ArticleCNS neuroscience & therapeutics2026
Aerobic Exercise Promotes Hippocampal Neurogenesis and Ameliorates Cognitive Dysfunction Induced by Unilateral Labyrinthectomy.
Article in CNS neuroscience & therapeutics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Aging in a highly polluted world: challenges and solutions to prevent Alzheimer's disease.Archives of toxicology · 2026Review
- Aerobic Exercise Promotes Hippocampal Neurogenesis and Ameliorates Cognitive Dysfunction Induced by Unilateral Labyrinthectomy.CNS neuroscience & therapeutics · 2026Article
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Authors and funding
14 authors.
Funding
Abstract
aimsVestibular dysfunction is strongly linked to cognitive impairment and dementia risk, yet its underlying mechanisms remain unclear, hindering treatment development. As a primary physical therapy intervention, aerobic exercise improves cognitive dysfunction. Thus, we investigated its potential to reverse cognitive deficits after vestibular dysfunction and explored the neurobiological mechanisms involved.
methodsBehavioral experiments were conducted to assess the cognitive impairment induced by unilateral labyrinthectomy (UL). Immunofluorescence staining was performed to assess neural stem cell proliferation and newborn neuron maturation in the hippocampal dentate gyrus. Aerobic exercise was applied as an intervention to examine its effects on cognitive and neurogenic recovery. RNA sequencing followed by qRT-PCR was used to characterize transcriptional changes. Pharmacological manipulation is applied to demonstrate the necessity and sufficiency of key candidate genes in mediating the exercise-induced effects.
resultsUL induced significant cognitive dysfunction and hippocampal neurogenesis inhibition, whereas aerobic exercise intervention reversed these impairments. Transcriptomic profiling showed that aerobic exercise normalized UL-disrupted gene expression, with enrichment observed in MHC class I/II-related (H2-K1, H2-Eb1, CD74) and neurodevelopmental (Cntn5, Mid1) pathways. Pharmacological experiments established causality: inhibition of neuroinflammatory signaling with AZD1480 enhanced neurogenesis and improved cognition after UL, whereas LPS-mediated activation of inflammation attenuated the beneficial effects of aerobic exercise.
conclusionThese findings provide a novel non-pharmacological strategy for cognitive rehabilitation, as well as early cognitive screening and exercise rehabilitation intervention for patients with vestibular disorders.
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