The progression of Alzheimer's disease (AD) can be arrested
by rescuing the Golgi apparatus, the part of the cell involved in packaging and
sorting protein cargo.
The study was carried out by researchers Yanzhuang Wang,
Gunjan Joshi, and colleagues at the University of Michigan, Ann Arbor. In order
to uncover the mechanism damaging the Golgi, they used a transgenic mouse and
tissue culture models of AD to look at what was happening inside the brain.
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
The study has paved a way for drugs hoping to slow AD