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Peer-reviewedCC BY 4.0Frontiers in Neurology

Dietary high salt drives cognitive impairment and Aβ accumulation via an insufficient compensatory mitophagy response

  • Jie Wen1
  • Hao Ren1
  • Fan Wen1
  • Junping Yu1
  • Haixia Fan2
  • Jincheng Liu1
  • Zhiyou Cai3
  1. 1Department of Neurology, Xiangyang Hospital of Traditional Chinese Medicine, Xiangyang Hospital affiliated to Hubei University of Chinese Medicine
  2. 2Department of Medical Administration, First Hospital of Shanxi Medical University
  3. 3Department of Neurology, Liangjiang Hospital of Chongqing Medical University, People Hospital of Chongqing Liangjiang New Area
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Abstract

There is mounting evidence that dietary habits are strongly correlated with cerebrovascular diseases and dementia, but the precise mechanism remains unclear how a salt-rich diet adversely affects the brain. Here, 12-month-old mice were fed a high-salt diet (HSD) for 2 months, and we observed salt-induced cognitive deficits in mice. The short-term HSD increased mitophagy-associated markers (PINK1, Parkin, and LC3-II) and decreased SQSTM1/p62, consistent with a compensatory mitophagy response that was insufficient to prevent cognitive decline. Neuro-2a cells were cultured in normal medium, NaCl medium (40 mM) or NaCl (40 mM) + CCCP group (20 μM) medium for 24 h, respectively. Short-term HSD feeding impaired learning and memory and increased amyloid-β (Aβ) burden, in parallel with altered PINK1/Parkin-associated mitophagy markers. These findings link a salt-rich diet to cognitive dysfunction, and suggest that enhancing PINK1/Parkin-mediated mitophagy may counteract the harmful effects of HSD on the brain. Therefore, the PINK1/Parkin mitophagy may be a potential target for combating the harmful effects on the brain caused by HSD or other diseases related to mitophagy.

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Cite

BibTeXRIS
BibTeX
@article{wen2026dietary,
  title = {{Dietary high salt drives cognitive impairment and Aβ accumulation via an insufficient compensatory mitophagy response}},
  author = {Jie Wen and Hao Ren and Fan Wen and Junping Yu and Haixia Fan and Jincheng Liu and Zhiyou Cai},
  journal = {Frontiers in Neurology},
  year = {2026},
  month = oct,
  doi = {10.3389/fneur.2026.1922997},
  url = {https://www.frontiersin.org/articles/10.3389/fneur.2026.1922997/full},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Dietary high salt drives cognitive impairment and Aβ accumulation via an insufficient compensatory mitophagy response
AU  - Jie Wen
AU  - Hao Ren
AU  - Fan Wen
AU  - Junping Yu
AU  - Haixia Fan
AU  - Jincheng Liu
AU  - Zhiyou Cai
PY  - 2026
DA  - 2026/10/26
JO  - Frontiers in Neurology
DO  - 10.3389/fneur.2026.1922997
UR  - https://www.frontiersin.org/articles/10.3389/fneur.2026.1922997/full
AB  - There is mounting evidence that dietary habits are strongly correlated with cerebrovascular diseases and dementia, but the precise mechanism remains unclear how a salt-rich diet adversely affects the brain. Here, 12-month-old mice were fed a high-salt diet (HSD) for 2 months, and we observed salt-induced cognitive deficits in mice. The short-term HSD increased mitophagy-associated markers (PINK1, Parkin, and LC3-II) and decreased SQSTM1/p62, consistent with a compensatory mitophagy response that was insufficient to prevent cognitive decline. Neuro-2a cells were cultured in normal medium, NaCl medium (40 mM) or NaCl (40 mM) + CCCP group (20 μM) medium for 24 h, respectively. Short-term HSD feeding impaired learning and memory and increased amyloid-β (Aβ) burden, in parallel with altered PINK1/Parkin-associated mitophagy markers. These findings link a salt-rich diet to cognitive dysfunction, and suggest that enhancing PINK1/Parkin-mediated mitophagy may counteract the harmful effects of HSD on the brain. Therefore, the PINK1/Parkin mitophagy may be a potential target for combating the harmful effects on the brain caused by HSD or other diseases related to mitophagy.
SN  - 1664-2295
ER  -