In this task, you are given an abstract of article. Your task is to generate label "True" if abstract is structured, otherwise generate "False". A structured abstract is composed of a topic sentence (or key sentence), relevant supporting sentences, and a closing (or transition) sentence. This structure is key to keeping your abstract focused on the main idea and creating a clear and concise image.
Q: Alzheimer's disease (AD) is hypothesized to be caused by an overproduction or reduced clearance of amyloid- (A) peptide. Autosomal dominant AD (ADAD) caused by mutations in the presenilin (PSEN) gene have been postulated to result from increased production of A42 compared to A40 in the central nervous system (CNS). This has been demonstrated in rodent models of ADAD but not in human mutation carriers. We used compartmental modeling of stable isotope labeling kinetic (SILK) studies in human carriers of PSEN mutations and related noncarriers to evaluate the pathophysiological effects of PSEN1 and PSEN2 mutations on the production and turnover of A isoforms. We compared these findings by mutation status and amount of fibrillar amyloid deposition as measured by positron emission tomography (PET) using the amyloid tracer Pittsburgh compound B (PIB). CNS A42 to A40 production rates were 24% higher in mutation carriers compared to noncarriers, and this was independent of fibrillar amyloid deposits quantified by PET PIB imaging. The fractional turnover rate of soluble A42 relative to A40 was 65% faster in mutation carriers and correlated with amyloid deposition, consistent with increased deposition of A42 into plaques, leading to reduced recovery of A42 in cerebrospinal fluid (CSF). Reversible exchange of A42 peptides with preexisting unlabeled peptide was observed in the presence of plaques. These findings support the hypothesis that A42 is overproduced in the CNS of humans with PSEN mutations that cause AD, and demonstrate that soluble A42 turnover and exchange processes are altered in the presence of amyloid plaques, causing a reduction in A42 concentrations in the CSF.
A:
False