Psy 468: Alzheimer's Disease, amyloid beta, & tau

both abnormal accumulations of amyloid beta and of tau may result in the cognitive losses of Alzheimer's dementia.

Current neuroenhancement medications are aimed at reducing production of amyloid beta; these slow decline but only temporarily.

Animal models (mice genetically engineered to develop brain pathology similar to Alzheimer's disease) suggest that treatment reducing the formation of mutant taus or even the normal protein may reduce memory loss and neurological deficits even with accumulating amyloid beta (see Roberson et al., 2007).

Mutant tau may activate microglial cells, the brain's immune cells. Treatment with an immunosuppressant decreases neuronal loss and life span in affected mice.

Also, tau binds to and stabilizes the microtubles which transport nutrients, proteins, and material in the neuronal axon. Tau become excessively phosphorylated in Alzheimer's brains, leading to it no longer binding properly to microtubules, that in turn deteriorate, leading to cell death.

Science, vol 316, 2007, pp. 1416-1417.