From San Francisco, at the International Stroke Conference
People who die from a stroke have accumulations of a protein called amyloid beta in the thalamus, a part of the brain involved in motor control, sensory processing, and signal relaying, researchers report.
In healthy people, the brain routinely makes and clears away amyloid beta, whose normal role is poorly understood. But in the brains of people with Alzheimer’s disease, amyloid beta gathers into waxy clumps—a development widely believed to contribute to this form of dementia.
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No clear connection between amyloid beta and stroke had ever been established in people, but animal tests suggested a link.
Biochemist Jukka Jolkkonen of the University of Kuopio in Finland and his colleagues examined stored brain tissues from 427 people who had died after a stroke had shut off blood to a portion of their brains and 57 people who had had no strokes. No patient in either group had been diagnosed with Alzheimer’s disease or any other form of dementia. The stroke and nonstroke groups had the same average age at death.
The stroke victims had significantly greater amyloid beta accumulations in the thalamus than did the others, even though the thalamus itself hadn’t suffered damage in the stroke patients, says Jolkkonen.
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The thalamus is near the end of arterial branches, making the area slow to routinely clear amyloid beta, says Jolkkonen. While the location puts it away from areas of direct stroke damage, Jolkkonen hypothesizes that the stress of a stroke in another part of the brain disrupts signals between those areas and the thalamus, further hindering amyloid beta clearance there.