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Diabetic encephalopathy: metabolic reprogramming as a potential driver of accelerated brain aging and cognitive decline
Huai JX, Chang EE, Zhu YR, Ma WL, Lv TS, Sun J, Zhou XQ.. Frontiers in cell and developmental biology, 2025-11-17
Topic: Brain proteins, microglia and lab models
Diabetic encephalopathy (DE) is a serious neurological complication of diabetes and is expressed as progressive decline in cognitive function, emotional disorders, and changes in brain structure. This review brings together the relevant evidence and demonstrates that metabolic reprogramming, the adaptive reconfiguration of the core metabolic pathway in response to hyperglycemia, is a potential driver of accelerated brain aging in DE. The main pathological characteristics are: abnormal brain insulin signaling, resulting in a decrease in neuronal glucose intake and a decrease in mitochondrial oxidative phosphorylation, oxidative stress and neuroinflammation caused by high blood sugar, in which excess reactive oxygen species (ROS), impairs mitochondrial integrity and leads to activation of microglia cells. The impaired mitophagy and the macrophages remove defects and cause the accumulation and energy collapse of the dysfunctional organelles. In addition, it promotes excessive glycolytic flux, lipolysis disorder, lactic acid accumulation, and ceramide-dependent synaptic damage. We further examine shared metabolic mechanisms between DE and neurodegenerative diseases such as alzheimer's disease (AD) and treatment strategies for pathological metabolic reprogramming including GLP-1 receptor agonists, NAD + boosters, and AMPK activators. This analysis laid the foundation for new intervention measures against the development of DE.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Huai, J. X., Chang, E. E., Zhu, Y. R., Ma, W. L., Lv, T. S., Sun, J., et al. (2025). Diabetic encephalopathy: metabolic reprogramming as a potential driver of accelerated brain aging and cognitive decline. Frontiers in cell and developmental biology. https://doi.org/10.3389/fcell.2025.1701406
Vancouver
Huai JX, Chang EE, Zhu YR, Ma WL, Lv TS, Sun J, et al. Diabetic encephalopathy: metabolic reprogramming as a potential driver of accelerated brain aging and cognitive decline. Frontiers in cell and developmental biology. 2025. doi:10.3389/fcell.2025.1701406. PMID: 41332987.
BibTeX
@article{huai2025-41332987,
author = {Huai, J. X. and Chang, E. E. and Zhu, Y. R. and Ma, W. L. and Lv, T. S. and Sun, J. and Zhou, X. Q.},
title = {{Diabetic encephalopathy: metabolic reprogramming as a potential driver of accelerated brain aging and cognitive decline}},
journal = {Frontiers in cell and developmental biology},
year = {2025},
doi = {10.3389/fcell.2025.1701406},
pmid = {41332987},
url = {https://doi.org/10.3389/fcell.2025.1701406}
}
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 7 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
- The main pathological characteristics are: abnormal brain insulin signaling, resulting in a decrease in neuronal glucose intake and a decrease in mitochondrial oxidative phosphorylation, oxidative stress and neuroinflammation caused by high blood sugar, in which excess reactive oxygen species (ROS), impairs mitochondrial integrity and leads to activation of microglia cells.
- The impaired mitophagy and the macrophages remove defects and cause the accumulation and energy collapse of the dysfunctional organelles.
- In addition, it promotes excessive glycolytic flux, lipolysis disorder, lactic acid accumulation, and ceramide-dependent synaptic damage.
- We further examine shared metabolic mechanisms between DE and neurodegenerative diseases such as alzheimer's disease (AD) and treatment strategies for pathological metabolic reprogramming including GLP-1 receptor agonists, NAD + boosters, and AMPK activators.
- This analysis laid the foundation for new intervention measures against the development of DE.
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Study details
- Evidence strengthLow
How this study scored 45/100
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. We have no data on journal's citation record, times cited, citations per year, impact for its field and year, cited by studies here, still being cited, senior author's track record, institution's track record and multicenter collaboration, so those were left out: it earned 26 of the 58 points we could judge it on, which is 45 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Frontiers in cell and developmental biology) |
| Journal's citation record | — / 4 | No journal record from OpenAlex — left out of this score |
| 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) |
| Randomized / blinded | 0 / 2 | No randomization or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | — / 7 | No citation count (not found in OpenAlex) — left out of this score |
| Citations per year | — / 5 | No citation count or no year — left out of this score |
| Impact for its field and year | — / 6 | No field-weighted citation impact (OpenAlex has none yet) — left out of this score |
| Cited by studies here | — / 6 | Not yet checked against this library's citation graph — left out of this score |
| Still being cited | — / 4 | No yearly citation counts — left out of this score |
| Senior author's track record | — / 4 | Senior author's record not available — left out of this score |
| Institution's track record | — / 3 | No institution listed in OpenAlex — left out of this score |
| Multicenter collaboration | — / 3 | Institutions not listed — left out of this score |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 41332987) |
| Free to read | 2 / 2 | Free to read |
| Points | 26 / 58 | Scored on 11 of 20 parts. We have no data for the rest, so they are left out: 26 of the 58 points we could judge it on is 45 out of 100. |
| Total | 45 / 100 | — |
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