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Chronic caffeine consumption prevents obesity-induced cognitive and memory impairments by reducing neuroinflammation and enhancing neuronal activity in the hippocampus
Adriana M. Capucho, José Ponce de Leão, Karine Corrêa Flôr, Gonçalo M. Melo, M. Fernandes, Joana F. Sacramento, Sílvia V. Conde. Pharmacological Research, 2026-02-13
Topic: Brain proteins, microglia and lab models
Obesity and its associated metabolic disturbances increase the risk of cognitive decline, dementia, and anxiety-related disorders. Chronic caffeine consumption was suggested to prevent synaptic and cognitive deficits, but the underlying mechanisms remain unclear. Here, we investigated whether caffeine protects against cognitive and memory deficits and anxiety induced by a hypercaloric diet, and explored the molecular mechanisms involved. Ten-week-old male Wistar rats were assigned to three groups: normal chow (control), high-fat high-sucrose (HFHSu, 25 weeks), and HFHSu plus caffeine (HFHSuCaff, 1 g/L last 11 weeks). Insulin sensitivity and glucose tolerance were assessed at weeks 14 and 25. Behavioral tests (open field, novel object recognition (NOR), Y-maze, block test, elevated plus maze (EPM)) evaluated memory, cognition, and anxiety. Hippocampal tissues were analyzed by Western blot and immunohistochemistry for insulin signaling, neuronal activity and microglia activation. HFHSu feeding promoted obesity, insulin resistance, and glucose intolerance, accompanied by impaired memory and cognition (reductions in Y-maze, NOR, and block test), increased anxiety (54.5 % time in EPM open arms), reduced hippocampal glutamatergic (41.1 % VGlut) and adenosinergic signaling (22.4 %, 11.1 %, 22.6 % in A1, A2A, A2B receptors), and elevated neuroinflammation (elevated GFAP, IBA-1, IL-6 receptor levels; altered microglial morphology) compared with control. Caffeine intake ameliorated metabolic, cognitive, and neuroinflammatory alterations, except for anxiety. Notably, caffeine increased hippocampal neuronal activity by 25.22, 94.84 and 61.51 % in CA1, CA2 and CA3 areas. In conclusion, chronic caffeine consumption mitigates obesity-induced cognitive and memory deficits via modulation of hippocampal glutamatergic and adenosinergic signaling and reduced neuroinflammation, highlighting its potential as a neuroprotective intervention.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Capucho, A. M., de Leão, J. P., Flôr, K. C., Melo, G. M., Fernandes, M., Sacramento, J. F., et al. (2026). Chronic caffeine consumption prevents obesity-induced cognitive and memory impairments by reducing neuroinflammation and enhancing neuronal activity in the hippocampus. Pharmacological Research. https://doi.org/10.1016/j.phrs.2026.108140
Vancouver
Capucho AM, de Leão JP, Flôr KC, Melo GM, Fernandes M, Sacramento JF, et al. Chronic caffeine consumption prevents obesity-induced cognitive and memory impairments by reducing neuroinflammation and enhancing neuronal activity in the hippocampus. Pharmacological Research. 2026. doi:10.1016/j.phrs.2026.108140. PMID: 41692039.
BibTeX
@article{capucho2026-41692039,
author = {Capucho, Adriana M. and de Leão, José Ponce and Flôr, Karine Corrêa and Melo, Gonçalo M. and Fernandes, M. and Sacramento, Joana F. and Conde, Sílvia V.},
title = {{Chronic caffeine consumption prevents obesity-induced cognitive and memory impairments by reducing neuroinflammation and enhancing neuronal activity in the hippocampus}},
journal = {Pharmacological Research},
year = {2026},
doi = {10.1016/j.phrs.2026.108140},
pmid = {41692039},
url = {https://doi.org/10.1016/j.phrs.2026.108140}
}
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
- HFHSu feeding promoted obesity, insulin resistance, and glucose intolerance, accompanied by impaired memory and cognition (reductions in Y-maze, NOR, and block test), increased anxiety (54.5 % time in EPM open arms), reduced hippocampal glutamatergic (41.1 % VGlut) and adenosinergic signaling (22.4 %, 11.1 %, 22.6 % in A1, A2A, A2B receptors), and elevated neuroinflammation (elevated GFAP, IBA-1, IL-6 receptor levels; altered microglial morphology) compared with control.
- In conclusion, chronic caffeine consumption mitigates obesity-induced cognitive and memory deficits via modulation of hippocampal glutamatergic and adenosinergic signaling and reduced neuroinflammation, highlighting its potential as a neuroprotective intervention.
Why it matters
In rats fed a high-fat high-sucrose diet, chronic caffeine reduced memory and cognitive deficits and anxiety, linked to changes in hippocampal signaling and reduced neuroinflammation. This is animal research, so it does not show that caffeine prevents cognitive decline or dementia in people.
Study details
- Evidence strengthLow
How this study scored 41/100
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 (Pharmacological Research) |
| Journal's citation record | 2 / 4 | Pharmacological Research: journal h-index 222 (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 | 5 / 5 | 2026 — within 1 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 | 2.0 citations a year over 2 year(s) since 2026 |
| Impact for its field and year | 4 / 6 | Cited 10.0× 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 | 2 / 4 | Last-listed author Sílvia V. Conde: h-index 33 (OpenAlex, whole career) |
| Institution's track record | 1 / 3 | Consejo Superior de Investigaciones Científicas: institution h-index 1,048 (OpenAlex) |
| Multi-centre collaboration | 2 / 3 | OpenAlex lists 4 institution(s) in 2 countries |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 41692039) |
| Free to read | 2 / 2 | Free to read |
| Total | 41 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
- DOI: 10.1016/j.phrs.2026.108140
- PubMed: 41692039
- Original source →
- Free full text: Pharmacological Research →
Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).
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