Exercise hormone irisin is a critical regulator of cognitive function.
@article{Islam2021ExerciseHI, title={Exercise hormone irisin is a critical regulator of cognitive function.}, author={Mohammad Rashedul Islam and Sophia Valaris and Michael F Young and Erin B Haley and Renhao Luo and Sabrina F Bond and Sofia Mazuera and Robert R. Kitchen and Barbara J. Caldarone and Luis E. B. Bettio and Brian R. Christie and Angela B. Schmider and Roy J. Soberman and Antoine Besnard and Mark P. Jedrychowski and Hyeonwoo Kim and Hua Tu and Eunhee Kim and Se Hoon Choi and Rudolph E. Tanzi and Bruce M Spiegelman and Christiane D Wrann}, journal={Nature metabolism}, year={2021}, volume={3 8}, pages={ 1058-1070 } }
Identifying secreted mediators that drive the cognitive benefits of exercise holds great promise for the treatment of cognitive decline in ageing or Alzheimer's disease (AD). Here, we show that irisin, the cleaved and circulating form of the exercise-induced membrane protein FNDC5, is sufficient to confer the benefits of exercise on cognitive function. Genetic deletion of Fndc5/irisin (global Fndc5 knock-out (KO) mice; F5KO) impairs cognitive function in exercise, ageing and AD. Diminished…
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References
SHOWING 1-10 OF 78 REFERENCES
Exercise-linked FNDC5/irisin rescues synaptic plasticity and memory defects in Alzheimer’s models
- Biology, PsychologyNature Medicine
- 2019
FNDC5/irisin is placed as a novel agent capable of opposing synapse failure and memory impairment in AD, and restoration of its expression can ameliorate these phenotypes in rodent models.
A PGC1α-dependent myokine that drives browning of white fat and thermogenesis
- BiologyNature
- 2012
It is shown in mouse that PGC1-α expression in muscle stimulates an increase in expression of FNDC5, a membrane protein that is cleaved and secreted as a newly identified hormone, irisin, which results in improvements in obesity and glucose homeostasis.
Exercise alters the immune profile in Tg2576 Alzheimer mice toward a response coincident with improved cognitive performance and decreased amyloid
- BiologyJournal of Neuroinflammation
- 2008
Exercise shifts the immune response from innate to an adaptive or alternative response, and this shift in immune response coincides with a decrease in Aβ in advanced pathological states.
Detection and Quantitation of Circulating Human Irisin by Tandem Mass Spectrometry.
- BiologyCell metabolism
- 2015
Mitophagy inhibits amyloid-β and tau pathology and reverses cognitive deficits in models of Alzheimer’s disease
- Biology, PsychologyNature Neuroscience
- 2019
Evidence that mitophagy is impaired in the hippocampus of AD patients, in induced pluripotent stem cell-derived human AD neurons, and in animal AD models is provided, suggesting that impaired removal of defective mitochondria is a pivotal event in AD pathogenesis and thatMitophagy represents a potential therapeutic intervention.
Voluntary Running Attenuates Memory Loss, Decreases Neuropathological Changes and Induces Neurogenesis in a Mouse Model of Alzheimer's Disease
- Biology, PsychologyBrain pathology
- 2016
In APPswe/PS1ΔE9 mice, voluntary running reduced all the neuropathological hallmarks of AD studied, reduced neuronal loss, increased hippocampal neurogenesis and reduced spatial memory loss, supporting that voluntary exercise might have therapeutic value on AD.
Ablation of Fmrp in adult neural stem cells disrupts hippocampus-dependent learning
- BiologyNature Medicine
- 2011
It is shown that ablation of FMRp in aNSCs by inducible gene recombination leads to reduced hippocampal neurogenesis in vitro and in vivo, as well as markedly impairing hippocampus-dependent learning in mice, and restoration of Fmrp expression specifically in a NSCs rescues these learning deficits in FmrP-deficient mice.
Adult hippocampal neurogenesis reduces memory interference in humans: opposing effects of aerobic exercise and depression
- Psychology, BiologyFront. Neurosci.
- 2013
The hypothesis that adult-born neurons in the DG contribute to the orthogonalization of incoming information that acts to reduce interference between highly similar inputs is supported.