Journal
MINI-REVIEWS IN MEDICINAL CHEMISTRY
Volume 14, Issue 5, Pages 393-400Publisher
BENTHAM SCIENCE PUBL LTD
DOI: 10.2174/1389557514666140506161458
Keywords
Cofilin-1; cofilin/actin rods; ATP depletion; neurodegeneration; ROS
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Funding
- MCT/CNPq Universal [470306/2011-4]
- PRONEX/FAPERGS [1000274]
- PRONEM/FAPERGS [11/2032-5]
- PqG/FAPERGS [2414-2551/12-8]
- MCT/CNPq INCT-TM [573671/2008-7]
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Cofilin-1 protein, which main function is to regulate actin cytoskeleton dynamics, appears to be involved with many steps in the neurotoxicity processes found in neurodegenerative diseases such as Alzheimer's disease (AD), Parkinson's disease (PD) and Huntington's disease (HD). As the dynamics of actin filaments play a major role in several cellular processes, the primary involvement of cofilin-1 dysfunctions in the pathophysiology of these disorders may be related to a cytoskeleton stress. However, recently cofilin-1 has also been related to other biological processes such as cell death by apoptosis. In both cases, ATP depletion associated with the presence of reactive species and other stressors regulate cofilin-1 by inducing the formation of aggregates composed primarily by actin and cofilin-1, known as cofilin/actin rods. These structures seem to be formed initially as a neuroprotective response to mitochondrial damage; but once the stressor persists they are thought to act as inducers of further impairments and loss of neuronal functions. Therefore, here we provide a brief overview of the current knowledge about the central role of cofilin/actin rods formation, where its dysregulation and malfunction might be the trigger to neurodegeneration.
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