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Pathomechanisms, genetic insights, and therapeutics in diabetes-associated dementia
Rakesh Meher, Roja Sahu, Santosh Kumar Ranajit, Trupti Rekha Swain, Biswajeet Acharya, Jack Feehan, Prafulla Kumar Sahu, Vasso Apostolopoulos. Journal of Endocrinology, 2025-11-01
Topic: Risk, prevention and care in population studies
Type 2 diabetes (T2DM) significantly increases the risk of dementia due to overlapping metabolic, molecular, and genetic factors. This review comprehensively analyzes the pathophysiological links between diabetes and cognitive decline, focusing on chronic hyperglycemia, insulin resistance, oxidative stress, mitochondrial dysfunction, neuroinflammation, and cerebrovascular complications. Key genetic and epigenetic contributors to diabetes-associated dementia (DAD), including variations in APOE, PICALM, SORL1, and GSK3B, are discussed. The roles of pathological proteins such as amyloid-beta (Aβ) and hyperphosphorylated tau in neurodegeneration are also highlighted. Preclinical and clinical evidence supports targeting insulin signaling pathways, oxidative damage, and inflammatory responses as potential therapeutic strategies. Promising therapies, including GLP-1 receptor agonists, SGLT2 inhibitors, DPP-4 inhibitors, and anti-inflammatory drugs, are reviewed alongside emerging approaches such as gene therapy, stem cell therapy, and immunomodulation. Despite encouraging advances, the clinical translation of these therapies remains challenging due to the complexity of DAD pathogenesis. This review aims to advance understanding of diabetes-induced cognitive impairment and guide the development of personalized dementia therapies by integrating molecular, genetic, and clinical insights. Future research should focus on elucidating the precise molecular mechanisms of DAD progression and on developing targeted, patient-specific therapeutic interventions to overcome translational barriers.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Meher, R., Sahu, R., Ranajit, S. K., Swain, T. R., Acharya, B., Feehan, J., et al. (2025). Pathomechanisms, genetic insights, and therapeutics in diabetes-associated dementia. Journal of Endocrinology. https://doi.org/10.1530/joe-25-0016
Vancouver
Meher R, Sahu R, Ranajit SK, Swain TR, Acharya B, Feehan J, et al. Pathomechanisms, genetic insights, and therapeutics in diabetes-associated dementia. Journal of Endocrinology. 2025. doi:10.1530/joe-25-0016. PMID: 41196686.
BibTeX
@article{meher2025-41196686,
author = {Meher, Rakesh and Sahu, Roja and Ranajit, Santosh Kumar and Swain, Trupti Rekha and Acharya, Biswajeet and Feehan, Jack and Sahu, Prafulla Kumar and Apostolopoulos, Vasso},
title = {{Pathomechanisms, genetic insights, and therapeutics in diabetes-associated dementia}},
journal = {Journal of Endocrinology},
year = {2025},
doi = {10.1530/joe-25-0016},
pmid = {41196686},
url = {https://doi.org/10.1530/joe-25-0016}
}
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 names 8 authors; APA and Vancouver show the first six, BibTeX and the downloads carry all of them. Check the citation against the original before you use it.
Key findings
- Type 2 diabetes (T2DM) significantly increases the risk of dementia due to overlapping metabolic, molecular, and genetic factors.
Why it matters
This review describes how type 2 diabetes increases dementia risk through overlapping metabolic, molecular, and genetic factors, and discusses potential therapies targeting insulin signaling, oxidative damage, and inflammation. It notes that clinical translation of these therapies remains challenging due to the complexity of diabetes-associated dementia.
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Study details
- Evidence strengthLow
How this study scored 36/100
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.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Journal of Endocrinology) |
| Journal's citation record | 2 / 4 | Journal of Endocrinology: journal h-index 220 (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 | 4 / 5 | 2025 — within 3 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 | 1 / 7 | Cited 4 times (OpenAlex, 2026-10-10) |
| Citations per year | 1 / 5 | 1.3 citations a year over 3 year(s) since 2025 |
| Impact for its field and year | 2 / 6 | Cited 2.5× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 0 / 6 | No other study in this library cites it |
| Still being cited | 1 / 4 | Cited 4 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 3 / 4 | Last-listed author Vasso Apostolopoulos: h-index 78 (OpenAlex, whole career) |
| Institution's track record | 0 / 3 | RMIT University: institution h-index 493 (OpenAlex) |
| Multi-centre collaboration | 2 / 3 | OpenAlex lists 4 institution(s) in 2 countries |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 41196686) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 36 / 100 | — |
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