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Are these brain-protecting cells actually contributing to Alzheimer’s?

| | May 7, 2018

[Neuroscientist Michael Heneka] and his team had eliminated a key inflammation gene from a strain of mouse that usually develops symptoms of Alzheimer’s disease. The modified mice seemed perfectly healthy. They sailed through memory tests and showed barely a sign of the sticky protein plaques that are a hallmark of the disease.

Since then, numerous studies have bolstered the link between dementia and the brain’s immune system, highlighting the cells and signals involved. But none has managed to fully pin it down.

Microglia have turned out to be central to the link between inflammation and neurodegeneration (see ‘Help or hinder’). The cells have two major functions. They take care of the general health of neurons and their synapses — the junctions between neurons where they communicate with one another. And they patrol the brain, searching for threats and problems.

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How might microglia, which evolved to keep the brain in good order, become a force for the bad in Alzheimer’s? Last year, Heneka and his colleagues published evidence suggesting a plausible mechanism for the switch, at least in their mice. They found that activated microglia discard the remnants of inflammasomes in tiny clumps called specks, and that these specks go on to seed new amyloid-β clusters, spreading the disease across the brain. “A perfect storm,” says Heneka. “Toxic amyloid-β promotes inflammation, which promotes more toxic amyloid-β.”

Read full, original post: Is ‘friendly fire’ in the brain provoking Alzheimer’s disease?

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