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Cinnamaldehyde improves the pathology of vascular cognitive impairment via astrocytic TRPA1

Nozomi Kato1, Ayaka Kawashita1, Hiroki Nakajima1

  • 1Department of Molecular Pharmacology, Graduate School of Pharmaceutical Sciences, Kyoto University, Japan.

Journal of Pharmacological Sciences
|June 16, 2026
PubMed

Insights

Activating astrocytic Transient Receptor Potential Ankyrin 1 (TRPA1) channels with cinnamaldehyde ameliorates vascular cognitive impairment (VCI) and white matter injury in mice. This suggests TRPA1 is a potential therapeutic target for VCI.

Area of Science:

  • Neuroscience
  • Pathology
  • Pharmacology

Background:

  • Vascular cognitive impairment (VCI) is a dementia form linked to vascular issues.
  • Chronic cerebral hypoperfusion (CCH) causes VCI via inflammation, oxidative stress, and white matter damage.
  • Current therapeutic strategies for VCI are limited, highlighting the need for novel targets.

Purpose of the Study:

  • To investigate the role of Transient Receptor Potential Ankyrin 1 (TRPA1) in VCI pathogenesis.
  • To explore TRPA1 stimulation as a therapeutic approach for late-stage VCI.
  • To determine if astrocytic TRPA1 mediates the protective effects of cinnamaldehyde.

Main Methods:

  • Utilized a mouse model of VCI induced by bilateral common carotid artery stenosis (BCAS).
  • Administered cinnamaldehyde to stimulate TRPA1 and assessed cognitive function and white matter integrity.
  • Generated astrocyte-specific TRPA1-deficient mice to elucidate the cellular mechanisms of TRPA1 action.

Main Results:

  • Cinnamaldehyde treatment improved cognitive deficits and white matter injury in CCH mice.
  • The therapeutic benefits of cinnamaldehyde were abolished in astrocyte-specific TRPA1-deficient mice.
  • Cinnamaldehyde administration reduced microglial activation (Iba1-positive cells) in the VCI model.

Conclusions:

  • Activation of astrocytic TRPA1 by cinnamaldehyde offers a promising therapeutic strategy for advanced VCI.
  • Astrocyte-derived factors released upon TRPA1 activation may suppress neuroinflammation by inhibiting microglial activity.
  • Targeting astrocytic TRPA1 presents a novel avenue for treating VCI and related dementias.

Keywords:
AstrocyteChronic cerebral hypoperfusionCinnamaldehydeTRPA1Vascular cognitive impairment

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