Cerebrospinal fluid neurological diseases

Tumani, H., et al. (1998). Beta-trace protein in cerebrospinal fluid a blood-CSF barrier-related evaluation in neurological diseases. Ann. Neurol. 44, 882-9. 

Other neurological diseases accompanied by the manifestation of monocytic oligocytosis this is the most complicated issue of cytological diagnostics in CSF. Borreliosis can be differentiated again by the presence of an antibody response in cerebrospinal fluid. 

K7. Kimura, S., Ikeda, L, Ito, T, et al., AndromedulUn concentration in CSE from patients with neurological diseases. In 52nd AACC Annual Meeting, CUnical Chemistry, 46(6), A26, 2000. K8. Kjellin, K. G., Xanthochromic compounds in cerebrospinal fluid Quantitative spectrophotometry and electromigration. In Neurobiology of Cerebrospinal Huid 2 (J. H., Wood, ed.). Chap. 33, pp. 559-570. Plenum Press, New York, 1983. 

V3. Vrethem, M., Ohman, S., and von Schenk, H., Comparison of concentration of orosomucoid in serum and cerebrospinal fluid in different neurological diseases. Acta Neurol. Scand. 75, 328-331 (1987). 

Montine TJ, Beal MF, Robertson D, Cudkowicz ME, Biaggioni I, O Donnell H, Zackert WE, Roberts LJ and Morrow JD. 1999. Cerebrospinal fluid F2-isoprostanes are elevated in Huntington s disease. Neurology 52 1104-1105. 

Puccioni-Sohler M, Rieckmann P, Kitze B, Lange P, Albrecht M, Flegenhauer K. A soluble form of tumor necrosis factor receptor in cerebrospinal fluid and serum of HTVLV-l-associated hyelopathy and other neurological diseases. Neurology 1995 242 239-242. 

Palmert MR, Usiak M, Mayeux R, Raskind M, Tourtellotte WW, Younkin SG. Soluble derivatives of the beta amyloid protein precursor in cerebrospinal fluid Alterations in normal aging and in Alzheimer s disease. Neurology 1990 40(7) 1028-1034. 

Decreased 3-amyloidl 2 in cerebrospinal fluid of patients with Creutzfeldt-Jakob disease. Neurology 54, 1099-1102. 

Proteases are essential for the conversion of inactive proprotein precursors into the active neuropeptides. Two main protease pathways have been elucidated for processing proneuropeptides and hormones the recently discovered cysteine protease cathepsin L with aminopeptidase B and the well-established subtilisin-like serine proteases that consist of prohormone con-vertases 1 and 2 followed by carboxypeptidase E/H. Endogenous regulators modulate these two protease pathways as endogenous peptide inhibitors, activators, and in vivo secretory vesicle proteins. Neuropeptides in CSE (cerebrospinal fluid) in neurological diseases can monitor brain nervous activity because neuropeptides represent active neurotransmission (93, 94). 

The brain barrier systems, i.e., the blood—brain and blood—cerebrospinal fluid barriers, ensure that there are adequate supplies of zinc, copper, and iron available for brain function and prevention of neurological diseases. Too much or too little will be detrimental to brain function. Specific transporters present on the BBB will ensure the passage of each of these metals across this barrier. 

Matsiota, P, Blancher, A., Doyon, B., Guilbert, B., Clanet, M., Kouvelas, E. D., et al., Comparative study of natural autoantibodies in the serum and cerebrospinal fluid of normal individuals and patients with multiple sclerosis and other neurological diseases, Ann. Inst. Pasteur Immunol., 139(99), 108, 1988. 

Cerebrospinal Fluid. The proteome of cerebrospinal fluid can provide clues to several neurological disorders, including Alzheimer disease, Parkinson disease, and multiple sclerosis. This study has identified five proteins involved in amyloid-beta metabolism and other metabolisms. These include apolipoprotein Al, cathepsin D, and hemopexin, which were downregulated in Alzheimer patients the transthyretin and pigment epidermal factors were elevated. 

Numerous applications are now encountered where FA chromatographic profiles of a human physiological fluid or tissue are correlated to certain pathological conditions. A few representative examples will now be mentioned that include both free (non-esterified) FA and the saponified lipids. The identification of a methyl-branched FA (phytanic acid) in plasma of the patients with Refsum s disease [360] is now a widely known example of the power of GC in studying various metabolic defects. The profiles of FA from brain ti.ssue lipids were investigated for various neurological disorders [361,362] and in experimental animals [363]. Tichy et al. [364] determined FA in different lipids isolated from the cerebrospinal fluid while the FA profiles in cerebrospinal fluid differ from those in blood serum, no obvious correlations between the FA composition and human neurological complications were established at this time. 

During the first phase of the disease, the most common laboratory abnormalities are a low white blood cell count (leukopenia) and a low platelet count (thrombocytopenia). Liver enzymes in the serum may also be mildly elevated. After the onset of neurological disease during the second phase, an increase in protein levels, an increase in the number of white blood cells or a decrease in the glucose levels in the cerebrospinal fluid (CSF) is usually found. 

Riekse RG, Li G, Petrie EC, Leverenz JB, Vavrek D, Vuletic S, Albers JJ, Montine TJ, Lee VM, Lee M, Seubert P, Galasko D, Schellenberg GD, Hazzard WR, Peskind ER (2006) Effect of statins on Alzheimer s disease biomarkers in cerebrospinal fluid. J Alzheimer Dis 10 399-406 Ridha BH, Josephs KA, Rosser MN (2005) Delusions and hallucinations in dementia with Lewy bodies worsening with memantine. Neurology 65 481 82 Roberts CK, Barnard RJ, Sindhu RK, Jurczak M, Ehdaie A, Vaziri ND (2006) Oxidative stress and dysregulation of NAD(P)H oxidase and antioxidant enzymes in diet-induced metabolic syndrome. Metabolism 55 928—934... 

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