Many older people have amyloid plaques in their brains but never progress to developing Alzheimer’s disease. It seems that amyloid accumulation on its own is not enough to cause dementia. So what is a trigger that starts the disease progression?

According to a recent study, it is an neuroinflammation, or in other words, an activation of the brain’s immune cells (microglial cells). The study showed that neuroinflammation is not a consequence, but rather an important driver of the disease progression.

To determine how harmful misfolded proteins (amyloid and tau) spread across the brain and lead to dementia, the researchers used live imaging to look deep into the brains of people with various stages of Alzheimer’s disease and healthy aging individuals.

The researchers found that neuroinflammation was more common in older people and that it was even more pronounced in people with mild cognitive impairment and Alzheimer’s. Bioinformatics analysis confirmed that tau generation depended on microglial activation. It means that microglial activation was a key element that links the effects of amyloid plaque aggregation to tau spread and, ultimately, cognitive impairment and dementia.

Based on this finding, targeting neuroinflammation might be beneficial for people with early-stage Alzheimer’s disease as it might help reverse or at least slow down the accumulation of harmful proteins in the brain and postpone Alzheimer’s.

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