Caveolin-1, a novel player in cognitive decline

Neurosci Biobehav Rev. 2021 Oct:129:95-106. doi: 10.1016/j.neubiorev.2021.06.044. Epub 2021 Jul 5.

Abstract

Cognitive decline (CD), which related to vascular dementia, Alzheimer's disease, Parkinson's disease, Huntington's disease, amyotrophic lateral sclerosis and diabetes mellitus, is a growing health concern that has a great impact on the patients' quality of life. Although extensive efforts, the mechanisms of CD are still far from being clarified, not to mention the effective treatment and prevention strategies. Caveolin-1 (Cav-1), a trans-membrane protein, is a major component of the caveolae structure and scaffolding proteins. Recently, ample evidence depicts a strong correlation between Cav-1 and CD, however, the specific role of Cav-1 in CD has not been clearly examined and how they might be connected have yet to be identified. This review seeks to provide a comprehensive overview about how Cav-1 modulates pathogeneses of CD-associated diseases. In summary, Cav-1 can promote structural and functional plasticity of neurons, improve neurogenesis, relieve mitochondrial dysfunction, inhibit inflammation and suppress oxidative stress, which have shed light on the idea that Cav-1 may be an efficacious therapeutic target to treat CD.

Keywords: Brain development; Caveolin-1; Cognitive decline-related diseases; Pathophysiologic mechanisms.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Caveolae / metabolism
  • Caveolin 1* / metabolism
  • Cognitive Dysfunction* / metabolism
  • Humans
  • Oxidative Stress
  • Quality of Life

Substances

  • Caveolin 1