Doggone it, flora, you got me on the "hunt" again this morning! hehehe.....
Ok.......I found an abstract regarding that article. Here are the three "markers" they found...........jeez, way back in 2003. Tell me news isn't slow.
http://www.neurology.org/cgi/content/ab ... 61/12/1720Neurofilament light protein and glial fibrillary acidic protein as biological markers in MS
C. Malmeström, MD, S. Haghighi, MD, L. Rosengren, MD PhD, O. Andersen, MD PhD and J. Lycke, MD PhD
From the Institute of Clinical Neuroscience, Department of Neurology, Göteborg University, Sahlgrenska University Hospital, Sweden.
Address correspondence and reprint requests to Dr. J. Lycke, Institute of Clinical Neuroscience, Department of Neurology, Göteborg University, Sahlgrenska University Hospital, SE-413 45 Göteborg, Sweden; e-mail: email@example.com
Objective: To determine if CNS-derived proteins present in the CSF of multiple sclerosis (MS) patients reflect different pathologic processes of MS and if these proteins could be useful as biologic markers of disease activity.
Methods: Concentrations of the neurofilament light protein (NFL), glial fibrillary acidic protein (GFAP), S100B, and the neuron-specific enolase protein (NSE)
were determined in the CSF of 66 MS patients and 50 healthy control subjects with immunoassays.
Results: The mean levels of the NFL were increased during all stages of MS compared with controls (p < 0.001), peaking almost 10 times higher during acute relapses. The highest levels of GFAP were found during the secondary progressive course (p < 0.001) with a strong correlation with neurologic deficits (Expanded Disability Status Scale score, r = 0.73, p < 0.001). No increase of S100B or NSE protein was found in the CSF of MS patients compared with control subjects. Conclusions: Increased level of NFL is a general feature of MS, indicating continuous axonal damage during the entire course of the disease with the most profound damage during acute relapses. GFAP may serve as a biomarker for disease progression, probably reflecting the increasing rate of astrogliosis.
Received March 31, 2003. Accepted in final form August 20, 2003.
Oh, this is interesting! Maybe a bit controversial. That above are the original findings by some other folks. (Which as I mentioned previously, we already knew there was axonal damage going on in MS, so nothing new there. Even with this research, it still doesn't tell the "why" at all. But Sharon and I have some "theories".
Dr. Avasarala had some questions for these researchers, expressing a little skepticism, even: http://www.neurology.org/cgi/eletters/61/12/1720#1009
And those original researchers responded. Part of what they said to Dr. Avasarala was:
....There are no methodological problems to measure S-100B or NSE in serum. However, the mechanism by which CNS proteins enter CSF and serum differ. Passage to CSF is relatively unrestricted, and consequently levels of markers in CSF reflect the glial and nerve cell injury. Passage to serum is influenced by the function of the blood brain barrier (the integrity of the endothelial lining of the vascular bed), which means that serum-S-100B not only reflects the glial cell injury. In MS patients, the parenchymal damage is probably too small even during acute relapses and the function of the blood-brain barrier is relatively undisturbed to allow increased levels of CNS-derived proteins in serum. Furthermore, both S-100B and NSE are found in extra neuronal tissue; S-100B in adipose tissue and NSE in neuroendocrine cells. Thus, in serum neither of these markers truly reflects specific damage of nerve and glial cells.
Then, in 2004, Dr. Avasarala did his/her own research, which I can't seem to get ahold of right at the moment:
J. R. Avasarala, J. N. Lycke, C. Malmestrom, S. Haghighi, L. Rosengren, and O. Andersen
Neurofilament light protein and glial fibrillary acidic protein as biological markers in MS
Neurology, August 10, 2004; 63(3): 599 - 599.
EDIT: Ah! I see. This Dr. Avasarala seems to concentrate on finding the "markers" for diagnosis and prognosis in MS. Here's another abstract from this doctor, just to show what I mean:
Arch Neurol. 2001 Dec;58(12):2044-5. Related Articles, Links Oligoclonal band number as a marker for prognosis in multiple sclerosis.
Avasarala JR, Cross AH, Trotter JL.
Department of Neurology, Washington University School of Medicine, Campus Box 8111, 660 S Euclid Ave, St Louis, MO 63017, USA. firstname.lastname@example.org
The natural course of disease in multiple sclerosis varies. Multiple sclerosis that is clinically apparent but causes minimal disability over time has been labeled benign multiple sclerosis. The ability to predict the subsequent clinical course of multiple sclerosis on the basis of clinical and other supportive data at presentation would be invaluable. In this article we report our findings based on a retrospective analysis of 1800 patients diagnosed as having multiple sclerosis, of which 44 patients met our inclusion criteria. There was a suggestion that a low or absent number of oligoclonal bands in the cerebrospinal fluid at the time of diagnosis predicts a better prognosis. However, quantification of oligoclonal bands in cerebrospinal fluid remains an insensitive prognostic indicator and must not be used to influence decisions regarding therapeutic options.
PMID: 11735778 [PubMed - indexed for MEDLINE]
SECOND EDIT: Darn, once you really start to read into this, you might see what I do. They still aren't even sure about THIS (i.e. flora's original article she found!) There is controversy and "some" contradiction amongst the researchers themselves. hmmmmmmmm........ Oh, well.........it sure would be nice, though, if they DO all agree and find these "markers" to definitely be indicative of MS, and axonal damage, etc. That would be in and of itself very useful in order to monitor progression, also. Let's keep our fingers crossed that something comes of it!