Why Humans Are Uniquely Vulnerable to Alzheimer’s Disease
Humans’ unique brain traits make them more prone to Alzheimer’s, while non-human primates resist age-related brain damage.
Complete the form below to unlock access to ALL audio articles.
A recent review in Aging (Albany NY) explores why humans are uniquely vulnerable to Alzheimer’s disease (AD) compared to non-human primates, such as chimpanzees, baboons and macaques. Authored by Ferrer Isidro from the University of Barcelona and Reial Acadèmia de Medicina de Catalunya, the work highlights evolutionary differences that may explain why Alzheimer’s causes severe cognitive decline and memory loss in humans, while non-human primates experience only mild aging-related changes.
Understanding the divergence in brain aging
Alzheimer’s affects over 50 million people globally, but non-human primates rarely exhibit the toxic protein deposits central to the disease. While aging primates can develop beta-amyloid plaques, these are less toxic than in humans and do not interact with tau tangles to trigger dementia. Tau tangles, harmful deposits of tau protein that damage brain cells and disrupt memory, are common in humans and emerge early in life. In contrast, these tangles are rare in non-human primates and typically confined to small regions of the brain.
Tau tangles
Abnormal accumulations of tau protein in brain cells, which impair cellular functions and contribute to Alzheimer’s disease progression.Beta-amyloid plaques
Clumps of protein fragments derived from amyloid precursor protein, found in the brains of Alzheimer’s patients. These plaques are toxic in humans but less harmful in non-human primates.This divergence underscores significant differences in aging-related brain processes. Humans’ longer lifespans, larger brains and higher cognitive abilities may contribute to their heightened susceptibility to Alzheimer’s. These traits, which emerged through evolution, likely came with trade-offs that make human brains more prone to aging-related damage.
Want more breaking news?
Subscribe to Technology Networks’ daily newsletter, delivering breaking science news straight to your inbox every day.
Subscribe for FREERethinking Alzheimer’s treatments
The review emphasizes that tau tangles, rather than beta-amyloid deposits, may play a more central role in Alzheimer’s progression. This perspective challenges the amyloid cascade hypothesis, which identifies beta-amyloid as the main driver of the disease. By shifting attention to tau pathology, the findings could inspire the development of treatments aimed at preventing or reducing tau deposits.
Amyloid cascade hypothesis
A widely accepted theory suggesting that beta-amyloid deposition is the primary trigger for Alzheimer’s disease.Lessons from non-human primates
Studying non-human primates may also uncover protective mechanisms that help their brains avoid severe aging-related damage. These insights could lead to novel strategies for delaying or preventing Alzheimer’s in humans. Understanding why primates resist the toxic cascade of tau and beta-amyloid interactions could transform approaches to managing brain aging.
Implications for Alzheimer’s research
This work highlights the need to refine current theories about Alzheimer’s development and progression. It also underscores the importance of studying diverse species to uncover biological mechanisms that could inform treatments. By identifying evolutionary vulnerabilities in human brain aging, scientists may find new opportunities to combat aging-related diseases like Alzheimer’s.
Reference: Isidro F. Brain aging and Alzheimer’s disease, a perspective from non-human primates. Aging. 2024. doi: 10.18632/aging.206143
This article has been republished from the following materials. Note: material may have been edited for length and content. For further information, please contact the cited source. Our press release publishing policy can be accessed here.
This content includes text that has been generated with the assistance of AI. Technology Networks' AI policy can be found here.
