In the past, atrophy of brain cells was considered untreatable, they could not be regenerated.
But with epigenetics, perhaps the gene expression for growth of new brain cells can be activated. What are your thoughts?
We have treated successfully gluten cerebellar ataxia on GFD in non-celiac patients with gluten sensitivity.
Thanks for your interesting response. Are there any reports that I can read (in Spanish or English) by which I can familiarize myself with the subject?
Today we know that apart of classic neurogenic niches there is a number of central nervous system areas in which neural stem cells are produced daily. Among them cerebellum has been demonstrated in some animal species to be a source of these cells. Stimulating its proliferation with growth factors may lead to a partial regeneration and functional improvement.
What we have to understand is that paradoxically, stimulating neuronal growth may have the opposite effect. While ataxia is usually degenerative, it is not so much lack of neurons or Purkinje cells but the in-coordination of signals that causes ataxia. It is by no means a given that stimulating neurons will give a positive result in humans
http://brain.oxfordjournals.org/content/126/3/685.full.pdf+html
This is an article about gluten sensitive sporadic ataxia. Among people with ataxia, anecdotally many try a gluten-free diet for a while - it is an easy and no-risk of side effects treatment.
Wonderful, thought provoking comments! Thank you all very much. Any further thoughts would be most welcome.
References on Gluten Ataxia can be found in: Neurogluten (Spanish) [REV NEUROL 2011;53:287-300] PMID: 21796607 [REV NEUROL 2011;53:287-300] PMID: 21796607
Brian
University of California Irvine researchers discovered the axon ceases to function in the absence of lactate, which is produced by the oligodendrocyte. When the oligodendrocyte is damaged or degenerative, addition of lactate to axons in vitrio revives the axon functions--without oligodendroctye involvement. Suggest you consider this as a genetic malfunction, not of the axon but of the oligodendrocyte. Read the info under Scholarly Articles as to the subject.
Hope this helps,
Does it mean that oligodendrocyte mainly work under anaerobic conditions?
I've been always interested in epigenetics, mainly in cardiovascular cells, but, as I encountered cerebellar disorders, linked to primary cilia dysfuntion, I had a dream, that is linking primary cilia signalling to gene expression and epigenetics in cell and animal models of ciliopathies. There are no reports in literature, but as some ciliary protein may translocate to the nucleus, and some pathways pivotal to neurogenesis are altered in these pathological conditions, I believe that the epigenetic profile (in terms of histone modifications, miRNA expression, activity of chromatin remodelling enzymes) of patients affected by cerebellar disorders is altered and restoring a correct gene expression network by EpiDrugs treatment may help to partially revert the phenotype. I'm working on this and I have some interesting data but I have still no papers out. I don't know if my opinion may help..
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