Interestingly, in Tg2575 model of amyloidosis which displays some pathological tau-related alterations but not NFT [26], Latina and colleagues demonstrated, via an elegant immunotherapy approach by using a neutralizing tau antibody against its toxic N-terminal fragment, that decreasing tau content yields abolishment of both Aβ and p-tau accumulation, as well as tuning down of some neuroinflammatory (i.e. increased GFAP but not Iba-1 expression) and synaptic (e.g. synaptophysin but not SNAP-25) impairments at the early stage of pathogenesis in the retina [33]. The gene discussed is GFAP; the disease is amyloidosis.