Samuel D. Crish

TL;DR: These data support a novel and flexible model of modest ocular hypertension with axon loss, and the maximal duration of IOP elevation will be further characterized in future studies.

TL;DR: It is shown that, like other neurodegenerations, distal axon injury appears early in mouse glaucoma, and myelinated RGC axons and their presynaptic terminals persist in the colliculus well after transport fails, suggesting distal transport loss is predegenerative and may represent a therapeutic target.

TL;DR: The results suggest that deficiency of microglial TREM2 leads to heightened tau pathology coupled with widespread increases in activated neuronal stress kinases, and offer new insight into the complex, multiple roles of TREM1 in regulating Aβ and tau pathologies.

TL;DR: Recent evidence on the pathological progression of neurodegeneration in glaucoma and some of the Ca(2+)-dependent mechanisms that could underlie these changes present clear implications for efforts to develop interventions targeting neuronal loss directly and make glau coma an attractive model for both interrogating and informing other Neurodegenerative diseases.

TL;DR: It is reported that irradiation induces transient reduction in proliferating microglia within the optic nerve head and glial lamina within the first week post-irradiation, accompanied by reduced microglial activation, with no effect on astrocyte gliosis in those regions.