ReviewMolecular neurobiology2025
The Cooperation of Neurogranin with Calmodulin Promotes the Treatment of Aging-Related Diseases via Regular Exercise.
Review in Molecular neurobiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Exercise orchestrates systemic metabolic and neuroimmune homeostasis via the brain-muscle-liver axis to slow down aging and neurodegeneration: a narrative review.European journal of medical research · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Research has demonstrated that engaging in regular exercise has the potential to enhance cognitive function, promote neuroplasticity, and mitigate the likelihood of experiencing cognitive decline. The underlying mechanisms responsible for these effects are intricate and encompass various pathways, including the interaction between neurogranin and calmodulin. The activation of calcium signaling pathways is a significant mechanism through which regular exercise facilitates the treatment of age-related diseases. The activation of neurogranin and calmodulin induced by exercise can provide protection against neurodegeneration by promoting neuronal survival, mitigating oxidative stress, and improving mitochondrial function through the regulation of calcium homeostasis and energy metabolism. In addition, there is evidence suggesting that engaging in regular exercise can lead to an upregulation of neurotrophic factors, specifically brain-derived neurotrophic factor (BDNF). These factors are crucial for the survival of neurons, the plasticity of synapses, and overall cognitive function. Researchers have discovered the involvement of neurogranin in the regulation of BDNF signaling, underscoring its significance in exercise-induced neuroprotection and cognitive enhancement. The current work offers valuable insights into how neurogranin/calmodulin cooperation, facilitated by regular exercise, promotes the treatment of aging-related diseases. The results suggest that regular exercise could enhance memory, learning, synaptic plasticity, and resilience to neurological damage; promote recovery after brain injury; and treat aging-related disorders such as Alzheimer's disease.
Indexed as
Identifiers
40285939What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.