acid, which improve cellular energy and fat burning, as well as omega-3 fatty acids (EPA/DHA) and curcumin, resveratrol, which support microglia and neuron health.

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Published by Kaoru Kashima

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