Disturbance of neuronal plasticity is a critical pathogenetic event in Alzheimer's disease.

Brain areas affected by AD pathology are primarily those structures that are invovled in the regulation of "higher brain functions". The functions these areas subserve such as learning, memory, perception, self-awareness, and consciousness require a life-long re-fittng of synaptic contacts that allows for the acquistion of new epigenetic information, a process based on a particularly high degree of structural plasticity. Here, we outline a hypothesis that it is the "labile state fo differentiation" of a subset of neurons in the adult brain that allows for ongoing neuroplastic processes after development is completed but at the same time renders these neurons particularly vulnerable. Mechanisms of molecular and cellular control of neuronal differentiation and proliferation might, thus, not only play a role during development but critically involved in the pathogenesis of neurodegeneration.