As we age, misfolded proteins such as amyloid beta, alpha synuclein and tau can accumulate in the brain. We know that this process is associated with neurodegenerative diseases and dementia, but it has never been entirely clear to what extent these accumulating proteins actually cause disease, vs simply being symptomatic of a deeper underlying cause.
If humans lived significantly longer than we do currently, would we all inevitably develop dementia due to a gradual build-up of misfolded proteins over decades? Perhaps not, suggests this study.
This six-year study of centenarians — people who are over 100 years old — found that despite high levels of a brain marker associated with cognitive decline, called amyloid beta, these centenarians were still sharp and performed well on cognitive tests. The researchers concluded these elderly subjects may have resilience mechanisms protecting them from memory loss.
In fact, they said the risk of dementia may not necessarily increase once you pass your 100th birthday.
Researchers still aren’t sure exactly why some people are protected from cognitive decline, while others are spared. The researchers in the study proposed some of these protective factors associated with cognitive performance could be education, frequent cognitive activity and even IQ. But there can be more at play.
“There could be protective immunologic and cardiovascular risk factors that help keep their brains resilient and cognitively functional even in old age,” said Dr. Gayatri Devi, a neurologist and psychiatrist at Lenox Hill Hospital in New York City.
“It’s important to understand that the presence of amyloid in the brain does not definitively mean a person will develop dementia. There are other factors and lifestyle behaviours that can make us resilient and resistant to cognitive decline.”
Research such as this, in addition to the apparent ineffectiveness of drugs targeting amyloid plaques, certainly supports the argument that protein misfolding is merely one of many factors that contribute to neurodegeneration and dementia. We know for example that inflammation can be both a cause and a consequence of protein accumulation and may be more central to the disease than the plaque itself.
One important caveat is that amyloid beta is measured post mortem and with consent of the participant, and was therefore only measured in 44 individuals. All study participants were also of the same nationality (Dutch). Consequently, more research is needed to confirm if these findings are widely applicable.
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