PMC:7523471 / 12024-13031 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/7523471","sourcedb":"PMC","sourceid":"7523471","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7523471","text":"Schematic illustration of retinal pathology in AD patients. A comparison between cognitively normal control and AD retinas along a continuum. AD attributed retinal pathology includes accumulation of Aβ and phosphorylated-tau proteins, degeneration and subsequent thinning, and an inflammatory response. AD retinal vessels display substantial thinning and pericyte loss alongside Aβ protein deposition. Modified illustration from Advances in Retinal Imaging: Retinal Amyloid Imaging (Koronyo-Hamaoui et al., 2020) with permission from Springer Nature via Copyright Clearance Center. Aβ, Amyloid-β protein; CTRL, control; GCL, ganglion cell layer; ILM, inner limiting membrane; INL, inner nuclear layer; IPL, inner plexiform layer; mRGCs, melanopsin-containing retinal ganglion cells; NFL, nerve fiber layer; NFT, neurofibrillary tangles; OPL, outer plexiform layer; ONL, outer nuclear layer; OLM, outer limiting membrane; PRL, photoreceptor layer; RGCs, retinal ganglion cells; pTau, hyperphosphorylated tau.","tracks":[]}