Other Neurological Diseases Group Research Articles

Elevated Serum Xanthine Oxidase and Its Correlation with Antioxidant Status in Patients with Parkinson's Disease.

Parkinson's disease (PD) is a neurodegenerative movement disorder associated with a loss of dopamine neurons in the substantia nigra. The diagnosis of PD is sensitive since it shows clinical features that are common with other neurodegenerative diseases. In addition, most symptoms arise at the late stage of the disease, where most dopaminergic neurons are already damaged. Several studies reported that oxidative stress is a key modulator in the development of PD. This condition occurs due to excess reactive oxygen species (ROS) production in the cellular system and the incapability of antioxidants to neutralize it. In this study, we focused on the pathology of PD by measuring serum xanthine oxidase (XO) activity, which is an enzyme that generates ROS. Interestingly, the serum XO activity of patients with PD was markedly upregulated compared to patients with other neurological diseases (ONDs) as a control. Moreover, serum XO activity in patients with PD showed a significant correlation with the disease severity based on the Hoehn and Yahr (HY) stages. The investigation of antioxidant status also revealed that serum uric acid levels were significantly lower in the severe group (HY ≥ 3) than in the ONDs group. Together, these results suggest that XO activity may contribute to the development of PD and might potentially be a biomarker for determining disease severity in patients with PD.

Detection and clinical significance of serum autoantibodies in patients with myasthenia gravis

Objective To investigate the expressions and clinical significance of serum anti - acetylcholine receptor antibodies (AChR-Ab), anti-Titin antibodies (Titin-Ab), and anti-Ryanodine receptor antibodies (RyR-Ab) in patients with myasthenia gravis (MG). Methods Serum AChR-Ab, Titin-Ab and RyR-Ab were detected with enzyme-linked immunosorbent assay (ELISA) in 182 MG patients, 105 patients of other neurological diseases (OND) and 62 normal controls. Results Serum AChR-Ab, Titin-Ab and RyR-Ab were detected positive respectively in 68.13% (124/182), 64.29% (117/182) and 67.03% (122/182) of patients in MG group. The positive rates of those antibodies in MG group were significantly higher than those in OND group ( P = 0.000, for all) and control group ( P = 0.000, for all). When 3 antibodies coexisted, the sensitivity in the diagnosis of MG was 41.21%, with 99.40% of specificity. There was no significant difference in the positive rate of serum AChR-Ab, Titin-Ab and RyR-Ab between early-onset MG subgroup and late-onset MG subgroup ( P > 0.05, for all). The positive rates of AChR-Ab were significantly higher in MG patients with thymoma than in those without thymoma ( P = 0.004). There was no significant difference in the positive rate of Titin-Ab and RyR-Ab between MG with thymoma subgroup and MG without thymoma subgroup ( P > 0.05, for all). The prevalence of AChR-Ab in generalized MG (GMG) atients (Ⅱa and Ⅱb) was higher than those in ocular MG (OMG) patients (typeⅠ; P = 0.005, 0.012). There was no significant difference in the positive rate of Titin-Ab and RyR-Ab between GMG subgroup and OMG subgroup ( P > 0.05, for all). Conclusions Serum AChR-Ab, Titin-Ab and RyR-Ab can be used as ndicators of the diagnosis of MG. Patients with 3 coexisted positive antibodies are highly suspected as MG. Higher AChR-Ab level in serum of OMG patients indicates the possibility of progressing to GMG. DOI: 10.3969/j.issn.1672-6731.2016.10.007

Hexosylceramides as intrathecal markers of worsening disability in multiple sclerosis

Background: Sphingolipids are important components of neurons and the myelin sheath whose levels are altered in multiple sclerosis (MS). Objectives: We aimed to determine if cerebrospinal fluid (CSF) sphingolipids can be used as markers of MS disease progression. Methods: Using liquid chromatography tandem mass spectrometry, we analysed sphingolipids in CSF from 134 individuals. The MS group included 65 patients divided into 41 relapsing–remitting MS (RRMS) and 24 progressive MS (ProgMS). In addition, a group of 13 early MS/clinically isolated syndrome (EarlyMS) and two control groups consisting of 38 individuals with other neurological diseases (OND) and 18 OND with signs of inflammation (iOND) were analysed. A follow-up study included 17 additional RRMS patients sampled at two time points 4.7±1.7 years apart. Results: Levels of sphingomyelin (SM)- and hexosylceramide (HexCer)-derived sphingolipids increased in the CSF of patients with MS independently of the fatty acid chain length in RRMS (p<0.05). Levels of palmitic acid (16:0)-containing HexCer (HexCer16:0) increased significantly in ProgMS compared with the OND (p<0.001), iOND (p<0.05) and EarlyMS (p<0.01) groups and correlated with Expanded Disability Status Scale in RRMS in both studies (p=0.048; p=0.027). Conclusion: HexCer16:0 is a promising candidate marker of disease progression in MS, especially in RRMS.

Cytoskeletal proteins in the cerebrospinal fluid as biomarker of multiple sclerosis

The axonal cytoskeleton is a finely organized system, essential for maintaining the integrity of the axon. Axonal degeneration is implicated in the pathogenesis of unremitting disability of multiple sclerosis (MS). Purpose of this study is to evaluate levels of cytoskeletal proteins such as neurofilament light protein (NFL), glial fibrillary acidic protein (GFAP), and β-tubulin (β-Tub) isoforms II and III in the cerebrospinal fluid (CSF) of MS patients and their correlation with MS clinical indices. CSF levels of cytoskeletal proteins were determined in 51 patients: 33 with MS and 18 with other neurological diseases (OND). NFL, GFAP and β-Tub II proteins were significantly higher (p < 0.0001) in MS than in OND group; no significant difference (p > 0.05) was found between MS and OND with regard to β-Tub III. Interestingly, levels of β-Tub III and NFL were higher in progressive than in remitting MS forms; on the contrary, higher levels of β-Tub II and GFAP were found in remitting MS forms. However, with the exception of β-Tub III, all proteins tend to decrease their CSF levels concomitantly with the increasing disability (EDSS) score. Overall, our results might indicate β-Tub II as a potential candidate for diagnostic and β-Tub III as a possible prognostic biomarker of MS. Therefore, further analyses are legitimated and desirable.

CSF angiotensin II and angiotensin-converting enzyme levels in anti-aquaporin-4 autoimmunity

Background Anti-aquaporin-4 (AQP4) antibody targets perivascular astrocyte foot processes, which contain abundant angiotensinogen, a precursor of angiotensin II, angiotensin-converting enzyme (ACE) and ACE2. Objective To disclose any abnormality in the intrathecal angiotensin II metabolic pathway in Japanese patients with neuromyelitis optica (NMO) or NMO spectrum disorders (NMOs) and positive for anti-AQP4 antibody. Methods We measured CSF angiotensin II, ACE and ACE2 levels in 15 anti-AQP4 antibody-positive patients with NMO or NMOs, 21 anti-AQP4 antibody-negative multiple sclerosis (MS) patients, 32 patients with other neurological diseases (OND) and 24 non-neurologic controls, using established ELISAs. Results CSF angiotensin II levels were lower in patients with NMO/NMOs (2.01 ± 1.82 pg/ml) and those with MS (3.15 ± 1.67 pg/ml) than in the OND (5.41 ± 2.34 pg/ml) and control groups (6.71 ± 2.65 pg/ml) ( P corr < 0.005). The difference in CSF angiotensin II levels between NMO/NMOs and MS patients was nearly significant ( P uncorr = 0.052). In NMO/NMOs and MS patients, angiotensin II levels were negatively correlated with CSF/serum albumin ratio ( P < 0.05). ACE levels in CSF were lower in patients with NMO/NMOs (34.3 ± 5.61 ng/ml) than in MS patients (42.5 ± 8.19 ng/ml, P corr = 0.035) and controls (44.7 ± 4.02 ng/ml, P corr < 0.0003) while ACE2 levels were lower in NMO/NMOs (1.13 ± 0.49 ng/ml) and MS (1.75 ± 0.86 ng/ml) patients than in controls (2.76 ± 0.23 ng/ml, P corr < 0.001 for both). Conclusion CSF angiotensin II, ACE, and ACE2 levels are decreased in NMO/NMOs patients with anti-AQP4 antibody, reflecting severe destruction of perivascular astrocytes.

The prevalence of human endogenous retroviruses in cerebrospinal fluids from patients with sporadic Creutzfeldt–Jakob disease

Background About 8% of human genome is constituted by retroviral sequences. Some of these have been classified as human endogenous retroviruses (HERVs), which have been implicated in both health and disease. Recently, indirect evidence for a possible role of retroviral elements in neurological diseases has been provided by several studies. Objectives In the present study, we aimed to evaluate the relationship between HERVs and sporadic Creutzfeldt–Jakob disease (CJD), one of the human forms of prion diseases. Study design We investigated the prevalence of HERV families by RT-PCR in cell-free cerebrospinal fluids (CSFs) samples from normal controls, patients with sporadic CJD and other neurological diseases (OND). Results The incidence rate of some HERV families were significantly different in CSF samples from the group of sporadic CJD compared to samples from normal individuals; HERV-W ( P = 0.001), T ( P = 0.039), FRD ( P < 0.001), L ( P = 0.003) and ERV-9 ( P < 0.001) and the incidence rate of HERV-W ( P = 0.021) and HERV-L ( P = 0.049) were significantly increased in CSF samples from the group of sporadic CJD compared to samples from OND group. Moreover, our results from combining frequencies of two HERV families indicated that the prevalence of many combination groups was significantly different between sporadic CJD and normal CSF samples and between two patients’ CSF samples. In addition, a large number of HERV sequences were newly identified in CSFs from normal and diseased individuals. Conclusions Our study about distinct prevalence patterns of HERVs reflects that some HERVs families may be associated with the development of prion diseases, and considered as a candidate marker for the diagnosis of sporadic CJD.

Intrathecal origin of CSF ribonuclease.

A CSF Poly(C)-avid ribonuclease (RNase) activity was determined in serum and CSF of 11 controls and 75 neurological patients (34 multiple sclerosis (MS), 18 infectious processes and 23 other neurological diseases (OND]. In controls, the blood-CSF ratio of RNase activity is low. This fact and the absence of correlation between serum and CSF RNase activity (except in OND group), and between CSF albumin and CSF RNase activity in controls and MS patients, suggest an intrathecal origin for the major part of this CSF RNase activity. A formula taking into account any plasmatic enrichment in RNase of the CSF is proposed to evaluate this intrathecal activity. The normal mean value of this intrathecal RNase activity is 27 +/- 3 units/ml (mean +/- SE) in our experimental conditions and using our formula. The highest intrathecal RNase activity is observed in infectious processes and this finding is associated with a significant increase in the local anti-RNA antibody synthesis. An increase in intrathecal RNase activity is rarely found in MS and local anti-RNA synthesis is only observed in one third of MS patients.

T-cells expressing natural killer (NK) receptors are altered in multiple sclerosis and responses to α-galactosylceramide are impaired

Multiple sclerosis (MS) is an autoimmune disorder characterised by clinical relapse and remission and pathological demyelination with varying inflammation. Because it is suggested that T-cells expressing natural killer cell receptors (NKR) play important roles in regulating human autoimmune diseases, we have quantified populations of T-cells expressing the NKR CD56, CD161 and CD94 in the peripheral blood of MS patients, in healthy control subjects (HS) and in patients with other neurological diseases (OND). CD161+ T-cells and CD94+ T-cells were significantly decreased in MS patients with primary progressive disease and secondary progressive disease respectively whereas CD56+ T-cell numbers were unchanged. In contrast NKT-cells that express the invariant Vα24-Jα18+ T-cell receptor identified here by specific receptor antibody and CD1d-tetrameric PBS57-loaded complexes, were increased in MS patients compared with HS. Reductions in CD161+ T-cells and CD94+ T-cells relative to HS were also observed in the OND group and this was particularly prominent in Parkinsonian patients. A striking functional finding was that while NKT-cells in unfractionated peripheral blood from healthy subjects expanded in number and produced IFN-γ upon stimulation with α-galactosylceramide, NKT-cells from MS patients did not. Thus we have identified alterations in a number of potentially important lymphocyte sub-populations warranting further investigation in the immune response in MS.

Antibodies to sulfatide in cerebrospinal fluid of patients with multiple sclerosis

The identity of target antigen(s) in multiple sclerosis (MS) remains elusive despite much effort to identify it. We analyzed cerebrospinal fluid (CSF) from patients with MS, other neurological diseases (OND), other diseases (OD) and healthy controls for antibodies against purified sulfatide, a major glycosphingolipid of human myelin, by an enzyme-linked immunosorbent assay (ELISA) and a thin-layer chromatogram (TLC)-immunostaining technique. Elevated anti-sulfatide antibodies were significantly higher in MS patients as compared with the OND group ( p<0.05) and all controls combined ( P<0.025). Binding of high titer antibodies to sulfatide was confirmed with TLC-immunostaining. Anti-sulfatide antibodies were detected in all subtypes of MS although the frequency was higher in patients with secondary progressive MS (SPMS) than in patients with primary progressive (PPMS) and relapsing–remitting MS (RRMS). The data demonstrate a humoral response to sulfatide in the CSF of patients with MS.

Uric acid levels in sera from patients with multiple sclerosis

The levels of uric acid (UA), a natural peroxynitrite scavenger, were measured in sera from 240 patients with multiple sclerosis (MS) and 104 sex- and age-matched control patients with other neurological diseases (OND). The mean serum UA concentration was lower in the MS than in the OND group, but the difference did not reach the level of statistical significance (P = 0.068). However, the mean serum UA level from patients with active MS (202.6 + 67.1 mumol/l) was significantly lower than that in inactive MS patients (226.5 + 78.6 mumol/l; P = 0.046) and OND controls (P = 0.007). We found a significant inverse correlation of serum UA concentration with female gender (P = 0.0001), disease activity (P = 0.012) and duration (P = 0.017), and a trend towards an inverse correlation with disability as assessed by EDSS score, which did not reach statistical significance (P = 0.067). Finally, multivariate linear regression analyses showed that UA concentration was independently correlated with gender (P = 0.0001), disease activity (P = 0.014) and duration of the disease (P = 0.043) in MS patients. These findings suggest that serum UA might serve as a possible marker of disease activity in MS. They also provide support to the potential beneficial therapeutic effect of radical-scavenging substances in MS.

Diagnostic utility of CSF soluble CD27 for primary central nervous system lymphoma in immunocompetent patient

The aim of this study is to determine the diagnostic utility of cerebrospinal fluid (CSF) soluble CD27 (sCD27) as a tumor marker for primary central nervous system lymphoma (PCNSL) in immunocompetent patients. A total of 93 CSF samples were collected from the following four patient groups: the PCNSL group, 13 patients (26 samples) with PCNSL, 12 samples obtained at initial diagnosis, 10 during therapy, four at complete remission; the other brain tumors (OBT) group, 30 patients (30 samples) with other brain tumors; the other neurological diseases (OND) group, 25 (25 samples) with other neurological diseases; the inflammatory neurological diseases (IND) group, 12 patients (12 samples) with inflammatory neurological diseases. sCD27 levels were determined by sandwich enzyme-linked immunosorbent assay. The optimal cut-off value was found to be 15 U ml~1. The CSF sCD27 levels were over 15 U ml~1 in 23 of the 26 PCNSL samples and were significantly higher than those in the OBT and OND groups in which all samples were below 15 U ml~1. Elevated CSF sCD27 levels were also observed in 11 of 12 IND samples. In the two PCNSL patients whose CSF sCF27 levels were studied longitudinally, the sCD27 levels correlated very well with remission and relapse of the disease. CSF sCD27 is useful as a tumor marker for PCNSL in immunocompetent patients, and is also useful to evaluate the effect of various types of treatment. Although there was a large cross-reactivity in the CSF sCD27 levels between PCNSL and IND group, white blood cell count in the CSF is helpful to distinguish these two diseases. [Neurol Res 2000; 22: 434-442]

IgG index in acute idiopathic peripheral facial palsy.

Etiologic hypotheses in acute idiopathic peripheral facial palsy (AIPFP) mostly point to an immunologic dysfunction, probably virus-induced. Though various immunologic abnormalities are reported, the problem is still unsolved. We investigated intrathecal immunoglobulin synthesis in AIPFP as a clue for central nervous system (CNS) immunopathology. We studied IgG index in 24 patients with AIPFP, 10 with other neurological diseases (OND) and 17 with multiple sclerosis (MS). CSF and serum IgG were measured by radial immunodiffusion technique. IgG index is calculated according to Tibbling's formula. IgG indexes were abnormal in 6 patients with AIPFP, 3 with OND and 10 with MS patients. There was no statistical difference between AIPFP and OND groups, while marked difference existed between AIPFP and MS groups. Though IgG indexes were high in 25% of AIPFP patients, statistical analyses did not show any significance of this finding. Lack of a positive result might reflect non-existence of an extensive immunologic pathology within CNS, excluding a very limited one.

Increased circulating antiganglioside antibodies in primary and secondary progressive multiple sclerosis.

Plasma samples from 70 patients with multiple sclerosis (MS), 41 patients with other neurological diseases (OND), and 38 healthy subjects were examined for antibodies against gangliosides GM1, GM3, GD1a, GD1b, and GD3 using enzyme-linked immunosorbent assays. The percentages of subjects with increased anti-GM3 responses were significantly higher in the primary progressive MS (56.3%) and secondary progressive MS (42.9%) groups than in the relapsing-remitting MS (2.9%), healthy subject (2.6%), and OND (14.6%) groups. Elevated antiganglioside antibodies may be secondary to axonal damage or may be a cause of axonal damage and accumulating disability in progressive MS. In either case, they may serve as a marker of axonal damage in MS.

Evidence for a missed signal to the CD8+ cells in CSF of multiple sclerosis patients.

Peripheral blood (PB) and cerebrospinal fluid (CSF) lymphocyte subpopulations, defined by various T-cell specific monoclonal antibodies and flow cytometry, were analysed in 44 relapsing remitting multiple sclerosis (RRMS) patients (including 21 subjects in the acute phase and 23 in the stable phase), 40 chronic-progressive multiple sclerosis (CPMS) patients, and 24 patients with other neurological diseases (OND), in order to verify the presence of any abnormality in the lymphocyte subset pattern. A significant increase in the total number of T-lymphocytes and the CD4+ subpopulation was found in the PB of the MS patients in comparison with the OND group. Moreover, a not statistically significant increase in CD4+ cells was observed in the CSF of MS patients. A statistically significant increase was also found in the CD4+ Leu 8+ (suppressor inducer) cells in the CSF of all of the MS groups. Finally, the CD8+ (suppressor/cytotoxic) cell levels, were significantly lower in the CSF of CPMS and stable RMS patients than in the CSF of the OND patients. As a whole, our data suggest that the immunosuppressive deficit that seems to be a constant finding in MS is not due to a decrease in suppressor inducer cell levels, as previously suggested, but may be caused by a missed or altered signal from the suppressor inducer to CD8+ suppressor cells.

Markers of Activated T Lymphocytes and T Cell Receptor Gamma/ Delta+ in Patients with Multiple Sclerosis

We studied interferon-gamma (IFN-gamma), alpha-tumor necrosis factor (alpha-TNF) and granulocyte macrophage colony-stimulating factor (GM-CSF) in the cerebrospinal fluid and serum of 18 patients with multiple sclerosis (MS) and 10 subjects with other neurological diseases (OND). We also studied the cerebrospinal-fluid CD 69 expression, and T cells with T cell receptor (TcR) gamma/delta+. We found an increase of IFN-gamma (14.0 +/- 3.5 U/ml) and GM-CSF (8.0 +/- 3.4 pg/ml) levels in the cerebrospinal fluid of MS patients compared to the OND group (p < 0.005 and p < 0.01, respectively). The frequency of detectable cerebrospinal-fluid and serum alpha-TNF was similar in patients with MS and with OND. The cerebrospinal-fluid CD69 expression in lymphocytes was significantly higher in MS patients (15.0 +/- 9.9%) than in the control group (3.7 +/- 6.2%; p < 0.005). Comparable serum levels of IFN-gamma and GM-CSF were detected in patients with MS and in OND subjects. No significant difference in the incidence of TcR gamma/delta+ in the cerebrospinal fluid was found between the two groups. These results indicate an activation of T lymphocytes and macrophages in patients with MS. Our data do not suggest a role for an increased incidence of TcR gamma/delta+. However, we cannot rule out the possibility that these T cells could be present at the plaque site of MS patients.

Increased levels of β2-microglobulin, soluble interleukin-2 receptor, and soluble CD8 in patients with subacute sclerosing panencephalitis

We measured β2-microglobulin (β2-M), soluble interleukin-2 receptor (sIL-2R), and soluble CD8 (sCD8) antigen levels in paired cerebrospinal fluid (CSF) and sera from patients with subacute sclerosing panencephalitis (SSPE), multiple sclerosis (MS), and other neurological diseases (OND) using enzyme-linked immunosorbent assay. β2-M was significantly increased in CSF of the SSPE group compared to the MS or the OND group. Similarly, β2-M in the MS versus OND group was significantly increased in CSF. Although serum levels of β2-M were similar in the three groups, the CSF/serum ratios were higher in SSPE versus the MS group and in the MS versus the OND group. Levels of sIL-2R and sCD8 were higher in SSPE CSF than OND CSF; however, there were no differences between levels in SSPE and MS CSF. The levels of sIL-2R were increased in SSPE sera compared to those of MS or the OND group, whereas levels of sCD8 in serum from the three groups were similar. The findings of increased CSF/serum ratio of β2-M and higher levels of serum sIL-2R and CSF sCD8 in SSPE patients are consistent with those seen in patients with acute and chronic viral infections. When the levels between the initial and follow-up CSF and serum samples from SSPE patients were compared, the data showed that CSF levels of sCD8 elevated during periods of clinical worsening and decreased during clinical improvement. In contrast, serum β2-M decreased during periods of worsening and increased during improvement. The measurement of serum β2-M and CSF sCD8 may be useful in SSPE patients as markers to monitor disease activity.

IgG1,3 and 4 oligoclonal bands in multiple sclerosis and other neurological diseases.

Cerebrospinal fluid (CSF) samples from 10 patients with Multiple Sclerosis (MS) and 7 with other neurological diseases (OND) were studied in order to detect oligoclonal restriction of IgG subclasses 1,3 and 4. Agarose isoelectric focusing (AGA-IEF) followed by Western capillary blotting and immunoperoxidase staining with specific monoclonal antibodies were used. All MS samples showed oligoclonal IgG1 and 6 of them also had IgG3 or IgG4 bands. In the OND group only patients with subacute sclerosing panencephalitis (SSPE) and Guillain-Barré disease (GBD) showed CSF oligoclonal patterns for IgG subclasses. Our results demonstrate that in MS CSF other IgG subclasses beside IgG1 may display an oligoclonal pattern. The finding of more than one subclass in the same band indicates a microheterogeneous composition of these oligoclonal bands.

Polymorphonuclear neutral protease activity in multiple sclerosis and other diseases.

Polymorphonuclear neutral protease activity (PMN-NPA) was examined in 87 patients with definite multiple sclerosis (MS) (48 active, 39 inactive), 49 patients with other neurological diseases (OND), 24 patients with immune-mediated non-neurological diseases (INND), and 32 normal subjects. PMN-NPA was found to be significantly increased in active MS compared with inactive MS and compared with each of the control groups. No differences were found between the group of normal subjects and the groups of patients with OND, INND, or inactive MS. Levels of PMN-NPA were significantly higher in the OND group than in inactive MS group. The differences for INND versus normal controls, neurological controls, and patients with inactive MS were not significant. No significant differences have been detected between active and inactive INND. These results suggest that PMN-NPA may be useful in the diagnosis and evaluation of MS.

Comparison of in vitro demyelination and cytotoxicity of humoral factors in multiple sclerosis and other neurological diseases

The distribution and nature of serum factors causing in vitro demyelination and glial lysis were investigated in multiple sclerosis (MS), other neurological diseases (OND), ill control and control groups. MS sera were unique in affecting only CNS myelin and glia whereas stroke and Guillain-Barré syndrome (GBS) sera brought changes to both CNS and PNS tissue. Through both visual scoring of myelin damage and the quantitative measurement of radiolabel release from cerebellar cultures, it was evident that the MS and OND groups have similar myelino- and cytotoxic effects. This may reflect MS and OND sera sharing similar humoral factors. 74% MS, 68% OND and 22% of control scores were above a score threshold designed to exclude culture handling trauma effects. When classified by their current disease state MS patients with severe and mild disease yielded higher in vitro scores than did those with moderate disease who comprised an older age group. No other clinical features of MS patients gave any association with in vitro serum effects. The rare demonstration of bound Fab IgG in cultures after MS serum tests indicates that immune mechanisms are unlikely to make a large contribution to serum-induced demyelination and cellular change in vitro.

Antibodies in cerebrospinal fluid to white matter glycoproteins in multiple sclerosis patients

Cerebrospinal fluid (CSF) specimens from 45 patients with multiple sclerosis (MS) and 45 age- and sex-matched controls with other neurological diseases (OND) were tested for antibodies to white matter (WM) membrane glycoprotein (GP) fractions prepared from MS and control WM membranes by lentil lectin chromatography. The binding of the CSF IgG to the 125I-labeled GP fractions was determined by immunoprecipitation using Protein A-Sepharose. CSF from patients with MS bound highly significantly more strongly to the GP fraction prepared from MS WM than did the OND CSF specimens ( P < 0.001). There was no such difference when control GP fraction was used as an antigen. No highly significant differences were observed when 20 paired serum specimens were tested. Electrophoresis of the immunoprecipitates showed that components with molecular weights (MWs) of 157,300, 135,600, 111,100, 93,000, 75,700, 63,300, 50,100, 24,300, 20,300 and 17,000 daltons were precipitated from the MS GP fraction by CSF specimens of both MS and OND groups, whereas components with MWs of 50,100, 24,300, 20,300 and 17,000 daltons were precipitated from the control GP fraction.