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We compared four equations for estimating intrathecal IgG synthesis (Tibbling and Link IgG index (T/L), Schuller and Sagar (S/S), Reiber and Felgenhauer (R/F), and Tourtellotte (T) equations) using data from chronic progressive MS patients. For normal albumin leakage (AL) (

Glycerylphosphorylcholine (GPC) phosphocholine phosphodiesterase activity (EC 3.1.4.38) is significantly reduced in multiple sclerosis plaques compared to adjacent tissue with a P less than 0.01 based upon the Student-Newman-Keuls or Tukey test. This finding is in accord with the proposal that this particular form of the enzyme is myelin-specific. Similar activities for GPC phosphocholine phosphodiesterase were obtained with samples from various regions of the same individual brain.

Transforming growth factor (TGF)beta plays a role in injury repair in sites surrounding brain injury. The present study tested the hypothesis that TGFbeta1 and TGFbeta2 levels in the postmortem CSF of patients with neurodegenerative disorders would be elevated compared to those in normal subjects. Free TGFbeta1 and total TGFbeta2 were measured by ELISA in postmortem ventricular cerebrospinal fluid (vCSF) of patients with Parkinson's disease (n = 30), Alzheimer's disease (n = 30), multiple sclerosis (n = 15), and schizophrenia (n = 12) and of normal controls (n = 16). In addition, albumin, IgG, and total protein in vCSF were measured. Both TGFbeta1 and TGFbeta2 were significantly different between groups (P0.002 and P0.001, respectively). Parkinson's disease vCSF showed significant increases in both TGFbeta1 (P = 0.015) and TGFbeta2 (P = 0.012) compared to normal controls. There was a trend for TGFbeta2 to be elevated in Alzheimer's disease and multiple sclerosis vCSFs, which failed to achieve significance. There were no differences between controls and schizophrenics in TGFbeta1 or TGFbeta2. Alzheimer's disease vCSF showed a significant decrease in protein compared to all other groups, which was not related to blood-brain barrier permeability, age, or autolysis differences. Evidence is presented suggesting that some TGFbeta1 may leak into the vCSF from plasma. Autopsy vCSF levels of TGFbeta isoforms were found to be distinctly different from those reported for human serum, especially for TGFbeta2, which is undetectable in plasma. These results indicate that further in vivo studies of TGFbeta2 in the CSF of Parkinson's disease patients are warranted to determine the relationship between clinical status, medication, and TGFbeta2 concentrations.

A blinded study was designed to determine if a glycoprotein fraction, G2, shown in previous studies to be specific for multiple sclerosis (MS), could be isolated from cryopre-served autopsy central nervous system (CNS) tissue. Coded tissue sections were obtained from the Human Neurospecimen Bank, Los Angeles, Calif; and the code was broken after all data were analyzed. Multiple sections of the CNS from 23 MS patients, 12 patients with other neurologic diseases (OND), and 10 individuals who died as a sudden death were utilized. Crossed immunoisoelectrophoresis (CIE) of G2 against anti-MS cytosole antibodies to MS-specific CNS antigens (MSG2) and tandem CIE of the G2 fraction with a known MSG2 preparation were carried out. MSG2 was found in one or more CNS sections from 78% of MS patients, all sections from MS spinal cord, and no sections from OND or control individuals. We propose that the MSG2 found in the MS CNS may contain a glycoprotein of a persistent virus, such as measles and/or myelin.

We have estimated the levels of partially purified multiple sclerosis (MS) specific glycoproteins (MSG2) in gray matter, white matter, spinal cord and brain stem of MS autopsy brains by an enzyme immunoassay in which antisera to a pooled MSG2 was employed. Similarly, the levels of KG2 (non-MS brain isolate corresponding to MSG2) were assayed in various topographic areas of non-MS autopsy brains. Comparison of data on MS and non-MS groups revealed that the MS specific antigens may be preferentially located in the normal appearing white matter of MS brains. The concentration of MS antigens was found to be highest in the normal appearing white matter of MS brains, followed by periplaque and finally plaque. These results indicate that the MS specific antigens are not the degraded products of MS brains. They further support the view that normal appearing white matter of MS brains should be the target tissue for the isolation of MS specific antigens.

The binding of partially purified multiple sclerosis (MS) specific brain antigens (MSG2) and of the corresponding antigens of non-MS brains (KG2) to cerebrospinal fluid IgG of patients with MS and other neurological diseases was assayed employing sandwich enzyme linked immunosorbent assay (ELISA). Assay of the antigen-antibody binding revealed that the concentration of MSG2 required for the optimum binding to IgG in the undiluted MS CSFs was lower than that of KG2 in all cases. The index for IgG binding capacity of an antigen (IgBC) was expressed as a ratio of the optical density of the enzymic products in ELISA at the optimal antigen-antibody binding to the lowest concentration of the antigen required for the optimal binding. The IgBC of MSG2 was found to be linearly correlated with the IgG concentration in the CSF of MS patients. These results indicate that IgG with specificity to MSG2 may be present in the CSF of MS patients.