Alzheimer's disease progresses inside the brain in a rising storm of cellular activity as deposits of the toxic protein, amyloid-beta, overwhelm neurons.

AD progresses in a rising storm of cellular activity inside the brain, as deposits of the toxic protein, amyloid-beta, overwhelm neurons. An apparent side effect of accumulating amyloid-beta is the Golgi fragmentation by activating a cell cycle kinase, cdk5. This Golgi function can be rescued by blocking cdk5 or shielding its downstream target protein in the Golgi, GRASP65. Rescuing the Golgi reduced amyloid beta accumulation significantly, apparently by re-opening a normal protein degradation pathway for the amyloid precursor protein (APP).
The study has paved a way for drugs hoping to slow AD progression.
Source-Medindia