A mouse model of retinal degeneration reveals a common mechanism for axonal degeneration and photoreceptor cell death and identifies SARM1 as a therapeutic candidate for retinopathies.

Mouse retina manifests homeostatic plasticity and adapts to photoreceptor degeneration to resist visual decline.

Lipid efflux by the retinal pigment epithelium is crucial for proper retinal integrity and function, and its impairment may contribute to diseases like age-related macular degeneration.

Regulating rod gene expression with a small molecule ligand for the orphan nuclear receptor Nr2e3 rescues photoreceptors from degeneration in a mouse model of retinitis pigmentosa.

TGFβ signaling to retinal microglia is central to the regulation of neuroinflammatory responses relevant to age-related macular degeneration (AMD), a leading cause of blindness in the developed world.

A combination of in vitro and in vivo experiments demonstrate a cell-autonomous role of the KIT ligand/KIT signaling pathway in protecting retinal photoreceptor cells from environmentally or genetically caused degeneration.

Transportomic analysis of the changes underlying neurodegeneration reveals the importance of Kif5a for neuronal survival and highlights the need to restore specific anterograde cargo transport to for regeneration.

A preclinical study using exogenous retinoids in a novel Usher syndrome 1F mouse model reveals a possible therapy to treat mutant PCDH15-mediated visual dysfunction.

Comprehensive mouse genetic analyses show, by having mTORC1 constitutively active, a RPC divides and exhausts mitotic capacity faster than neighboring RPCs, and thus produces retinal cells that degenerate with aging-related changes in the mature mouse retina.

A novel therapy for a common blinding retinal disease uses an innovative CCR1 blocking-based strategy.