Cellular Mechanisms of Neurodegeneration – CMN
NOTE: Starts with the October 2026 Council round submission dates (Cycle I due dates). This study section was evaluated as part of CSR’s ENQUIRE process to align study sections with advances in science. Learn more about ENQUIRE.
The Cellular Mechanisms of Neurodegeneration reviews applications to study cellular and molecular aspects of neurodegeneration at the mechanistic level. Also considered are the role of genetic factors, trophic molecules and extrinsic influences in neurodegenerative disorders.
Disorders of interest include Alzheimer’s disease, frontotemporal dementias, tauopathies, Parkinson’s disease, spinal muscular atrophy, amyotrophic lateral sclerosis and, Huntington’s disease, spinobulbar muscular atrophy, spinocerebellar, peripheral neuropathy, and Friedreich’s ataxias. Applications may include studies with cellular and molecular endpoints in vitro, in cells including those from human and non-human primate origins, and/or in vivo higher vertebrate animal genetic models as well as model organisms such as C. elegans, Drosophila, Yeast and zebrafish.
Review Dates
A roster for the panel will be posted here, at least 30 days prior to the review meeting
Membership Panel
When the panel is chartered as a standing panel, members will be listed here. Expected in 2026.
Topics
- Studies of pathogenic RNA mechanisms, changes in splicing and RNA processing, and RAN translation in neurodegeneration.
- Characterization of molecular and cellular mechanisms underlying triple nucleotide repeat expansion neurodegenerative disorders.
- Consequences for loss-and-gain-of function mechanisms leading to neurodegenerative disorders.
- Organelle quality control and trafficking pathways such as autophagy, lysosomal degradation, vesicular sorting, and mitophagy.
- Studies of nuclear and epigenetic mechanisms such as nuclear architecture, DNA damage, DNA methylation and histone modifications in transcriptional disturbances observed in neurodegenerative diseases.
- Studies of disease-associated alterations in neurotransmission and intracellular signaling.