Home › Research › Prevention and risk
Dietary salt promotes neurovascular and cognitive dysfunction through a gut-initiated TH17 response
Faraco G, Brea D, Garcia-Bonilla L, Wang G, Racchumi G, Chang H, Buendia I, Santisteban MM et al.. Nature neuroscience, 2018-01-15
Topic: Brain proteins, microglia and lab models
A diet rich in salt is linked to an increased risk of cerebrovascular diseases and dementia, but it remains unclear how dietary salt harms the brain. We report that, in mice, excess dietary salt suppresses resting cerebral blood flow and endothelial function, leading to cognitive impairment. The effect depends on expansion of TH17 cells in the small intestine, resulting in a marked increase in plasma interleukin-17 (IL-17). Circulating IL-17, in turn, promotes endothelial dysfunction and cognitive impairment by the Rho kinase-dependent inhibitory phosphorylation of endothelial nitric oxide synthase and reduced nitric oxide production in cerebral endothelial cells. The findings reveal a new gut-brain axis linking dietary habits to cognitive impairment through a gut-initiated adaptive immune response compromising brain function via circulating IL-17. Thus, the TH17 cell-IL-17 pathway is a putative target to counter the deleterious brain effects induced by dietary salt and other diseases associated with TH17 polarization.
Key findings
- A diet rich in salt is linked to an increased risk of cerebrovascular diseases and dementia, but it remains unclear how dietary salt harms the brain.
- Thus, the TH17 cell-IL-17 pathway is a putative target to counter the deleterious brain effects induced by dietary salt and other diseases associated with TH17 polarization.
Why it matters
In mice, a high-salt diet impaired cerebral blood flow and endothelial function and led to cognitive impairment through a gut-initiated immune response involving TH17 cells and IL-17. This is animal research identifying a possible mechanism and a putative target, not evidence that reducing salt prevents dementia in people.
New to this subject? Start with our plain-English guide: Prevention →
Study details
- Evidence strengthLow
How this study scored 53/100
Published in a leading specialty 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 | 9 / 10 | Tier 2 — leading specialty journal (Nature neuroscience) |
| Journal's citation record | 4 / 4 | Nature Neuroscience: journal h-index 593 (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 343 times (OpenAlex, 2026-10-10) |
| Citations per year | 4 / 5 | 34.3 citations a year over 10 year(s) since 2018 |
| Impact for its field and year | 5 / 6 | Cited 21.2× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 2 / 6 | Cited by 9 other studies in this library |
| Still being cited | 3 / 4 | Cited 110 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 4 / 4 | Last-listed author Costantino Iadecola: h-index 128 (OpenAlex, whole career) |
| Institution's track record | 1 / 3 | Weill Cornell Medicine: institution h-index 1,163 (OpenAlex) |
| Multi-centre collaboration | 0 / 3 | OpenAlex lists 1 institution(s) in 1 country — scores zero (affiliation lists can be incomplete) |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 29335605) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 53 / 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. 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
Faraco, G., Brea, D., Garcia-Bonilla, L., Wang, G., Racchumi, G., Chang, H., et al. (2018). Dietary salt promotes neurovascular and cognitive dysfunction through a gut-initiated TH17 response. Nature neuroscience. https://doi.org/10.1038/s41593-017-0059-z
Vancouver
Faraco G, Brea D, Garcia-Bonilla L, Wang G, Racchumi G, Chang H, et al. Dietary salt promotes neurovascular and cognitive dysfunction through a gut-initiated TH17 response. Nature neuroscience. 2018. doi:10.1038/s41593-017-0059-z. PMID: 29335605.
BibTeX
@article{faraco2018-29335605,
author = {Faraco, G. and Brea, D. and Garcia-Bonilla, L. and Wang, G. and Racchumi, G. and Chang, H. and Buendia, I. and Santisteban, M. M. and others},
title = {{Dietary salt promotes neurovascular and cognitive dysfunction through a gut-initiated TH17 response}},
journal = {Nature neuroscience},
year = {2018},
doi = {10.1038/s41593-017-0059-z},
pmid = {29335605},
url = {https://doi.org/10.1038/s41593-017-0059-z}
}
Studies this one cites
Referenced by this study and also in the alzhub library, so you can read them here.
Later studies that cite this one
9 studies in the alzhub library list this one in their references. Showing the 8 highest-scoring.