Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2020 Aug;15(8):1451-1459.
doi: 10.4103/1673-5374.274330.

The role of cofilin in age-related neuroinflammation

Affiliations
Review

The role of cofilin in age-related neuroinflammation

Amsha S Alsegiani et al. Neural Regen Res. 2020 Aug.

Abstract

Aging brain becomes susceptible to neurodegenerative diseases due to the shifting of microglia and astrocyte phenotypes to an active "pro-inflammatory" state, causing chronic low-grade neuroinflammation. Despite the fact that the role of neuroinflammation during aging has been extensively studied in recent years, the underlying causes remain unclear. The identification of relevant proteins and understanding their potential roles in neuroinflammation can help explain their potential of becoming biomarkers in the aging brain and as drug targets for prevention and treatment. This will eventually reduce the chances of developing neurodegenerative diseases and promote healthier lives in the elderly. In this review, we have summarized the morphological and cellular changes in the aging brain, the effects of age-related neuroinflammation, and the potential role of cofilin-1 during neuroinflammation. We also discuss other factors contributing to brain aging and neuroinflammation.

Keywords: aging; astrocyte-activation; cofilin; cofilin inhibitor; cofilin/actin rods; inflammaging; microglial activation; neurogenesis; neuroinflammation.

PubMed Disclaimer

Conflict of interest statement

None

Figures

Figure 1
Figure 1
Cofilin activation in aged microglia leads to neuroinflammation. In normal aging, the microglia morphology changed from ramified phenotype in resting state to dystrophic phenotype. We hypothesize that the morphological change due to an increase in the expression of active cofilin in aged microglia compared with young, resulting in activated other microglial cells, induce neuroinflammation, astrocyte activation and promote neuronal death.

References

    1. ADAPT Research Group, Martin BK, Szekely C, Brandt J, Piantadosi S, Breitner JC, Craft S, Evans D, Green R, Mullan M. Cognitive function over time in the Alzheimer’s Disease Anti-inflammatory Prevention Trial (ADAPT): results of a randomized, controlled trial of naproxen and celecoxib. Arch Neurol. 2008;65:896–905. - PMC - PubMed
    1. Alhadidi Q, Nash KM, Alaqel S, Sayeed MSB, Shah ZA. Cofilin knockdown attenuates hemorrhagic brain injury-induced oxidative stress and microglial activation in mice. Neuroscience. 2018;383:33–45. - PMC - PubMed
    1. Alhadidi Q, Shah ZA. Cofilin mediates LPS-induced microglial cell activation and associated neurotoxicity through activation of NF-kappaB and JAK-STAT pathway. Mol Neurobiol. 2018;55:1676–1691. - PMC - PubMed
    1. Aloisi F. The role of microglia and astrocytes in CNS immune surveillance and immunopathology. Adv Exp Med Biol. 1999;468:123–133. - PubMed
    1. Ambach A, Saunus J, Konstandin M, Wesselborg S, Meuer SC, Samstag Y. The serine phosphatases PP1 and PP2A associate with and activate the actin-binding protein cofilin in human T lymphocytes. Eur J Immunol. 2000;30:3422–3431. - PubMed