23 research outputs found

    Measuring linguistic complexity in long-term L2 speakers of English and L1 attriters of German

    Get PDF
    Linguistic complexity is neither easily defined nor measured. The challenge in finding reliable ways to measure linguistic complexity is even more pronounced when the variation of contexts in which complexity is measured is taken into account. This paper therefore aims at finding measures for assessing syntactic and lexical complexity that are sensitive and non-overlapping even in a less frequently studied context: spontaneous speech of L1 attriters and highly proficient L2 English speakers. To evaluate operationalizations of syntactic and lexical complexity, several previously proposed measures are applied to a corpus of spontaneous speech and a principal component analysis is conducted. The results show which of the measures group together as underlying variables of syntactic and lexical complexity and how this can inform future operationalizations of complexity

    Brain Region Specific Pre-Synaptic and Post-Synaptic Degeneration Are Early Components of Neuropathology in Prion Disease

    Get PDF
    Synaptic abnormalities, one of the key features of prion disease pathogenesis, gives rise to functional deficits and contributes to the devastating clinical outcome. The synaptic compartment is the first to succumb in several neurodegenerative diseases linked with protein misfolding but the mechanisms underpinning this are poorly defined. In our current study we document that a focal intrahippocampal injection of the mouse-adapted 22L scrapie strain produces a complex, region-specific pathology in the brain. Our findings reveal that early synaptic changes in the stratum radiatum of the hippocampus, identical to those observed with the ME7 strain, occur when 22L strain is introduced into the hippocampus. The pathology was defined by degenerating Type I pre-synaptic elements progressively enveloped by the post-synaptic density of the dendritic spine. In contrast, the pathology in the cerebellum suggested that dendritic disintegration rather than pre-synaptic abnormalities dominate the early degenerative changes associated with the Purkinje cells. Indeed, both of the major synaptic inputs into the cerebellum, which arise from the parallel and climbing fibers, remained intact even at late stage disease. Immunolabeling with pathway selective antibodies reinforced these findings. These observations demonstrate that neuronal vulnerability to pathological protein misfolding is strongly dependent on the structure and function of the target neurons
    corecore