Fat deposits implied

It may be possible to improve the fortunes of patients with Alzheimer’s disease by giving them a drug that targets the fatty plaques that form in their brains early in the development of the disease, suggests work by Quebec researchers .

Postdoctoral researcher Laura Hamilton from the CHUM Research Center and her colleague Karl Fernandes, associate researcher at CRCHUM and professor-researcher at the University of Sherbrooke, reported in 2015 that fatty deposits (not to be confused with plaques of proteins, better known in the context of Alzheimer’s disease) clogs patients’ brains. These fat accumulations were first seen in the brains of mice, then their presence in human brains was confirmed during an autopsy. Their new work, published in the prestigious journal Nature, is “the second chapter,” Mr Fernandes said, as they are interested in how we might target the enzyme responsible for forming these lipid deposits. More specifically, the new paper focuses specifically on the hippocampus, a brain structure essential for memory and learning.

“What we’ve seen is that when we put this drug in the (mouse) brain, which inhibits the enzyme that makes this fatty acid that we think is toxic, we turn off a lot of the genes involved in Alzheimer’s disease involved can switch off at rates like wild mice, so (…) at a more normal pace,” Ms Hamilton summarized. In addition, the affected genes play a key role in various facets of Alzheimer’s disease, she added. These fatty deposits appear to form in the brain very early in the disease process, well before many other changes that eventually cause the usual symptoms of Alzheimer’s disease, but after the accumulation of amyloid proteins early in the disease. “The drug we used will change the composition of fatty acids and correct memory,” Fernandes said. It’s sort of the missing link between the trigger, the amyloid, and all the things you see afterwards. »

The drug (SCDi) also had the effect of fighting inflammation in the brain and restoring connections between cells, Hamilton said. The mice that received it regained the same memory capacities as a mouse that had never been sick after just a month of treatment, even if they already showed obvious memory loss. Ms. Hamilton and Mr. Fernandes can almost claim to have been the ones who, back in 2015, got the scientific community on the trail of these fat accumulations in the brain linked to Alzheimer’s disease. But if we go back to the scientific literature, says Mr. Fernandes, we see that Dr. Alois Alzheimer also described these lipid aggregates a hundred years ago. “But after a few years, people didn’t think it was important, so it fell out of the literature,” he said.

In any case, as of 2015, several other researchers are interested in the role that SCDi could play in combating other neurodegenerative diseases such as Parkinson’s and multiple sclerosis. A clinical study on the treatment of Parkinson’s was even initiated last year. The two Quebec researchers would be the only ones currently studying in detail the role of these fatty deposits in Alzheimer’s disease. Their work could eventually lead to the development of new tests for the disease and, they hope, new treatments, given that the necessary inhibitors are already on the market, having been developed for other health conditions. said Mr Fernandes.

“We were able to regulate memory after just one month with one drug,” emphasized Ms. Hamilton. If we treat longer, sooner or later, we might even be able to achieve extraordinary effects. We don’t know, but it’s very promising for us. »

Photo credit: iStock

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