Procollagen Type I C-terminal propeptide, procollagen Type III N-terminal propeptide, hyaluronic acid, and laminin in the cerebrospinal fluid of rats with communicating hydrocephalus.

OBJECT: Fibrosis along the route of CSF flow is indicated by the development of hydrocephalus. The changes of fibrosis index might reflect the level of hydrocephalus and even become a diagnostic index of hydrocephalus. The object of this study was to analyze the levels of procollagen Type I C-terminal propeptide (PICP), procollagen Type III N-terminal propeptide (PIIINP), hyaluronic acid (HA), and laminin (LN) and their significance in the CSF of communicating hydrocephalus rat models. METHODS: Thirty adult Sprague-Dawley rats were randomly divided into 3 groups: hydrocephalus group (20 rats) with intraventricular kaolin injections, sham control group (5 rats) with saline injections, and normal group (5 rats) without any processing. The levels of PICP, PIIINP, HA, and LN in the CSF were detected using ELISA. RESULTS: Levels of PICP, PIIINP, HA, and LN in the hydrocephalus group were significantly higher than those in the saline control group (p < 0.05). It was revealed by correlation analysis that the increase was positively correlated with the severity of ventricular dilation. CONCLUSIONS: Results indicated that PICP, PIIINP, HA, and LN continue to rise dramatically in experimental hydrocephalus and may serve as the diagnostic index of hydrocephalus.

Measurement of laminins in the cerebrospinal fluid obtained from patients with Alzheimer's disease and vascular dementia using a modified enzyme-linked immunosorbent assay.

We developed a new enzyme-linked immunosorbent assay (ELISA) system using antibodies against intact human laminin, laminin alpha(5)-chain, laminin beta(1)-chain, laminin gamma(1)-chain and laminin alpha(1)-chain peptide (YFQRYLI). Using this ELISA, we measured the anti-laminin immunoreactivity levels in the cerebrospinal fluid (CSF) obtained from patients with Alzheimer's disease (AD), vascular dementia (VaD), and other disorders. The present study showed the levels of certain laminins in CSF to demonstrate significant differences in the chain levels in different dementias. The AD group showed a significantly lower level of anti-laminin gamma(1) immunoreactivity. The late-onset AD group showed significantly elevated anti-laminin alpha(1)-peptide (YFQRYLI) immunoreactivity levels in comparison with the early-onset AD group and controls. On the other hand, the VaD group showed significantly higher levels of anti-intact human laminin and anti-laminin beta(1) immunoreactivity. The assays of anti-laminin immunoreactivity levels in CSF provided an efficient sensitivity (85.0%) and specificity (93.7%) for the diagnosis of AD by using the ratio of tau to anti-intact human laminin immunoreactivity levels. These results suggest that CSF laminin or its derivatives may correlate with the pathogenesis of AD and VaD, and the prevention of the proteolytic activity may be an effective therapeutic method for either preventing or slowing down the progression of AD. Furthermore, it was shown that performing ELISA for CSF laminins may prove to be useful for detecting the biological markers of AD and VaD.

Secretion of laminin alpha 2 chain in cerebrospinal fluid.

The absence of laminin alpha 2 chain causes muscle cell degeneration and peripheral dysmyelination in congenital muscular dystrophy patients and dy mice, suggesting its role in the maintenance of sarcolemmal architecture and peripheral myelinogenesis. Here we demonstrate the secretion of laminin alpha 2 chain in cerebrospinal fluid (CSF). Laminin alpha 2 chain was detected as a minor component of the total CSF proteins or glycoproteins. Laminin alpha 2 chain was localized in the cytoplasm of epithelial cells of choroid plexus, suggesting active secretion. Our results suggest that immunochemical analysis of CSF laminin alpha 2 chain could be useful as an aid for the diagnosis of congenital muscular dystrophy.

Laminin concentrations in serum and cerebrospinal fluid in aging and Alzheimer's disease.

Laminin, a basement membrane protein, and a potent promoter of neurite outgrowth, surrounds all peripheral nerves. It appears in the central nervous system during development and reappears in response to injury. In Alzheimer's disease (AD), there is a progressive loss of neurons in specific areas of the brain along with the presence of an increased number of senile plaques and neurofibrillary tangles. Laminin levels have been shown to be increased in injury, so we undertook to examine levels of laminin by radioimmunoassay (RIA), in cerebrospinal fluid and serum of patients with AD and age-matched controls. No difference in the CSF and serum laminin concentrations was found between Alzheimer's disease and age-matched controls. We found a lack of correlation between severity of clinical dementia and laminin concentrations. Finally, we show that the CSF and serum laminin concentrations increase with age.