Abstract
Original language | English |
---|---|
Pages (from-to) | 728-740 |
Number of pages | 13 |
Journal | Alzheimer's and Dementia |
Volume | 20 |
Issue number | 1 |
Early online date | 2023 |
DOIs | |
Publication status | Published - Jan 2024 |
Keywords
- Alzheimer's disease
- amyloid pathology
- imaging
- recruitment of clinical trials
- retina
- tau pathology
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In: Alzheimer's and Dementia, Vol. 20, No. 1, 01.2024, p. 728-740.
Research output: Contribution to journal › Article › Academic › peer-review
TY - JOUR
T1 - Retina pathology as a target for biomarkers for Alzheimer's disease
T2 - Current status, ophthalmopathological background, challenges, and future directions
AU - Alber, Jessica
AU - Bouwman, Femke
AU - den Haan, Jurre
AU - Rissman, Robert A.
AU - de Groef, Lies
AU - Koronyo-Hamaoui, Maya
AU - Lengyel, Imre
AU - Thal, Dietmar Rudolf
N1 - Funding Information: This manuscript was facilitated by the Alzheimer's Association International Society to Advance Alzheimer's Research and Treatment (ISTAART) through the “The Eye as a Biomarker for Alzheimer's Disease” Professional Interest Area (PIA). The views and opinions expressed by the authors in this publication represent those of the authors and do not necessarily reflect those of the PIA membership, ISTAART, or the Alzheimer's Association. The authors are very grateful to Jodi Titiner and Rebecca Edelmayer from the Alzheimer's Association for their help keeping the “The Eye as a Biomarker for Alzheimer's Disease” PIA going and for organizing the meetings that allowed the coordination of this manuscript. JA receives grants for AD research from the National Institutes of Health (NIH)/National Institute on Aging (NIA) grants R21AG074153 and R01AG079241, and the Warren Alpert Foundation. JdH is supported by Alzheimer Nederland by grant WE.03-2021-14. RAR is supported by NIH/NIA grants AG018440, AG058252, AG078109 AG058533, AG073979, and AG057437. LDG is funded by Stichting Alzheimer Onderzoek (2021/0036, SAO/FRA, Belgium). MKH receives grants for AD research from the NIH/NIA grants R01AG055865, R01AG056478, and R01AG075998. In addition, MKH receives funding from the Tom Gordon Foundation, The Jona Goldrich Foundation, and The Wilstein Foundation. IL is supported by the Medical Research Council/National Institute for Health Research Deep and Frequent Phenotyping Study for Alzheimer's Diseases grant (MR/N029941/1), Alzheimer's Society UK (ASPG213 project grant, and an unrestricted research grant from Optos Plc for his work on dementia. DRT receives grants for AD research from Fonds Wetenschappelijk Onderzoek (G0F8516N and G065721N, FWO, Belgium), Stichting Alzheimer Onderzoek (2020/017, SAO/FRA, Belgium), KU-Leuven Onderzoeksraad (C3/20/057), and Alzheimer's Association (22-AAIIA-963171, USA). Funding Information: This manuscript was facilitated by the Alzheimer's Association International Society to Advance Alzheimer's Research and Treatment (ISTAART) through the “The Eye as a Biomarker for Alzheimer's Disease” Professional Interest Area (PIA). The views and opinions expressed by the authors in this publication represent those of the authors and do not necessarily reflect those of the PIA membership, ISTAART, or the Alzheimer's Association. The authors are very grateful to Jodi Titiner and Rebecca Edelmayer from the Alzheimer's Association for their help keeping the “The Eye as a Biomarker for Alzheimer's Disease” PIA going and for organizing the meetings that allowed the coordination of this manuscript. JA receives grants for AD research from the National Institutes of Health (NIH)/National Institute on Aging (NIA) grants R21AG074153 and R01AG079241, and the Warren Alpert Foundation. JdH is supported by Alzheimer Nederland by grant WE.03‐2021‐14. RAR is supported by NIH/NIA grants AG018440, AG058252, AG078109 AG058533, AG073979, and AG057437. LDG is funded by Stichting Alzheimer Onderzoek (2021/0036, SAO/FRA, Belgium). MKH receives grants for AD research from the NIH/NIA grants R01AG055865, R01AG056478, and R01AG075998. In addition, MKH receives funding from the Tom Gordon Foundation, The Jona Goldrich Foundation, and The Wilstein Foundation. IL is supported by the Medical Research Council/National Institute for Health Research Deep and Frequent Phenotyping Study for Alzheimer's Diseases grant (MR/N029941/1), Alzheimer's Society UK (ASPG213 project grant, and an unrestricted research grant from Optos Plc for his work on dementia. DRT receives grants for AD research from Fonds Wetenschappelijk Onderzoek (G0F8516N and G065721N, FWO, Belgium), Stichting Alzheimer Onderzoek (2020/017, SAO/FRA, Belgium), KU‐Leuven Onderzoeksraad (C3/20/057), and Alzheimer's Association (22‐AAIIA‐963171, USA). Publisher Copyright: © 2023 The Authors. Alzheimer's & Dementia published by Wiley Periodicals LLC on behalf of Alzheimer's Association.
PY - 2024/1
Y1 - 2024/1
N2 - There is emerging evidence that amyloid beta protein (Aβ) and tau-related lesions in the retina are associated with Alzheimer's disease (AD). Aβ and hyperphosphorylated (p)-tau deposits have been described in the retina and were associated with small amyloid spots visualized by in vivo imaging techniques as well as degeneration of the retina. These changes correlate with brain amyloid deposition as determined by histological quantification, positron emission tomography (PET) or clinical diagnosis of AD. However, the literature is not coherent on these histopathological and in vivo imaging findings. One important reason for this is the variability in the methods and the interpretation of findings across different studies. In this perspective, we indicate the critical methodological deviations among different groups and suggest a roadmap moving forward on how to harmonize (i) histopathologic examination of retinal tissue; (ii) in vivo imaging among different methods, devices, and interpretation algorithms; and (iii) inclusion/exclusion criteria for studies aiming at retinal biomarker validation.
AB - There is emerging evidence that amyloid beta protein (Aβ) and tau-related lesions in the retina are associated with Alzheimer's disease (AD). Aβ and hyperphosphorylated (p)-tau deposits have been described in the retina and were associated with small amyloid spots visualized by in vivo imaging techniques as well as degeneration of the retina. These changes correlate with brain amyloid deposition as determined by histological quantification, positron emission tomography (PET) or clinical diagnosis of AD. However, the literature is not coherent on these histopathological and in vivo imaging findings. One important reason for this is the variability in the methods and the interpretation of findings across different studies. In this perspective, we indicate the critical methodological deviations among different groups and suggest a roadmap moving forward on how to harmonize (i) histopathologic examination of retinal tissue; (ii) in vivo imaging among different methods, devices, and interpretation algorithms; and (iii) inclusion/exclusion criteria for studies aiming at retinal biomarker validation.
KW - Alzheimer's disease
KW - amyloid pathology
KW - imaging
KW - recruitment of clinical trials
KW - retina
KW - tau pathology
UR - http://www.scopus.com/inward/record.url?scp=85175707867&partnerID=8YFLogxK
U2 - https://doi.org/10.1002/alz.13529
DO - https://doi.org/10.1002/alz.13529
M3 - Article
C2 - 37917365
SN - 1552-5260
VL - 20
SP - 728
EP - 740
JO - Alzheimer's and Dementia
JF - Alzheimer's and Dementia
IS - 1
ER -