Study reveals Alzheimer’s spreads differently than previously thought

pharmafile | November 3, 2021 | News story | Research and Development  

A University of Cambridge research team has used human data to quantify the speed of different processes that lead to Alzheimer’s disease, and have found that it develops in a different way to how we had once perceived, according to LabOnline.

The team’s results are published in the journal Science Advances, and could revolutionise the development of future treatments for the disease.

In Alzheimer’s disease, two proteins known as tau and amyloid-beta aggregate, which kills brain cells, thus resulting in memory loss and a decrease in quality of life.

Since this disease is difficulty to study, researchers have relied largely on animal models to study it. Researchers have implanted neural immune cells grown from human stem cells into the brains of mice, to mimic the brain inflammation that the disease causes.

In this new study, researchers used post-mortem brain samples from Alzheimer’s patients, as well as PET scans from living patients, who ranged from those with mild cognitive impairment to those with late-stage Alzheimer’s disease, to track the aggregation of tau. The researchers found that the mechanism controlling the rate of progression in Alzheimer’s is the replication of aggregates in individual regions of the brain, and not the spread of aggregates from one region to another.

Dr Georg Meisl from the University of Cambridge, first author on the study, said: “The thinking had been that Alzheimer’s develops in a way that’s similar to many cancers: the aggregates form in one region and then spread through the brain. But instead, we found that when Alzheimer’s starts there are already aggregates in multiple regions of the brain, and so trying to stop the spread between regions will do little to slow the disease.”

Lina Adams

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