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Alzheimer's Retinopathy: Seeing Disease in the Eyes
Mirzaei N, Shi H, Oviatt M, Doustar J, Rentsendorj A, Fuchs DT, Sheyn J, Black KL et al.. Frontiers in neuroscience, 2020-09-08
Topic: Amyloid, tau and blood-test diagnosis
Plain-language summary
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.
What this study adds
Evidence grade: Low
This is a narrative review. This review describes evidence that the retina shows signs of Alzheimer's disease pathology, including amyloid plaques, hyperphosphorylated tau, neuronal degeneration, retinal thinning, vascular abnormalities and gliosis. It suggests the retina may be a site for noninvasive imaging, but does not report a treatment or cure.
Taken from this record’s own fields, not from reading the paper. The grade is assigned from the abstract’s wording; what that means.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Mirzaei, N., Shi, H., Oviatt, M., Doustar, J., Rentsendorj, A., Fuchs, D. T., et al. (2020). Alzheimer's Retinopathy: Seeing Disease in the Eyes. Frontiers in neuroscience. https://doi.org/10.3389/fnins.2020.00921
Vancouver
Mirzaei N, Shi H, Oviatt M, Doustar J, Rentsendorj A, Fuchs DT, et al. Alzheimer's Retinopathy: Seeing Disease in the Eyes. Frontiers in neuroscience. 2020. doi:10.3389/fnins.2020.00921. PMID: 33041751.
BibTeX
@article{mirzaei2020-33041751,
author = {Mirzaei, N. and Shi, H. and Oviatt, M. and Doustar, J. and Rentsendorj, A. and Fuchs, D. T. and Sheyn, J. and Black, K. L. and others},
title = {{Alzheimer's Retinopathy: Seeing Disease in the Eyes}},
journal = {Frontiers in neuroscience},
year = {2020},
doi = {10.3389/fnins.2020.00921},
pmid = {33041751},
url = {https://doi.org/10.3389/fnins.2020.00921}
}
Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. The record's author list ends in “et al.”, so not every author is named. Check the citation against the original before you use it.
Key findings
- 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.
- 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.
- This progressive loss was closely associated with increased retinal vascular amyloidosis and predicted cerebral amyloid angiopathy scores.
- 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.
Why it matters
This review describes evidence that the retina shows signs of Alzheimer's disease pathology, including amyloid plaques, hyperphosphorylated tau, neuronal degeneration, retinal thinning, vascular abnormalities and gliosis. It suggests the retina may be a site for noninvasive imaging, but does not report a treatment or cure.
Study details
- Evidence strengthLow
How this study scored 46/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people and randomized / blinded because the record does not state it.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Frontiers in neuroscience) |
| Journal's citation record | 2 / 4 | Frontiers in Neuroscience: journal h-index 226 (OpenAlex, 2026-10-29) |
| Study design | 0 / 12 | No study design recorded — scores zero, not guessed (not stated in the record — scored 0) |
| Strength of evidence | 1 / 5 | Rated “low” in our summary |
| Peer-review validation | 10 / 10 | Peer-reviewed. Published as an article in a named peer-reviewed journal. |
| How recent | 2 / 5 | 2020 — within 10 year(s) of the newest study here |
| Sample size | 0 / 4 | Participant count not stated — scores zero (not stated in the record — scored 0) |
| Effect reported | 0 / 3 | No effect size reported — scores zero (not stated in the record — scored 0) |
| Studied in people | 0 / 3 | Not stated whether this was studied in people — scores zero (not stated in the record — scored 0) |
| Randomized / blinded | 0 / 2 | No randomization or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 5 / 7 | Cited 127 times (OpenAlex, 2026-10-10) |
| Citations per year | 3 / 5 | 15.9 citations a year over 8 year(s) since 2020 |
| Impact for its field and year | 4 / 6 | Cited 8.1× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 2 / 6 | Cited by 3 other studies in this library |
| Still being cited | 3 / 4 | Cited 63 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 2 / 4 | Last-listed author Maya Koronyo‐Hamaoui: h-index 42 (OpenAlex, whole career) |
| Institution's track record | 1 / 3 | Cedars-Sinai Medical Center: institution h-index 866 (OpenAlex) |
| Multicenter collaboration | 0 / 3 | OpenAlex lists 1 institution(s) in 1 country — scores zero (affiliation lists can be incomplete) |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 33041751) |
| Free to read | 2 / 2 | Free to read |
| Total | 46 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
- DOI: 10.3389/fnins.2020.00921
- PubMed: 33041751
- Original source →
- Free full text: Frontiers in Neuroscience →
Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).
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