UseCases_ArguminSci_Discourse  

PubMed:17409200 JSONTXT 6 Projects

Annnotations TAB TSV DIC JSON TextAE

Id Subject Object Predicate Lexical cue
T1 0-113 DRI_Outcome denotes Triplet repeat mutation length gains correlate with cell-type specific vulnerability in Huntington disease brain.
T2 114-244 DRI_Background denotes Huntington disease is caused by the expansion of a CAG repeat encoding an extended glutamine tract in a protein called huntingtin.
T3 245-423 DRI_Outcome denotes Here, we provide evidence supporting the hypothesis that somatic increases of mutation length play a role in the progressive nature and cell-selective aspects of HD pathogenesis.
T4 424-682 DRI_Outcome denotes Results from micro-dissected tissue and individual laser-dissected cells obtained from human HD cases and knock-in HD mice indicate that the CAG repeat is unstable in all cell types tested although neurons tend to have longer mutation length gains than glia.
T5 683-793 DRI_Challenge denotes Mutation length gains occur early in the disease process and continue to accumulate as the disease progresses.
T6 794-994 DRI_Challenge denotes In keeping with observed patterns of cell loss, neuronal mutation length gains tend to be more prominent in the striatum than in the cortex of low-grade human HD cases, less so in more advanced cases.
T7 995-1307 DRI_Outcome denotes Interestingly, neuronal sub-populations of HD mice appear to have different propensities for mutation length gains; in particular, smaller mutation length gains occur in nitric oxide synthase-positive striatal interneurons (a relatively spared cell type in HD) compared with the pan-striatal neuronal population.
T8 1308-1465 DRI_Outcome denotes More generally, the data demonstrate that neuronal changes in HD repeat length can be at least as great, if not greater, than those observed in the germline.
T9 1466-1707 DRI_Outcome denotes The fact that significant CAG repeat length gains occur in non-replicating cells also argues that processes such as inappropriate mismatch repair rather than DNA replication are involved in generating mutation instability in HD brain tissue.