New research from Emory University is challenging current theories on the origins of Alzheimer’s disease, a leading cause of dementia globally. Scientists at the Goizueta Brain Health Institute have discovered that proteins accumulating around amyloid-beta deposits may play a crucial role in the progression of the disease.
Amyloid beta deposits, known as plaques, build up in the brains of Alzheimer’s patients and disrupt brain functions, causing cognitive decline. The widely accepted hypothesis is that the amyloid buildup disrupts cell-to-cell communication and activates immune cells, ultimately destroying brain cells.
However, researchers Todd E. Golde and Yona Levites have presented a new hypothesis, highlighting a different role for amyloid beta. Using advanced analytical technologies, they identified over 8,000 proteins in human brains with Alzheimer’s and similar proteins in mice. They found more than 20 proteins that co-accumulate with amyloid beta in both humans and mice.
The study suggests that these additional proteins may accelerate amyloid aggregation and play a crucial role in the disease’s pathology rather than the amyloid itself. This finding offers new directions for treatment and potential therapeutic approaches.
The research has significant implications, not only for Alzheimer’s but also for other diseases characterized by amyloid buildup, including more than 30 human disorders affecting various tissues and organs throughout the body.
Source: https://scitechdaily.com/the-real-cause-of-alzheimers-might-not-be-amyloid-groundbreaking-discovery-challenges-decades-old-theories/