An experimental study from Lund University in Sweden has revealed that the Alzheimer’s protein amyloid-beta accumulates inside nerve cells, and that the misfolded protein may then spread from cell to cell via nerve fibres. This happens at an earlier stage than the formation of amyloid-beta plaques in the brain, something that is associated with the progression of Alzheimer’s disease.
International clinical trial yields mixed results with unclear cognitive effects but promising biomarker results
A new therapy prompts immune defense cells to swallow misshapen proteins, amyloid beta plaques and tau tangles, whose buildup is known to kill nearby brain cells as part of Alzheimer’s disease.
Researchers at University of California San Diego School of Medicine, with colleagues elsewhere, have used gene therapy to prevent learning and memory loss in a mouse model of Alzheimer’s disease (AD), a key step toward eventually testing the approach in humans with the neurodegenerative disease.