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.
Keywords: Cofilin-1, cofilin/actin rods, ATP depletion, neurodegeneration, ROS.
Rights & PermissionsPrintExport