A new study reveals that a previously undiscovered mouse gene reduces the two major pathological perturbations commonly associated with Alzheimer's disease (AD). The research, published by Cell Press in the November 12 issue of the journal Neuron, finds that the novel gene interacts with a key cellular enzyme previously-linked with AD pathology, thereby uncovering a new strategy for treating this devastating disorder.
AD is an incurable neurodegenerative disease characterized by a pathological accumulation of extracellular sticky amyloid beta (a-beta) protein plaques and intracellular hyperphosphorylated tau protein aggregations, called neurofibrillary tangles (NFT), in the brain. Previous research has suggested that glycogen synthase kinase-3 (GSK-3), an enzyme that is essential for many critical cellular functions, may play a role in both a-beta plaque and NFT generation.
"Because GSK-3 regulates two major pathological hallmarks of AD, manipulation of its activity is an attractive potential therapeutic strategy for AD," explains senior study author Dr. Huaxi Xu, professor and acting director of the Neurodegenerative Disease Research Program at the Burnham Institute for Medical Research in La Jolla, California.