The Cause of Alzheimer's Might Not Be Amyloid

Recent research from Emory University challenges the long-held belief that amyloid-beta deposits are the primary cause of Alzheimer's disease. Instead, scientists suggest that proteins accumulating around these deposits may be responsible for the progression of the disease. The study, published in Cell Reports Medicine, indicates that amyloid-beta serves as a scaffold for other proteins, which could disrupt brain cell function and lead to cognitive decline. Researchers identified over 20 proteins that co-accumulate with amyloid-beta in both human and mouse brains, with two specific proteins, midkine and pleiotrophin, shown to accelerate amyloid aggregation. This new understanding of Alzheimer's pathology suggests that targeting these additional proteins could lead to novel therapeutic approaches. The findings highlight the complexity of Alzheimer's disease, moving away from the simplistic amyloid cascade hypothesis and opening avenues for research into treatment strategies for Alzheimer's and potentially other diseases linked to amyloid buildup.

- New research suggests proteins around amyloid-beta may drive Alzheimer's progression.

- Over 20 proteins identified that co-accumulate with amyloid-beta in affected brains.

- Midkine and pleiotrophin proteins may play a significant role in brain damage.

- The study challenges the traditional amyloid cascade hypothesis of Alzheimer's.

- Findings could lead to new therapeutic strategies for Alzheimer's and related disorders.