Pathogenic Tau Presence in Optic Nerve Crushed Mouse Model

Irreversible loss of retinal ganglion cells after neurodegenerative disorders may result in blindness. Thus, it is of crucial importance to identify and suppress the destructive irremediable loss of ganglion cells. Recent studies showed Tau pathology process as a major destructive neurodegeneration factor upon traumatic brain injury. It has recently been demonstrated that Cis-p Tau conformers are extremely neurotoxic and trigger neurodegeneration process. In the current study, we examined pathogenic Tau presence in the crushed cell body and axonal structure of mouse retinal ganglion cells for the first time.

We performed an interventional experiment on retinal ganglion cells. Optic nerve crush injury was induced in C57 mouse, so the axons of the ganglion cells were damaged and the connection between the eye and the optic nerve was affected. Mice vision and behavior was analyzed using Visual cliff test after surgery to confirm the effect of surgery on optic nerve crush. Pathogenic Tau was observed using immunofluorescent staining via specific antibody for Tau on retinal ganglion cell body and optic nerve axons 60 days post crush. The results were analyzed via Prism software.

The first signs of pathogenic Tau accumulation were seen 24 hours post-crush in the ganglion cell layer after staining with Tau antibody which increased during the following days in more areas. On the 60th day post-crush, we detected pathogenic Tau presence in the ganglion cell nucleus. Proof of increase in pathogenic Tau expression was also quantified in another study.

It seems that the pathogenic Tau accumulates in the retinal cells of C57 mice after optic nerve crush. So, we could consider pathogenic Tau presence as one of the destructive factors of retinal ganglion cells after optic nerve crush qualitatively and, also, the rate of increase in its expression was proved in another study. This is the first time such a finding is reported in retina.