Alexandra K. Zaleta

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The clinical phenotype of Huntington's disease (HD) is far more complex and variable than depictions of it as a progressive movement disorder dominated by neostriatal pathology represent. The availability of novel neuro-imaging methods has enabled us to evaluate cerebral cortical changes in HD, which we have found to occur early and to be topographically(More)
Atrophy of cortical and subcortical gray matter is apparent in Huntington's disease (HD) before symptoms manifest. We hypothesized that the white matter (WM) connecting cortical and subcortical regions must also be affected early and that select clinical symptoms were related to systems degeneration. We used diffusion tensor magnetic resonance imaging (DTI)(More)
The corpus callosum (CC) is the major conduit for information transfer between the cerebral hemispheres and plays an integral role in relaying sensory, motor and cognitive information between homologous cortical regions. The majority of fibers that make up the CC arise from large pyramidal neurons in layers III and V, which project contra-laterally. These(More)
Humans exhibit significant interindividual variability in behavioral reaction time (RT) performance yet the underlying neural mechanisms for this variability remain largely unknown. It has been proposed that interindividual variability in RT performance may be due to differences in white matter (WM) physiological properties, although such a relationship has(More)
Significant advances are being made in our understanding of basic pathophyiological and biochemical mechanisms that cause Huntington's disease (HD). There is increasing reason to believe that pathologic alterations occur in the brain for years before symptoms manifest. The "classic" hallmark of neuropathology in HD is selective neurodegeneration in which(More)
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