Special Issue "Changes in Inhibitory Synapse Composition and Plasticity along the Progression of Neurodegenerative Diseases"
Deadline for manuscript submissions: 31 March 2022.
Interests: Alzheimer's disease; inhibitory synapses; gephyrin; neurodegeneration; neuorinflammation; microglia
The still incompletely understood pathogenesis of neurodegenerative diseases represents one important reason previous therapeutic approaches failed to effectively cure or delay their progression. Synaptic dysfunction, including altered synaptic plasticity, seems to be a central pathophysiological process in several neurodegenerative diseases, including Alzheimer’s disease, Parkinson’s disease, amyotrophic lateral sclerosis, and Huntington’s disease. Research in recent years has strongly supported the involvement of GABAergic neurotransmission in both early and late pathogenesis of these groups of diseases. The GABAergic system might undergo dynamic remodeling and play different roles in the pathology at various disease stages. This seems to include stage-dependent alterations in presynaptic and postsynaptic components of inhibitory synapses and particularly scaffolding, anchoring and supporting proteins of GABAA receptors which influence the plasticity of the GABAergic system. The modulation of GABAergic neurotransmission through targeting inhibitory synapse proteins and their interactions (e.g., receptor–scaffold protein interactions) was proposed as a promising pharmacological strategy to normalize synapse dynamics and restore cognitive function.
This Special Issue of IJMS encourages primarily original research articles and short communications that expand present and identify new perspectives and molecular details for a more profound understanding of the GABAergic system along neurodegeneration. Review articles covering the most recent discoveries in this area and new therapeutic approaches targeting GABAergic synapses are also welcome.
Dr. Eva Kiss
Manuscript Submission Information
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- inhibitory synapse
- synaptic plasticity
- scaffolding proteins
- animal models