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Alzheimer's Research Takes a New Turn

Study suggests that gummed-up synapses -- not plaque -- may be at the root of aging brain diseases

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"Our findings may well explain the long-mysterious vulnerability specifically of the aging brain to neurodegenerative disease," he said. "Kids don't get Alzheimer's or Parkinson's," Barres pointed out.

"Profound activation of the complement cascade, associated with massive synapse loss, is the cardinal feature of Alzheimer's disease and many other neurodegenerative disorders. People have thought this was because synapse loss triggers inflammation. But our findings here suggest that activation of the complement cascade is driving synapse loss, not the other way around," Barres explained.

Heather Snyder, director of medical and scientific operations for the Alzheimer's Association, said the new study "adds to the body of information that looks at how the immune system might work in Alzheimer's disease." She added that there are many hypotheses that need to be explored about what may be happening in Alzheimer's.

Noting that much of the research in the current study involved mice, Snyder said future studies need to focus on how C1q affects human brains.

"This is really opening the door that this should be explored further," she said. "It needs to be replicated in the laboratory and also correlated to what it may mean in human beings."

More than 5 million Americans have Alzheimer's disease, and that number is expected to rise significantly as the baby boom generation ages.

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