Autopsy samples from these patients revealed that in
all cases there was an almost complete absence of inflammatory
markers in the brain, notably of T cells. On
the other hand, there was significant staining for amyloid
precursor protein (APP) inclusions, a marker of
acute axonal damage (Fig. 5). This suggested that even
though inflammation had been abolished, neurodegeneration
was still proceeding in the brains of these patients,
and thus that neurodegeneration was not a direct
consequence, at least in the short-term,of inflammatory
damage to the nervous system.These data are consistent
with the observation from MRI studies that the rate of
brain atrophy is high in patients who have received
hematopoietic stem cell grafts in spite of an apparent
complete cessation of inflammatory lesion activity
From Bruck W J Neurol (2005) 252 [Suppl 5]: V/10–V/15
DOI 10.1007/s00415-005-5003-6 I own a copy of that paper.
The case study posted by Dignan is most certainly of value taken together with other material such as this autopsy work.
Those of us in the 'degenerative not autoimmune' camp are perfectly justified in taking that position.
However I'd like to be clear that saying degenertive does not exclude the immune system activity being there after the fact and even being a problem. I believe that in the end it will be clarified that there is a triggering factor to the immune activation (perhaps Zambonis mechanical trauma hypothesis) and eventually some clarity that the immune activataion even though "justified" from a physiologic point of view, was over active and part of what causes the eventual damage.
here's a good example; spinal cord injury. If you get a broken back they now know that the inflammatory response causes a lot of the damage. Mitigating that effectively is going to be part of the solution to better outcomes.
however if you never broke it in the first place you'd do best of all