Five million Americans suffer from Alzheimer’s disease, but scientists still have more questions about it than answers. Arguments abound over whether the hallmark protein clusters that accumulate in the brain are a cause or an effect of the illness, and current treatments do not address the main problem that causes impaired thinking: broken synapses, the junctions that allow neurons to communicate with one another. Researchers are now zeroing in on a promising missing link: mitochondria, the cell components responsible for energy regulation. In October researchers at Columbia University reported that young mice predisposed to acquiring Alzheimer’s accumulate protein clusters in synaptic mitochondria and that these clusters directly impair synapse function.
The link between mitochondria and Alzheimer’s is not exactly new. In the 1990s studies suggested that in the diseased brains of people and mice, mitochondria do not produce and distribute energy normally. And as early as 1994 researchers at the University of Kentucky showed that amyloid-beta protein fragments, the type found in Alzheimer’s, interfere with mitochondrial function. But no one knew how, exactly, mitochondria were linked to synaptic problems, if at all.
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