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Longevity Briefs: Alzheimer’s Disease May Not Develop The Way We Previously Thought

Posted on 9 November 2021

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Longevity briefs provides a short summary of novel research in biology, medicine, or biotechnology that caught the attention of our researchers in Oxford, due to its potential to improve our health, wellbeing, and longevity.

Why is this research important: Alzheimer’s disease is associated with the aggregation of proteins called tau and amyloid beta, which are hypothesised to drive Alzheimer’s by killing neurons throughout the brain. Understanding how these proteins spread during the course of the disease has important implications for future treatments. Animal models suggest that protein aggregates in Alzheimer’s disease begin to form at a single starting point in the brain, then spread to other regions in a ‘chain reaction’. If that’s true, then preventing the spread of aggregates between brain regions could be an effective way to slow disease progression. Unfortunately, animals like mice make poor models for Alzheimer’s disease in humans, as most experimental animals do not live long enough to get Alzheimer’s naturally, meaning that a greatly accelerated form of the disease must be induced.

What did the researchers do: In this study, researchers combined 5 different human datasets, including post-mortem brain samples from Alzheimer’s patients and PET scans from living patients at various stages of the disease. They specifically studied the presence of tau aggregates throughout the brain, and used a mathematical model to identify which mechanism was ultimately most important for the rate of disease progression.

A and B respectively are illustrations of the spreading and replication of tau aggregates. In spreading, existing aggregates relocate to other brain regions, while in replication, tau aggregates grow and multiply within a given brain region.
C and D show expected patterns of distribution of tau aggregates with time, depending on whether disease progression is limited by spread or by replication. If aggregation is spread limited, then aggregate load should decline sharply after a certain distance from the origin point, with aggregates spreading further as time progresses (C). If aggregation is limited by replication, then aggregate load should be mostly the same regardless of location, but should become higher as time progresses (D).

Key takeaway(s) from this research: Contrary to what has been observed in animal models, the researchers found that tau aggregates were already present in multiple brain regions at the start of Alzheimer’s disease, and it was the rate at which the aggregates subsequently replicated and killed neurons in these regions that determined how quickly the disease progressed during the mid and late stages. This would suggest that the replication of aggregates, rather than their spread throughout the brain, may be a more valuable target for drugs in the future.

They also found that the rate of tau aggregate replication was much slower in the human brain than that which has been observed in the test tube, suggesting that neurons are very good at slowing down this process. Indeed, tau replication was so slow that it cannot alone explain the high levels of tau protein found in late-stage Alzheimer’s, suggesting that other routes of tau formation might come into play.

This study is quite significant because it is the first to use human data to track the processes controlling Alzheimer’s development.

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