The age increase of GFAP may also be a factor in
Alzheimer disease (AD), because aging is the major risk factor
for AD, with the risk of AD doubling every 5 years after
65 [16]. In AD, synapse loss showed inverse correlations with
astrocyte volume [3]. According to our hypothesis, synapse
loss during aging could be intensified by GFAP-driven as trocytic changes during the progression of AD. The greater
induction of GFAP in lesions of old brains [11,12,35] and in
the present culture models are consistent with feed-forward
cascades of neurodegeneration and astrocytosis.