Was this another rhetorical comment? If it wasn't, I'd have to correct you. During the past years several MS researchers have stated that MS could be a two-stage disease, where inflammatory phase (RRMS) is often followed by degenerative phase (SPMS, PPMS). Naturally I haven't bought it ;-)TonyJegs wrote:Neurogenerative disorders (of any kind) never have been considered as “two-stage” disorders, they are always complex, all structures and all cells are involved simultaneously in certain degree.
I hear you. In other words you're stating that demyelination in lesions has to come before axonal injury, not vice versa in any circumstances, right? And it would be impossible for any kind of axonal dysfunction to cause local demyelination seen as lesions?TonyJegs wrote:It is physiologically impossible to have a myelinated axon, say 7 inches long, and have isolated local demyelination of it, say between 3,5 and 4 inches, only. Any axonal damage causes the demyelination distantly of the site of damage as well as proximally later.
In case of MS we have a situation when several hundreds of axons of different length, different size, different thickness of myelin, from neurons of different location in gray matter, met somewhere in the middle of the brain in local (bordered) lesion, but axons are not the cause here. They are victims :)
2. You got me right about axonal injury in WM, myelin damage comes first.
Lyon wrote:This is not in the least intended to be hostile because in your time here much of what you've said seems very sensible and it seems you have a direct knowledge of neurological functions. On the other hand, some things you mention directly contradict what we're used to hearing.
I'm in the search of truth so I have nothing against....and in fact I look forward to strong evidence which contradicts conventional knowledge, but in order to give it any weight I need more to go on.
Thanks to administration of this forum for possibility to share opinions in an unobstructed way
Axons, which went through the site of damage (MS lesion), reacted to this ‘catastrophe’ differently.
My knowledge of myelin thickness was limited to the assumed differences between the genders (based on the mice studies--men have thicker myelin than women I think ??) and I didn't realize there was so much general variation in myelin thickness that was itself dependent on the thickness of the axon. Did I understand that correctly? It's always possible I didn't.
What do you think this 'catastrophe' is (I'm assuming you didn't mean it's the lesion itself)? What in your opinion initiates the 'catastrophe' (damage to the myelin)? Or, is that something that's still an unknown?
Why women are protected from MS relapses during pregnancy? The level of estrogens goes down as protection from abortion (biological common sense)
Our data give further support to the notion that progression in MS is an age dependent process independent of relapses.
In both animals and humans, vitamin D serves as an important endogenous and/or exogenous regulator of neuroprotection, antiepileptic and anticalcification effects, neuro-immunomodulation, interplay with neurotransmitters and hormones, modulation of behaviors, brain ageing, and some other, less-explored, brain processes. SUMMARY: Vitamin D emerges as an important neurosteroid hormone in the brain, with a strong potential for age-specific applications…..
Users browsing this forum: wombat