Alzheimer’s disease(AD)is a neurodegenerative disorder characterized by progressive cognitive impairment suggested to be induced by the accumulation of amyloid-β(Aβ)in the brain,especially in the hippocampus.Cerebral Aβdeposits may be detected through positron emission tomography(PET)as early as two decades before clinically diagnosed AD-associated dementia,which provides the opportunity for early therapeutic interventions(Wang and Mao,2021).PET may not be suitable for AD screening since it is invasive,costly,and inaccessible for routine clinical use or population screening.Aβdeposits have also been identified throughout the retina,which is a developmental outgrowth of the diencephalon and shares physiological and pathological pathways with the central nervous system(London et al.,2013).Patients with mild cognitive impairment and early AD are reported to have visual disturbances involving visual field loss with reported thinning of the retinal layers including the retinal nerve fiber layer,ganglion cell layer,and inner plexiform layer(Koronyo-Hamaoui et al.,2011;Wang and Mao,2021).Retinal Aβdeposits have been detected prior to the manifestation of cerebral Aβdeposits in transgenic mice models of AD(Koronyo-Hamaoui et al.,2011;Habiba et al.,2021).Since the retina provides an easily accessible location for non-invasive imaging,retinal Aβmay have the potential to be a surrogate for cerebral Aβand a biomarker for the detection of AD prior to irreversible cognitive impairment.
展开▼
