Amyloid B hypothesis: Abnormal elevation or insufficent clearance of AB oligomers may underlie AD pathology. AB oligomers thought to be more injurious than AB-plaques
AB Oligomers diffuse into synaptic cleft and disrupt signal transmission. Oligomers will eventually aggregate forming plaques
Tau hypothesis: aggregates of hyperphosphorylated tau protein form NFT. Amyloid B is thought to promote phosphorylation of Tau.
Mitochondrial hypothesis: APP induces mitochondrial dysfunction in neuronal cells
- Donepezil= cholinesterase inhibitor to increase Ach levels
- Memantine= prevent glutamate reuptake by nerve cells