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The in vivo imaging probe [11C]-PIB (Pittsburgh Compound B, N-methyl[11C]2-(4'-methylaminophenyl-6-hydroxybenzathiazole) is under evaluation as a key imaging tool in Alzheimer's disease (AD) and to date has been assumed to bind with high affinity and specificity to the amyloid structures associated with classical plaques (CPs), one of the pathological hallmarks of the disease. However, no studies have systematically investigated PIB binding to human neuropathological brain specimens at the tracer concentrations achieved during in vivo imaging scans. Using a combination of autoradiography and histochemical techniques, we demonstrate that PIB, in addition to binding CPs clearly delineates diffuse plaques and cerebrovascular amyloid angiopathy (CAA). The interaction of PIB with CAA was not fully displaceable and this may be linked to the apolipoprotein E-epsilon4 allele. PIB was also found to label neurofibrillary tangles, although the overall intensity of this binding was markedly lower than that associated with the amyloid-beta (Abeta) pathology. The data provide a molecular explanation for PIB's limited specificity in diagnosing and monitoring disease progression in AD and instead indicate that the ligand is primarily a non-specific marker of Abeta-peptide related cerebral amyloidosis. [ABSTRACT FROM AUTHOR]

Evaluates the spectrum and regulation of matrix metalloproteinases (MMP) in bacterial meningitis (BM) by measuring concentrations of MMP-2, MMP-3, MMP-8 and MMP-9 and endogenous inhibitors of metalloproteinases in the cerebrospinal fluid (CSF) of children with BM. Role of MMP in glial and neuronal cell death; Comparison of the CSF levels of MMP-9 in patients who developed hearing impairment and those who recovered without neurological deficits.