Aging is the major risk factor for numerous brain diseases. This is especially true for Alzheimer's disease (AD), a peculiar neurodegenerative disorder in that it results from the synergy of two simultaneous but distinct degenerating processes: A beta and tau pathologies. For AD, and for most neurodegenerative disorders, aggregation of full length or truncated proteins, in neurons or glial cells, or in the parenchyma, is central, but still a mystery. In addition, the late onset of these pathologies links them to ageing processes. Cause or consequence? Experimental models, that allow us to dissect these pathophysiological defects, are presented.