Early Rehabilitation Exercise Promotes Vestibular Compensation in UVN Mice by Regulating Microglial Polarization Balance via the PGC-1alpha/FNDC5/BDNF Pathway

Acute unilateral vestibular lesions cause disabling vertigo, postural imbalance, and gait instability. Functional recovery depends on vestibular compensation (VC), a neuroplastic process whose cellular and molecular mechanisms remain incompletely understood. Although vestibular rehabilitation effectively accelerates recovery in clinical practice, the underlying pathways are still elusive....

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This is a mouse study using a specific signaling pathway (PGC-1α/FNDC5/BDNF); no actionable change to human vestibular rehabilitation protocols is warranted until human trials replicate these findings.

Identifying the PGC-1α/FNDC5/BDNF pathway as a mechanistic driver of exercise-induced vestibular compensation could eventually guide the timing and design of rehabilitation programs for patients with unilateral vestibular loss.

1. 01Early exercise after unilateral vestibular nerve lesion accelerated balance recovery in mice.
2. 02The mechanism involves microglial polarization — shifting brain immune cells from a harmful to a healing state.
3. 03The PGC-1α/FNDC5/BDNF signaling chain appears to mediate the exercise benefit.
4. 04Study published in Molecular Neurobiology (2026); findings are preclinical only.
5. 05No direct clinical translation yet — human vestibular rehabilitation implications remain speculative.

PMID

42503585

DOI

10.1007/s12035-026-06089-z.

Journal

Molecular Neurobiology

Publication type

research_article

Evidence level

4

Population

Mice with surgically induced unilateral vestibular nerve lesion (UVN model)

Intervention

Early post-lesion rehabilitation exercise

Comparator

No-exercise / delayed-exercise control animals