I've never seen any reason to think that it could happen the other way around
22% axonal loss at segment C7, but grossly normal immunostaining for myelin
Confocal and electron microscopy revealed myelin sheaths without axonal content
CONCLUSIONS: These studies confirm axonal degeneration in the absence of myelin loss as one histopathologic correlate to abnormal MR findings in patients with MS
Lyon wrote:I was going to ask you where you got those quotes but then I noticed that the text is a link. One of these days you're going to have to tell me how to do that!
I think you mentioned this and "tinyurl" a long time ago and I didn't understand this part so I downloaded tinyurl. I like this option better!NHE wrote: Note that using the above code for URLs keeps very long URLs from causing the browser page to stretch to a new width to accomodate the long URL. This can make reading a thread both annoying and difficult as it requires scrolling the window back and forth to read each line. NHE
Didn't seem in the time since to change what other researchers think?
The traditional notion that multiple sclerosis is a primary demyelinating disease has led to a plaque-centred view of both aetiology and the pathogenesis of disease progression. The presence of axonal loss has received increasing recognition. However, the relative roles of demyelination and axonal loss have not been fully clarified in multiple sclerosis nor have their possible interrelationships been elucidated.
Unexpectedly, after adjusting for sex, age and duration of disease, correlations between total plaque load and axonal loss in both the corticospinal tract and sensory tracts were weak or absent at each level investigated. Since there was little correlation between plaque load and axonal loss, the possibility that demyelination is not the primary determinant of spinal cord axonal loss warrants consideration.
All of this calls for the concept of MS as a focal, inflammatory demyelinating, WM disease to be reexamined and to start viewing MS as a diffuse CNS disease with an important neurodegenerative component. This is central for identifying novel and effective treatment strategies
.Our efforts have been directed towards discovery and development of small, blood brain barrier penetrant molecules to promote endogenous proliferation of neural stem cells within the brain. These endeavors have led to the discovery that the neurosteroid alloprognanolone (APalpha) is a potent and highly efficacious proliferative agent in vitro and in vivo of both rodent and human neural stem cells. Results of our in vitro studies coupled with our more recent analyses in the triple transgenic mouse model of AD suggest that APalpha is a promising strategy for promoting neurogenesis in the aged brain and potentially for restoration of neuronal populations in brains recovering from neurodegenerative disease or injury
I haven't had a chance to read any more so I'm still as in the dark as I was last night.Shayk wrote:Generally speaking I think it most definitely has but not nearly enough IMO.
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