Advances in Retinal Imaging: Retinal Amyloid Imaging

Koronyo‐Hamaoui, Maya; Doustar, Jonah; Oviatt, Mia; Black, Keith L.; Koronyo, Yosef

doi:10.1007/978-3-030-26269-3_6

Cited by 2 publications

(3 citation statements)

References 199 publications

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“…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.…”

Section: Retinal Aβ Pathology In Alzheimer's Patientsmentioning

confidence: 99%

“…Mounting evidence demonstrate AD-related retinal pathology in AD patients and animal models. Recent studies documented parallels between the brain and retinal pathology found both in AD patients and animal models (Koronyo-Hamaoui et al, 2011;Koronyo et al, 2012;Shi et al, 2014;Hart et al, 2016;Doustar et al, 2017;Koronyo et al, 2017;Koronyo-Hamaoui et al, 2020). While early examinations of postmortem eyes isolated from AD patients revealed loss of optic nerve integrity and RGC degeneration (Hinton et al, 1986;Blanks et al, 1989;Sadun and Bassi, 1990;Blanks et al, 1996a,b), it was not until 2010 that Koronyo-Hamaoui and colleagues were able to identify the existence of pathological hallmarks, Aβ deposits, in retinas isolated from these patients (Koronyo-Hamaoui et al, 2011).…”

Section: Introductionmentioning

confidence: 99%

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Alzheimer’s Retinopathy: Seeing Disease in the Eyes

et al. 2020

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The neurosensory retina emerges as a prominent site of Alzheimer's disease (AD) pathology. As a CNS extension of the brain, the neuro retina is easily accessible for noninvasive, high-resolution imaging. Studies have shown that along with cognitive decline, patients with mild cognitive impairment (MCI) and AD often suffer from visual impairments, abnormal electroretinogram patterns, and circadian rhythm disturbances that can, at least in part, be attributed to retinal damage. Over a decade ago, our group identified the main pathological hallmark of AD, amyloid β-protein (Aβ) plaques, in the retina of patients including early-stage clinical cases. Subsequent histological, biochemical and in vivo retinal imaging studies in animal models and in humans corroborated these findings and further revealed other signs of AD neuropathology in the retina. Among these signs, hyperphosphorylated tau, neuronal degeneration, retinal thinning, vascular abnormalities and gliosis were documented. Further, linear correlations between the severity of retinal and brain Aβ concentrations and plaque pathology were described. More recently, extensive retinal pericyte loss along with vascular platelet-derived growth factor receptor-β deficiency were discovered in postmortem retinas of MCI and AD patients. This progressive loss was closely associated with increased retinal vascular amyloidosis and predicted cerebral amyloid angiopathy scores. These studies brought excitement to the field of retinal exploration in AD. Indeed, many questions still remain open, such as queries related to the temporal progression of AD-related pathology in the retina compared to the brain, the relations between retinal and cerebral changes and whether retinal signs can predict cognitive decline. The extent to which AD affects the retina, including the susceptibility of certain topographical regions and cell types, is currently under intense investigation. Advances in retinal amyloid imaging, hyperspectral imaging, optical coherence tomography, and OCT-angiography encourage the use of such modalities to achieve more accurate, patient-and user-friendly, noninvasive detection and monitoring of AD. In this review, we summarize the current status in the field while addressing the many unknowns regarding Alzheimer's retinopathy.

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Section: Retinal Aβ Pathology In Alzheimer's Patientsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Alzheimer’s Retinopathy: Seeing Disease in the Eyes

et al. 2020

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“…Histopathologic findings have shown that the superior peripheral hemiretina is generally the most atrophic region. 35 A recent study also showed a higher Aβ 42 density in the periphery versus the central retina in human donor eyes affected by MCI or AD. 36 The propensity of amyloid proteins to accumulate in peripheral areas of the retina implies that analyzing ultra-widefield topographic OCTA metrics in preclinical AD could provide valuable insights into the natural history of retinal amyloid pathology.…”

Section: Discussionmentioning

confidence: 94%

Choriocapillaris and Retinal Vascular Alterations in Presymptomatic Alzheimer's Disease

Corradetti,

Oncel,

Kadomoto

et al. 2024

Invest. Ophthalmol. Vis. Sci.

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Purpose To compare optical coherence tomography angiography (OCTA) retina metrics between cognitively healthy subjects with pathological versus normal cerebrospinal fluid (CSF) Aβ 42 /tau ratios. Methods Swept-source OCTA scans were collected using the Zeiss PLEX Elite 9000 and analyzed on 23 cognitively healthy (CH) subjects who had previously undergone CSF analysis. Thirteen subjects had a pathological Aβ 42 /tau (PAT) ratio of <2.7132, indicative of presymptomatic Alzheimer's disease (AD), and 10 had a normal Aβ 42 /tau (NAT) ratio of ≥2.7132. OCTA en face images of the superficial vascular complex (SVC) and deep vascular complex were binarized and skeletonized to quantify the perfusion density (PD), vessel length density (VLD), and fractal dimension (FrD). The foveal avascular zone (FAZ) area was calculated using the SVC slab. Choriocapillaris flow deficits (CCFDs) were computed from the en face OCTA slab of the CC. The above parameters were compared between CH-PATs and CH-NATs. Results Compared to CH-NATs, CH-PATs showed significantly decreased PD, VLD, and FrD in the SVC, with a significantly increased FAZ area and CCFDs. Conclusions Swept-source OCTA analysis of the SVC and CC suggests a significant vascular loss at the CH stage of pre-AD that might be an indicator of a neurodegenerative process initiated by the impaired clearance of Aβ 42 in the blood vessel wall and by phosphorylated tau accumulation in the perivascular spaces, a process that most likely mirrors that in the brain. If confirmed in larger longitudinal studies, OCTA retinal and inner choroidal metrics may be important biomarkers for assessing presymptomatic AD.

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Advances in Retinal Imaging: Retinal Amyloid Imaging

Cited by 2 publications

References 199 publications

Alzheimer’s Retinopathy: Seeing Disease in the Eyes

Alzheimer’s Retinopathy: Seeing Disease in the Eyes

Choriocapillaris and Retinal Vascular Alterations in Presymptomatic Alzheimer's Disease

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