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The full study is a bit heavy for the average reader (including myself) but the bottom line is clear: "Our results suggest that damaged cerebellar neurons can be substantially rescued by increased myelination" and "for the first time, our results provide strong evidence that VGF has the ability to stimulate OP proliferation, trigger myelination, revert neural damage, and prolong lifespan."
Yes, this research was done on mice, not humans. Yes, this research covered only running (it's rather challenging to make mice cycle or play squash). But overall, it is becoming clearer and clearer that aerobic exercise may play a large role in containing multiple sclerosis progression. - D
Voluntary Running Triggers VGF-Mediated Oligodendrogenesis to Prolong the Lifespan of Snf2h-Null Ataxic Mice
Matías Alvarez-Saavedra
Highlights
•Running promotes the survival of mice with cerebellar ataxia following Snf2h inactivation
•Running ataxic mice show enhanced oligodendrogenesis and de novo myelination
•Comparative RNA-seq studies identify VGF as a contributor to brain repair
•VGF overexpression improves ataxic phenotype in mice without exercise
Summary
Exercise has been argued to enhance cognitive function and slow progressive neurodegenerative disease. Although exercise promotes neurogenesis, oligodendrogenesis and adaptive myelination are also significant contributors to brain repair and brain health. Nonetheless, the molecular details underlying these effects remain poorly understood. Conditional ablation of the Snf2h gene impairs cerebellar development producing mice with poor motor function, progressive ataxia, and death between postnatal days 25–45. Here, we show that voluntary running induced an endogenous brain repair mechanism that resulted in a striking increase in hindbrain myelination and the long-term survival of Snf2h cKO mice. Further experiments identified the VGF growth factor as a major driver underlying this effect. VGF neuropeptides promote oligodendrogenesis in*vitro, whereas Snf2h cKO mice treated with full-length VGF-encoding adenoviruses removed the requirement of exercise for survival. Together, these results suggest that VGF delivery could represent a therapeutic strategy for cerebellar ataxia and other pathologies of the CNS.
FULL STUDY:
http://www.cell.com/cell-reports/ful...247(16)31252-9
Yes, this research was done on mice, not humans. Yes, this research covered only running (it's rather challenging to make mice cycle or play squash). But overall, it is becoming clearer and clearer that aerobic exercise may play a large role in containing multiple sclerosis progression. - D
Running helps repair brain damage in mice, Ottawa researchers find
Researchers at The Ottawa Hospital and the University of Ottawa have discovered that a molecule triggered by running can help repair certain types of brain damage in mice.
The molecule, called VGF nerve growth factor, had previously been discovered to promote an anti-depressant response, but its importance in preventing or delaying brain damage wasn't as clear.
But in a study*published Tuesday in the scientific journal*Cell Reports, the researchers discovered the production of VGF nerve growth factor*assists with the healing of the protective coating that insulates nerve fibres.
The discovery was made when researchers were studying mice with genetically modified cerebellums, the part of the brain that controls motor movement co-ordination and balance.
....it helps to explain the effect that exercises, like running, have on people suffering from neurodegenerative diseases that involve damaged nerve insulation like multiple sclerosis.
....when mice stopped exercising they began to debilitate again.
STORY: http://www.cbc.ca/news/canada/ottawa...mage-1.3800121
Researchers at The Ottawa Hospital and the University of Ottawa have discovered that a molecule triggered by running can help repair certain types of brain damage in mice.
The molecule, called VGF nerve growth factor, had previously been discovered to promote an anti-depressant response, but its importance in preventing or delaying brain damage wasn't as clear.
But in a study*published Tuesday in the scientific journal*Cell Reports, the researchers discovered the production of VGF nerve growth factor*assists with the healing of the protective coating that insulates nerve fibres.
The discovery was made when researchers were studying mice with genetically modified cerebellums, the part of the brain that controls motor movement co-ordination and balance.
....it helps to explain the effect that exercises, like running, have on people suffering from neurodegenerative diseases that involve damaged nerve insulation like multiple sclerosis.
....when mice stopped exercising they began to debilitate again.
STORY: http://www.cbc.ca/news/canada/ottawa...mage-1.3800121
Matías Alvarez-Saavedra
Highlights
•Running promotes the survival of mice with cerebellar ataxia following Snf2h inactivation
•Running ataxic mice show enhanced oligodendrogenesis and de novo myelination
•Comparative RNA-seq studies identify VGF as a contributor to brain repair
•VGF overexpression improves ataxic phenotype in mice without exercise
Summary
Exercise has been argued to enhance cognitive function and slow progressive neurodegenerative disease. Although exercise promotes neurogenesis, oligodendrogenesis and adaptive myelination are also significant contributors to brain repair and brain health. Nonetheless, the molecular details underlying these effects remain poorly understood. Conditional ablation of the Snf2h gene impairs cerebellar development producing mice with poor motor function, progressive ataxia, and death between postnatal days 25–45. Here, we show that voluntary running induced an endogenous brain repair mechanism that resulted in a striking increase in hindbrain myelination and the long-term survival of Snf2h cKO mice. Further experiments identified the VGF growth factor as a major driver underlying this effect. VGF neuropeptides promote oligodendrogenesis in*vitro, whereas Snf2h cKO mice treated with full-length VGF-encoding adenoviruses removed the requirement of exercise for survival. Together, these results suggest that VGF delivery could represent a therapeutic strategy for cerebellar ataxia and other pathologies of the CNS.
FULL STUDY:
http://www.cell.com/cell-reports/ful...247(16)31252-9
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