Abstract
Small guanosine triphosphatases (GTPases) of the Ras superfamily are key regulators of many key cellular events such as proliferation, differentiation, cell cycle regulation, migration, or apoptosis. To control these biological responses, GTPases activity is regulated by guanine nucleotide exchange factors (GEFs), GTPase activating proteins (GAPs), and in some small GTPases also guanine nucleotide dissociation inhibitors (GDIs). Moreover, small GTPases transduce signals by their downstream effector molecules. Many studies demonstrate that small GTPases of the Ras family are involved in neurodegeneration processes. Here, in this review, we focus on the signaling pathways controlled by these small protein superfamilies that culminate in neurodegenerative pathologies, such as Alzheimer’s disease (AD) and Parkinson’s disease (PD). Specifically, we concentrate on the two most studied families of the Ras superfamily: the Ras and Rho families. We summarize the latest findings of small GTPases of the Ras and Rho families in neurodegeneration in order to highlight these small proteins as potential therapeutic targets capable of slowing down different neurodegenerative diseases.
Highlights
Eukaryotic cells permanently maintain communication with the extracellular medium through some molecules such as growth factors, hormones, peptides, and ions
The role of small guanosine triphosphatase (GTPase) of the Ras superfamily has been overlooked for a long time in neurodegenerative diseases
Rho GTPases in physiological conditions are responsible for the actin cytoskeleton remodeling, and their alteration may produce abnormalities such as spine loss in neurons
Summary
Eukaryotic cells permanently maintain communication with the extracellular medium through some molecules such as growth factors, hormones, peptides, and ions. The original trigger of neuronal death is still unknown, aging is considered a risk factor for neurodegenerative diseases Many of these disorders share an abnormal accumulation of misfolded peptides or proteins in the brain and spinal cord. The dysregulation of specific GTPases of the Ras superfamily, or their regulators or effector molecules, leads to aberrant signaling pathways and/or pathological cell responses that could cause neurodegeneration in AD and PD. Understanding how these GTPase-mediated molecular events are dysregulated in neurodegenerative diseases can help us understand the cause of neurodegeneration. We summarize the latest findings to highlight the role of small GTPases of the Ras and Rho families in neurodegenerative processes
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