We associate Alzheimer’s with physical deterioration in the brain, but new research shows the nerve damage responsible for Alzheimer’s onset might actually originate outside the brain, as a cascade of breakdowns that begin elsewhere in the body. The findings could open a whole new pathway for research into the devastating degenerative neurological condition.
The brains of Alzheimer’s patients exhibit an excess of a protein called amyloid-beta, which coalesces into “plaques” that disrupt neurological function. Until now, scientists have generally believed that deposits of amyloid-beta found in the brain originate in the brain. But the protein can be synthesized in peripheral tissues anywhere in the body.
[S]cientists surgically joined healthy mice to mice that had been genetically modified with high concentrations of amyloid-beta. Then they monitored the mice’s brains for signs of the Alzheimer’s disease-associated plaques. After a year, the healthy mice developed the same telling neurological symptoms as the genetically modified mice.
[S]ince the cell walls separating our blood vessels from our brain’s gray matter become weaker as we get older, the amyloid-beta in our bodies could cross over into our brains, making them a catalyst for dementia.
[Editor's note: Read the full study (behind paywall)]
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