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This page is alzhub.org's plain-English summary of a published study, not the paper itself. It is generated from the record we hold for this study, sourced and linked below — check the original for the full text and methods.

✓ Peer-reviewed alzhub usefulness score 56 out of 100. Risk factors

Topic: Risk, prevention and care in population studies

The concept of diabetic retinopathy as a microvascular disease has evolved, in that it is now considered a more complex diabetic complication in which neurodegeneration plays a significant role. In this article we provide a critical overview of the role of microvascular abnormalities and neurodegeneration in the pathogenesis of diabetic retinopathy. A special emphasis is placed on the pathophysiology of the neurovascular unit (NVU), including the contributions of microvascular and neural elements. The potential mechanisms linking retinal neurodegeneration and early microvascular impairment, and the effects of neuroprotective drugs are summarised. Additionally, we discuss how the assessment of retinal neurodegeneration could be an important index of cognitive status, thus helping to identify individuals at risk of dementia, which will impact on current procedures for diabetes management. We conclude that glial, neural and microvascular dysfunction are interdependent and essential for the development of diabetic retinopathy. Despite this intricate relationship, retinal neurodegeneration is a critical endpoint and neuroprotection, itself, can be considered a therapeutic target, independently of its potential impact on microvascular disease. In addition, interventional studies targeting pathogenic pathways that impact the NVU are needed. Findings from these studies will be crucial, not only for increasing our understanding of diabetic retinopathy, but also to help to implement a timely and efficient personalised medicine approach for treating this diabetic complication.

Key findings

Why it matters

This review argues that retinal neurodegeneration is a critical endpoint in diabetic retinopathy and that neuroprotection itself can be considered a therapeutic target. It also suggests that assessing retinal neurodegeneration could help identify people at risk of dementia, but notes that interventional studies targeting these pathways are still needed.

Study details

How this study scored 56/100
How this study's score is builtJournal tier 7 of 10; Journal's citation record 3 of 4; Study design 0 of 12; Strength of evidence 1 of 5; Peer-review validation 10 of 10; How recent 2 of 5; Sample size 0 of 4; Effect reported 0 of 3; Studied in people 0 of 3; Randomised / blinded 0 of 2; Times cited 6 of 7; Citations per year 5 of 5; Impact for its field and year 6 of 6; Cited by studies here 1 of 6; Still being cited 4 of 4; Senior author's track record 3 of 4; Institution's track record 2 of 3; Multi-centre collaboration 2 of 3; Indexed in PubMed 2 of 2; Free to read 2 of 2. Total 56 of 100.56 of 100 points earned44 not earned

Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people and randomised / blinded because the record does not state it.

ComponentPointsWhy
Journal tier 7 / 10 Tier 3 — peer-reviewed journal (Diabetologia)
Journal's citation record 3 / 4 Diabetologia: journal h-index 337 (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 2018 — 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)
Randomised / blinded 0 / 2 No randomisation or blinding stated — scores zero (not stated in the record — scored 0)
Times cited 6 / 7 Cited 593 times (OpenAlex, 2026-10-10)
Citations per year 5 / 5 59.3 citations a year over 10 year(s) since 2018
Impact for its field and year 6 / 6 Cited 43.0× the average for papers of its field and year (OpenAlex FWCI)
Cited by studies here 1 / 6 Cited by 2 other studies in this library
Still being cited 4 / 4 Cited 230 times in 2024–2026 (2026 still in progress; OpenAlex)
Senior author's track record 3 / 4 Last-listed author Thomas W. Gardner: h-index 72 (OpenAlex, whole career)
Institution's track record 2 / 3 University of Michigan: institution h-index 2,240 (OpenAlex)
Multi-centre collaboration 2 / 3 OpenAlex lists 7 institution(s) in 3 countries
Indexed in PubMed 2 / 2 Indexed in PubMed (PMID 30030554)
Free to read 2 / 2 Free to read
Total 56 / 100 —

What each of these 20 components measures, and what this score is not →

Read the original

Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).

Cite this study APA, Vancouver, BibTeX · download .bib or .ris

Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. Check the citation against the original before you use it.

APA 7th

Simó, R., Stitt, A. W., & Gardner, T. W. (2018). Neurodegeneration in diabetic retinopathy: does it really matter? Diabetologia. https://doi.org/10.1007/s00125-018-4692-1

Vancouver

Simó R, Stitt AW, Gardner TW. Neurodegeneration in diabetic retinopathy: does it really matter? Diabetologia. 2018. doi:10.1007/s00125-018-4692-1. PMID: 30030554.

BibTeX

@article{simo2018-30030554,
  author  = {Simó, R. and Stitt, A. W. and Gardner, T. W.},
  title   = {{Neurodegeneration in diabetic retinopathy: does it really matter?}},
  journal = {Diabetologia},
  year    = {2018},
  doi     = {10.1007/s00125-018-4692-1},
  pmid    = {30030554},
  url     = {https://doi.org/10.1007/s00125-018-4692-1}
}

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