Diabetic retinopathy and Alzheimer's disease: Convergence of the unfolded protein response in neurodegeneration

Diabetic retinopathy (DR) and Alzheimer's disease (AD) are progressive neurodegenerative disorders affecting the eye and the brain, respectively. Despite targeting different organs, they share common molecular mechanisms. A central process connecting these conditions is the unfolded protein res...

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Published inAlzheimer's & dementia Vol. 21; no. 8; pp. e70497 - n/a
Main Authors Palacios, Adrián G., Zhang, Sarah X., Acosta, Mónica L.
Format Journal Article
LanguageEnglish
Published United States John Wiley and Sons Inc 01.08.2025
Subjects
aging
Alzheimer Disease - metabolism
Alzheimer's disease
Animals
diabetes
Diabetic Retinopathy - metabolism
Endoplasmic Reticulum Stress
Humans
Oxidative Stress
retina
Review
unfolded protein response
Unfolded Protein Response - physiology
unfolded protein response
aging
retina
Alzheimer's disease
diabetes
Online AccessGet full text
ISSN1552-5260
1552-5279
1552-5279
DOI10.1002/alz.70497

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Abstract Diabetic retinopathy (DR) and Alzheimer's disease (AD) are progressive neurodegenerative disorders affecting the eye and the brain, respectively. Despite targeting different organs, they share common molecular mechanisms. A central process connecting these conditions is the unfolded protein response (UPR), which maintains protein homeostasis in the endoplasmic reticulum (ER). Dysregulation of UPR pathways, particularly the IRE1‐XBP1 and PERK‐eIF2α pathways, can lead to inflammation, oxidative stress, and neurodegeneration. While the IRE1‐XBP1 pathway regulates protein folding and inflammatory signaling, the PERK‐eIF2α pathway reduces protein synthesis but may trigger apoptosis if persistently activated. Emerging therapies targeting UPR pathways and ER chaperones show promise in mitigating neurodegenerative damage in DR and AD. This review highlights shared pathophysiological mechanisms, explore retinal biomarkers for early AD detection, and emphasizes UPR modulation as a therapeutic strategy for neurodegeneration in aging‐related diseases. Highlights Diabetic retinopathy (DR, ocular disorder) and Alzheimer's disease (AD, cerebral disorder) share common molecular mechanisms, including oxidative stress, inflammation, and proteostasis dysfunction. UPR is a critical pathway linking both diseases through endoplasmic reticulum (ER) stress and neurodegeneration and targeting unfolded protein response (UPR) pathways, ER chaperones (e.g., P58IPK), and anti‐inflammatory treatments show promise. The IRE1‐XBP1 pathway regulates protein homeostasis and inflammation; XBP1s protects against ER stress in both retinal and brain neurons. The PERK‐eIF2α pathway suppresses protein synthesis under stress but may induce apoptosis via ATF4 and CHOP if chronically activated. Age‐related decline in metabolism, proteostasis, and neurovascular function intensifies disease progression and exacerbates molecular and cellular damage in both DR and AD.
AbstractList Diabetic retinopathy (DR) and Alzheimer's disease (AD) are progressive neurodegenerative disorders affecting the eye and the brain, respectively. Despite targeting different organs, they share common molecular mechanisms. A central process connecting these conditions is the unfolded protein response (UPR), which maintains protein homeostasis in the endoplasmic reticulum (ER). Dysregulation of UPR pathways, particularly the IRE1-XBP1 and PERK-eIF2α pathways, can lead to inflammation, oxidative stress, and neurodegeneration. While the IRE1-XBP1 pathway regulates protein folding and inflammatory signaling, the PERK-eIF2α pathway reduces protein synthesis but may trigger apoptosis if persistently activated. Emerging therapies targeting UPR pathways and ER chaperones show promise in mitigating neurodegenerative damage in DR and AD. This review highlights shared pathophysiological mechanisms, explore retinal biomarkers for early AD detection, and emphasizes UPR modulation as a therapeutic strategy for neurodegeneration in aging-related diseases. HIGHLIGHTS: Diabetic retinopathy (DR, ocular disorder) and Alzheimer's disease (AD, cerebral disorder) share common molecular mechanisms, including oxidative stress, inflammation, and proteostasis dysfunction. UPR is a critical pathway linking both diseases through endoplasmic reticulum (ER) stress and neurodegeneration and targeting unfolded protein response (UPR) pathways, ER chaperones (e.g., P58IPK), and anti-inflammatory treatments show promise. The IRE1-XBP1 pathway regulates protein homeostasis and inflammation; XBP1s protects against ER stress in both retinal and brain neurons. The PERK-eIF2α pathway suppresses protein synthesis under stress but may induce apoptosis via ATF4 and CHOP if chronically activated. Age-related decline in metabolism, proteostasis, and neurovascular function intensifies disease progression and exacerbates molecular and cellular damage in both DR and AD.
Diabetic retinopathy (DR) and Alzheimer's disease (AD) are progressive neurodegenerative disorders affecting the eye and the brain, respectively. Despite targeting different organs, they share common molecular mechanisms. A central process connecting these conditions is the unfolded protein response (UPR), which maintains protein homeostasis in the endoplasmic reticulum (ER). Dysregulation of UPR pathways, particularly the IRE1-XBP1 and PERK-eIF2α pathways, can lead to inflammation, oxidative stress, and neurodegeneration. While the IRE1-XBP1 pathway regulates protein folding and inflammatory signaling, the PERK-eIF2α pathway reduces protein synthesis but may trigger apoptosis if persistently activated. Emerging therapies targeting UPR pathways and ER chaperones show promise in mitigating neurodegenerative damage in DR and AD. This review highlights shared pathophysiological mechanisms, explore retinal biomarkers for early AD detection, and emphasizes UPR modulation as a therapeutic strategy for neurodegeneration in aging-related diseases. HIGHLIGHTS: Diabetic retinopathy (DR, ocular disorder) and Alzheimer's disease (AD, cerebral disorder) share common molecular mechanisms, including oxidative stress, inflammation, and proteostasis dysfunction. UPR is a critical pathway linking both diseases through endoplasmic reticulum (ER) stress and neurodegeneration and targeting unfolded protein response (UPR) pathways, ER chaperones (e.g., P58IPK), and anti-inflammatory treatments show promise. The IRE1-XBP1 pathway regulates protein homeostasis and inflammation; XBP1s protects against ER stress in both retinal and brain neurons. The PERK-eIF2α pathway suppresses protein synthesis under stress but may induce apoptosis via ATF4 and CHOP if chronically activated. Age-related decline in metabolism, proteostasis, and neurovascular function intensifies disease progression and exacerbates molecular and cellular damage in both DR and AD.Diabetic retinopathy (DR) and Alzheimer's disease (AD) are progressive neurodegenerative disorders affecting the eye and the brain, respectively. Despite targeting different organs, they share common molecular mechanisms. A central process connecting these conditions is the unfolded protein response (UPR), which maintains protein homeostasis in the endoplasmic reticulum (ER). Dysregulation of UPR pathways, particularly the IRE1-XBP1 and PERK-eIF2α pathways, can lead to inflammation, oxidative stress, and neurodegeneration. While the IRE1-XBP1 pathway regulates protein folding and inflammatory signaling, the PERK-eIF2α pathway reduces protein synthesis but may trigger apoptosis if persistently activated. Emerging therapies targeting UPR pathways and ER chaperones show promise in mitigating neurodegenerative damage in DR and AD. This review highlights shared pathophysiological mechanisms, explore retinal biomarkers for early AD detection, and emphasizes UPR modulation as a therapeutic strategy for neurodegeneration in aging-related diseases. HIGHLIGHTS: Diabetic retinopathy (DR, ocular disorder) and Alzheimer's disease (AD, cerebral disorder) share common molecular mechanisms, including oxidative stress, inflammation, and proteostasis dysfunction. UPR is a critical pathway linking both diseases through endoplasmic reticulum (ER) stress and neurodegeneration and targeting unfolded protein response (UPR) pathways, ER chaperones (e.g., P58IPK), and anti-inflammatory treatments show promise. The IRE1-XBP1 pathway regulates protein homeostasis and inflammation; XBP1s protects against ER stress in both retinal and brain neurons. The PERK-eIF2α pathway suppresses protein synthesis under stress but may induce apoptosis via ATF4 and CHOP if chronically activated. Age-related decline in metabolism, proteostasis, and neurovascular function intensifies disease progression and exacerbates molecular and cellular damage in both DR and AD.
Diabetic retinopathy (DR) and Alzheimer's disease (AD) are progressive neurodegenerative disorders affecting the eye and the brain, respectively. Despite targeting different organs, they share common molecular mechanisms. A central process connecting these conditions is the unfolded protein response (UPR), which maintains protein homeostasis in the endoplasmic reticulum (ER). Dysregulation of UPR pathways, particularly the IRE1‐XBP1 and PERK‐eIF2α pathways, can lead to inflammation, oxidative stress, and neurodegeneration. While the IRE1‐XBP1 pathway regulates protein folding and inflammatory signaling, the PERK‐eIF2α pathway reduces protein synthesis but may trigger apoptosis if persistently activated. Emerging therapies targeting UPR pathways and ER chaperones show promise in mitigating neurodegenerative damage in DR and AD. This review highlights shared pathophysiological mechanisms, explore retinal biomarkers for early AD detection, and emphasizes UPR modulation as a therapeutic strategy for neurodegeneration in aging‐related diseases. Highlights Diabetic retinopathy (DR, ocular disorder) and Alzheimer's disease (AD, cerebral disorder) share common molecular mechanisms, including oxidative stress, inflammation, and proteostasis dysfunction. UPR is a critical pathway linking both diseases through endoplasmic reticulum (ER) stress and neurodegeneration and targeting unfolded protein response (UPR) pathways, ER chaperones (e.g., P58IPK), and anti‐inflammatory treatments show promise. The IRE1‐XBP1 pathway regulates protein homeostasis and inflammation; XBP1s protects against ER stress in both retinal and brain neurons. The PERK‐eIF2α pathway suppresses protein synthesis under stress but may induce apoptosis via ATF4 and CHOP if chronically activated. Age‐related decline in metabolism, proteostasis, and neurovascular function intensifies disease progression and exacerbates molecular and cellular damage in both DR and AD.
Diabetic retinopathy (DR) and Alzheimer's disease (AD) are progressive neurodegenerative disorders affecting the eye and the brain, respectively. Despite targeting different organs, they share common molecular mechanisms. A central process connecting these conditions is the unfolded protein response (UPR), which maintains protein homeostasis in the endoplasmic reticulum (ER). Dysregulation of UPR pathways, particularly the IRE1‐XBP1 and PERK‐eIF2α pathways, can lead to inflammation, oxidative stress, and neurodegeneration. While the IRE1‐XBP1 pathway regulates protein folding and inflammatory signaling, the PERK‐eIF2α pathway reduces protein synthesis but may trigger apoptosis if persistently activated. Emerging therapies targeting UPR pathways and ER chaperones show promise in mitigating neurodegenerative damage in DR and AD. This review highlights shared pathophysiological mechanisms, explore retinal biomarkers for early AD detection, and emphasizes UPR modulation as a therapeutic strategy for neurodegeneration in aging‐related diseases.
Author Palacios, Adrián G.
Zhang, Sarah X.
Acosta, Mónica L.
AuthorAffiliation 2 Departments of Ophthalmology and Biochemistry, Ross Eye Institute University at Buffalo, State University of New York Buffalo New York USA
1 Instituto de Neurociencia and Centro Interdisciplinario de Neurociencia de Valparaíso, Facultad de Ciencias Universidad de Valparaíso Valparaiso Chile
3 New Zealand National Eye Centre, Centre for Brain Research and School of Optometry and Vision Science The University of Auckland Auckland New Zealand
AuthorAffiliation_xml – name: 1 Instituto de Neurociencia and Centro Interdisciplinario de Neurociencia de Valparaíso, Facultad de Ciencias Universidad de Valparaíso Valparaiso Chile
– name: 3 New Zealand National Eye Centre, Centre for Brain Research and School of Optometry and Vision Science The University of Auckland Auckland New Zealand
– name: 2 Departments of Ophthalmology and Biochemistry, Ross Eye Institute University at Buffalo, State University of New York Buffalo New York USA
Author_xml – sequence: 1
  givenname: Adrián G.
  orcidid: 0000-0003-1532-7527
  surname: Palacios
  fullname: Palacios, Adrián G.
  email: adrian.palacios@uv.cl
  organization: Universidad de Valparaíso
– sequence: 2
  givenname: Sarah X.
  orcidid: 0000-0002-7848-3263
  surname: Zhang
  fullname: Zhang, Sarah X.
  email: xzhang38@buffalo.edu
  organization: University at Buffalo, State University of New York
– sequence: 3
  givenname: Mónica L.
  orcidid: 0000-0002-5018-339X
  surname: Acosta
  fullname: Acosta, Mónica L.
  email: m.acosta@auckland.ac.nz
  organization: The University of Auckland
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Sat Aug 09 01:32:42 EDT 2025
Wed Sep 03 16:33:01 EDT 2025
Thu Aug 28 10:10:37 EDT 2025
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Issue 8
Keywords unfolded protein response
aging
retina
Alzheimer's disease
diabetes
Language English
License Attribution-NonCommercial
2025 The Author(s). Alzheimer's & Dementia published by Wiley Periodicals LLC on behalf of Alzheimer's Association.
This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.
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Snippet Diabetic retinopathy (DR) and Alzheimer's disease (AD) are progressive neurodegenerative disorders affecting the eye and the brain, respectively. Despite...
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SubjectTerms aging
Alzheimer Disease - metabolism
Alzheimer's disease
Animals
diabetes
Diabetic Retinopathy - metabolism
Endoplasmic Reticulum Stress
Humans
Oxidative Stress
retina
Review
unfolded protein response
Unfolded Protein Response - physiology
Title Diabetic retinopathy and Alzheimer's disease: Convergence of the unfolded protein response in neurodegeneration
URI https://onlinelibrary.wiley.com/doi/abs/10.1002%2Falz.70497
https://www.ncbi.nlm.nih.gov/pubmed/40760071
https://www.proquest.com/docview/3236679207
https://pubmed.ncbi.nlm.nih.gov/PMC12321509
Volume 21
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