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Peer-reviewedCC BYMolecular brain

Proteomic analysis of transcutaneous auricular vagus nerve stimulation induced cognitive restoration in a mouse model of vascular cognitive impairment.

  • Seunghwan Choi1
  • Jae Hyun Park2
  • Chan Su Kim2
  • Sun Kwang Kim3,4
4 affiliations
  1. 1Department of Physiology, College of Korean Medicine, Kyung Hee University, Seoul, 02447, Korea.
  2. 2Department of East-West Medicine, Graduate School, Kyung Hee University, Seoul, 02447, Korea.
  3. 3Department of Physiology, College of Korean Medicine, Kyung Hee University, Seoul, 02447, Korea. [email protected].
  4. 4Department of East-West Medicine, Graduate School, Kyung Hee University, Seoul, 02447, Korea. [email protected].
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Abstract

Vascular cognitive impairment (VCI) is a major cause of dementia with limited treatment options. Transcutaneous auricular vagus nerve stimulation (taVNS) is a noninvasive neuromodulation approach that has shown cognitive benefits, but its molecular basis remains unclear. Here, we employed a mouse model of transient bilateral common carotid artery occlusion (tBCCAO) to identify molecular candidates underlying the cognitive restorative effects of taVNS. tBCCAO impaired cognitive function as revealed by behavioral assessments, whereas taVNS restored behavioral performance. Hippocampal proteomic analysis identified 58 proteins altered in tBCCAO compared with sham, and 16 proteins significantly modulated by taVNS compared with tBCCAO. Among these, a core set of taVNS-responsive proteins exhibited a normalization-like pattern, suggesting that taVNS shifted ischemia-associated proteomic alterations toward a near-normal state rather than simply amplifying or suppressing the overall response. These findings suggest that taVNS may improve VCI by restoring hippocampal protein dysregulation following transient cerebral hypoperfusion and highlight molecular targets as candidate mechanisms for further investigation.

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Cite

BibTeXRIS
BibTeX
@article{choi2026proteomic,
  title = {{Proteomic analysis of transcutaneous auricular vagus nerve stimulation induced cognitive restoration in a mouse model of vascular cognitive impairment.}},
  author = {Seunghwan Choi and Jae Hyun Park and Chan Su Kim and Sun Kwang Kim},
  journal = {Molecular brain},
  year = {2026},
  month = jul,
  doi = {10.1186/s13041-026-01339-6},
  url = {https://europepmc.org/article/MED/42902301},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - Proteomic analysis of transcutaneous auricular vagus nerve stimulation induced cognitive restoration in a mouse model of vascular cognitive impairment.
AU  - Seunghwan Choi
AU  - Jae Hyun Park
AU  - Chan Su Kim
AU  - Sun Kwang Kim
PY  - 2026
DA  - 2026/07/01
JO  - Molecular brain
DO  - 10.1186/s13041-026-01339-6
UR  - https://europepmc.org/article/MED/42902301
AB  - Vascular cognitive impairment (VCI) is a major cause of dementia with limited treatment options. Transcutaneous auricular vagus nerve stimulation (taVNS) is a noninvasive neuromodulation approach that has shown cognitive benefits, but its molecular basis remains unclear. Here, we employed a mouse model of transient bilateral common carotid artery occlusion (tBCCAO) to identify molecular candidates underlying the cognitive restorative effects of taVNS. tBCCAO impaired cognitive function as revealed by behavioral assessments, whereas taVNS restored behavioral performance. Hippocampal proteomic analysis identified 58 proteins altered in tBCCAO compared with sham, and 16 proteins significantly modulated by taVNS compared with tBCCAO. Among these, a core set of taVNS-responsive proteins exhibited a normalization-like pattern, suggesting that taVNS shifted ischemia-associated proteomic alterations toward a near-normal state rather than simply amplifying or suppressing the overall response. These findings suggest that taVNS may improve VCI by restoring hippocampal protein dysregulation following transient cerebral hypoperfusion and highlight molecular targets as candidate mechanisms for further investigation.
SN  - 1756-6606
ER  -