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In the brain affected by Alzheimer’s, abnormal levels of the beta-amyloid protein clump together to form plaques that collect between neurons and disrupt cell function. Abnormal collections of the tau protein accumulate and form tangles within neurons, harming synaptic communication between nerve cells. Credit: National Institute on Aging, NIH
In the brains of those who suffer from Alzheimer’s, amyloids accumulate and build up into sticky plaque that disrupts brain functions and causes cognitive decline. The big unknown has been exactly how that occurs. According to the most widely adopted hypothesis, the amyloid beta buildup disrupts cell-to-cell communication and activates immune cells in a process that eventually destroys brain cells.
While the basics of Alzheimer’s have been understood for more than a century, the search for a cure has been slow, often marked by repeated cycles of initially promising treatments that didn’t work in trials, as well as continuing controversy over competing theories to best explain how the disease damages the brain. As the researchers put it, “The initial notion of a purely linear amyloid cascade is now recognized as simplistic.
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