Abstract
Alzheimer’s disease (AD), a primary cause of dementia in the aging population, is characterized by extracellular amyloid-beta peptides aggregation, intracellular deposits of hyperphosphorylated tau, neurodegeneration and glial activation in the brain. It is commonly thought that the lack of early diagnostic criteria is among the main causes of pharmacological therapy and clinical trials failure; therefore, the actual challenge is to define new biomarkers and non-invasive technologies to measure neuropathological changes in vivo at pre-symptomatic stages. Recent evidences obtained from human samples and mouse models indicate the possibility to detect protein aggregates and other pathological features in the retina, paving the road for non-invasive rapid detection of AD biomarkers. Here, we report the presence of amyloid beta plaques, tau tangles, neurodegeneration and detrimental astrocyte and microglia activation according to a disease associated microglia phenotype (DAM). Thus, we propose the human retina as a useful site for the detection of cellular and molecular changes associated with Alzheimer’s disease.
Highlights
Alzheimer’s disease (AD) is a neurodegenerative disorder leading to dementia during elderly
The accumulation of Aβ and phosphorilated Tau (pTau) aggregates in the retinal tissue has been reported on both AD human tissue (Koronyo-Hamaoui et al, 2011; Koronyo et al, 2017) and mouse models (Criscuolo et al, 2018; Grimaldi et al, 2018), suggesting a putative use of the eye as a valuable structure for the study and the diagnosis of AD and other neurodegenerative disease
Michael’s Hospital Human Eye Biobank), we first confirmed the presence of Aβ and pTau aggregates in the retinal layers
Summary
Alzheimer’s disease (AD) is a neurodegenerative disorder leading to dementia during elderly. AD cases are constantly increasing and it is estimated that by the year 2050 AD will globally affects about 115 million people (Alzheimer’s Disease International World Alzheimer Report, 2009; Scheltens et al, 2016) posing a growing concern on public health. Studies from post-mortem brains revealed that, at the neuropathological level, distinctive features of AD include aggregation of amyloid beta protein (Aβ) and tau protein hyperphosphorylation (pTau), which cause synapses loss and neuronal degeneration. These plaques and tangles are generally associated with activated microglia and reactive astrocytes in AD brain (Ahmed et al, 2017; Henstridge et al, 2019). Over the years several candidate drugs have been proposed as a putative therapy for AD. Despite many attempts, a definitive cure has not been found yet and only symptomatic treatments are available
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