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Differential central pathology and cognitive impairment in pre-diabetic and diabetic mice
Ramos-Rodriguez JJ, Ortiz O, Jimenez-Palomares M, Kay KR, Berrocoso E, Murillo-Carretero MI, Perdomo G, Spires-Jones T et al.. Psychoneuroendocrinology, 2013-06-21
Topic: Brain proteins, microglia and lab models
Although age remains the main risk factor to suffer Alzheimer's disease (AD) and vascular dementia (VD), type 2 diabetes (T2D) has turned up as a relevant risk factor for dementia. However, the ultimate underlying mechanisms for this association remain unclear. In the present study we analyzed central nervous system (CNS) morphological and functional consequences of long-term insulin resistance and T2D in db/db mice (leptin receptor KO mice). We also included C57Bl6 mice fed with high fat diet (HFD) and a third group of C57Bl6 streptozotocin (STZ) treated mice. Db/db mice exhibited pathological characteristics that mimic both AD and VD, including age dependent cognitive deterioration, brain atrophy, increased spontaneous hemorrhages and tau phosphorylation, affecting the cortex preferentially. A similar profile was observed in STZ-induced diabetic mice. Moreover metabolic parameters, such as body weight, glucose and insulin levels are good predictors of many of these alterations in db/db mice. In addition, in HFD-induced hyperinsulinemia in C57Bl6 mice, we only observed mild CNS alterations, suggesting that central nervous system dysfunction is associated with well established T2D. Altogether our results suggest that T2D may promote many of the pathological and behavioral alterations observed in dementia, supporting that interventions devoted to control glucose homeostasis could improve dementia progress and prognosis.
Key findings
- In addition, in HFD-induced hyperinsulinemia in C57Bl6 mice, we only observed mild CNS alterations, suggesting that central nervous system dysfunction is associated with well established T2D.
- Altogether our results suggest that T2D may promote many of the pathological and behavioral alterations observed in dementia, supporting that interventions devoted to control glucose homeostasis could improve dementia progress and prognosis.
Why it matters
In this mouse study, diabetic db/db mice showed cognitive deterioration, brain atrophy, haemorrhages and tau phosphorylation resembling features of both Alzheimer's disease and vascular dementia, while mice with high-fat-diet-induced hyperinsulinemia showed only mild brain changes. The authors suggest controlling glucose homeostasis could improve dementia progress and prognosis, but this is animal research and has not been shown in people.
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Study details
- Evidence strengthLow
How this study scored 46/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported and randomised / blinded because the record does not state it.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Psychoneuroendocrinology) |
| Journal's citation record | 3 / 4 | Psychoneuroendocrinology: journal h-index 254 (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 | 1 / 5 | 2013 — within 20 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 | Laboratory or animal study (title names “mice”) — scores zero |
| Randomised / blinded | 0 / 2 | No randomisation or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 5 / 7 | Cited 147 times (OpenAlex, 2026-10-10) |
| Citations per year | 3 / 5 | 9.8 citations a year over 15 year(s) since 2013 |
| Impact for its field and year | 3 / 6 | Cited 6.8× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 2 / 6 | Cited by 4 other studies in this library |
| Still being cited | 2 / 4 | Cited 27 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 2 / 4 | Last-listed author Mónica Garcı́a-Alloza: h-index 43 (OpenAlex, whole career) |
| Institution's track record | 3 / 3 | Harvard University: institution h-index 3,235 (OpenAlex) |
| Multi-centre collaboration | 2 / 3 | OpenAlex lists 6 institution(s) in 2 countries |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 23790682) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 46 / 100 | — |
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Read the original
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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. The record's author list ends in “et al.”, so not every author is named. Check the citation against the original before you use it.
APA 7th
Ramos-Rodriguez, J. J., Ortiz, O., Jimenez-Palomares, M., Kay, K. R., Berrocoso, E., Murillo-Carretero, M. I., et al. (2013). Differential central pathology and cognitive impairment in pre-diabetic and diabetic mice. Psychoneuroendocrinology. https://doi.org/10.1016/j.psyneuen.2013.05.010
Vancouver
Ramos-Rodriguez JJ, Ortiz O, Jimenez-Palomares M, Kay KR, Berrocoso E, Murillo-Carretero MI, et al. Differential central pathology and cognitive impairment in pre-diabetic and diabetic mice. Psychoneuroendocrinology. 2013. doi:10.1016/j.psyneuen.2013.05.010. PMID: 23790682.
BibTeX
@article{ramosrodriguez2013-23790682,
author = {Ramos-Rodriguez, J. J. and Ortiz, O. and Jimenez-Palomares, M. and Kay, K. R. and Berrocoso, E. and Murillo-Carretero, M. I. and Perdomo, G. and Spires-Jones, T. and others},
title = {{Differential central pathology and cognitive impairment in pre-diabetic and diabetic mice}},
journal = {Psychoneuroendocrinology},
year = {2013},
doi = {10.1016/j.psyneuen.2013.05.010},
pmid = {23790682},
url = {https://doi.org/10.1016/j.psyneuen.2013.05.010}
}
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