Neuronal Stress, Death, and Survival – NSDS
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 which functions to align study sections with advances in science. Learn more about ENQUIRE.
The Neuronal Stress, Death, and Survival Study Section reviews applications studying the molecular mechanisms of neuronal cell stress and death involving aging, neurodegenerative diseases, programmed cell death, necrosis, autophagy, and excitotoxicity; oxidative stress associated with neural injury; and mitochondrial biology of neurons and glia in healthy and diseased states across the life span. Also considered are the roles of genetic factors and DNA damage, trophic molecules and extrinsic influences (including toxins, hormones, and environmental substances) in these processes, as well as basic aspects of disease, injury, and repair or neuroprotective strategies. Applications use vertebrate animal and cellular models as well as model organisms such as Yeast, C. elegans, Drosophila 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
- A wide variety of cell stress pathways such as oxidative stress in disease states including Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, Amyotrophic Lateral Sclerosis, and stroke and ischemia.
Mitochondrial function and dysfunction in mitochondrial diseases, neurodegenerative diseases and stroke; metabolic and bioenergetic demands of neurons, glia and the whole brain; mitochondrial fission, fusion, dynamics and mitophagy.
Neuronal cell signaling pathways in cell survival and cell death such as apoptosis, necrosis, autophagy, excitotoxicity. Functions and mechanisms of action of signaling molecules in regulating cell death and survival.
Studies of mechanisms relevant to the development of neuroprotective or cell survival strategies.
Molecular mechanisms underlying neural injury associated with ischemia, reperfusion injury, traumatic brain injury, hypoxia, hypoglycemia, neurotoxic insults, and excitotoxicity.
Gene regulatory mechanisms and post translational modifications as relates to neuronal cell death and cell survival.
Vertebrate and invertebrate animal models as well as neuronal cell and stem cell models of neurodegenerative disease, injury and neuroprotection.
Shared Interests and Overlaps
There is overlapping and shared interest with the following review panels:
There is shared interest between NSDS and the Neuronal Communications (NC) Study Section in oxidative stress, mitochondrial biology, calcium homeostasis, synaptic plasticity, and signal transduction, particularly as these processes relate to neurodegenerative disease and neural injury. Applications focused more on how energy metabolism or mitochondrial biology affects these processes in neurodegeneration or neuroprotection can be reviewed in NSDS. Applications focused more on how these processes influence synaptic structure, synaptic transmission, and neural circuit function can be reviewed in NC.
There is shared interest between NSDR and NSDS study section in applications that study plasticity, cell death, survival, and regeneration in normal aging as well as acute or chronic conditions caused by injury, disease or environmental factors. NSDS may review applications with a focus on degenerative or protective outcomes or when these outcomes are used to identify mitochondrial or oxidative involvement in neurodegeneration or protection. NSDR can review when the focus is on cellular and molecular mechanisms of synaptic plasticity, neurogenesis and regeneration of axonal or synaptic connections in the context of neurodegeneration or protection.
There is shared interest between NSDS and CMN in the mechanisms of cell death in neurodegeneration. NSDS can review if applications involve oxidative stress, cell signaling pathways or neuroprotection while CMN reviews applications on neurodegeneration that emphasize genetic factors, tropic molecules and extrinsic influences in neurodegeneration.
There is shared interest between NSDS and PPAN in the mechanisms of cell death in neurodegeneration. NSDS can review if applications involve oxidative stress, cell signaling pathways or neuroprotection while PPAN reviews applications on neurodegeneration that emphasize on proteostasis and defects in protein misfolding that underlie neurodegenerative disorders
There is shared interests BMGS and NSDS in the role of glia and neurovasculature in neurodegeneration. NSDS can review when mitochondrial function and/or oxidative stress are involved, while BMGS reviews applications focusing on neurodegenerative processes that primarily involve glia.
There is shared interest between CDIN and NSDS in neuronal cell death and protection. NSDS can review when molecular mechanisms of cell death and protection are the focus, including basic science using vertebrate and invertebrate models, while CDIN reviews applications that focus on pre-clinical, integrated physiological aspects of neurodegeneration as consequences of cellular disturbances, and possible therapeutic strategies.
There is shared interest with NP A-81 and NSDS in applications studying neural injury and brain ischemia applications. NSDS reviews applications investigating components of basic molecular signaling in cell death or protection pathways as well as applications dealing with cellular bioenergetics, while NP A-81 reviews applications on brain and neuronal injury and neurovascular disorders that are preclinical and translational.
There is shared interest with CMAD in applications that study aging. Applications on metabolic and mitochondrial function on health are reviewed in CMAD. Applications involving neuronal function or neurodegenerative diseases can be reviewed in NSDS.
