Biomedical subjects

H Diana Rosas

Publications and source records attributed to H Diana Rosas.

6 recordsLinked to original sources

PubMed2006

White matter alterations in cerebral amyloid angiopathy measured by diffusion tensor imaging.

BACKGROUND AND PURPOSE: Cerebral amyloid angiopathy (CAA) represents beta-amyloid deposition in the small- and medium-sized vessels of the brain and meninges. CAA contributes to altered vessel function and is associated with white matter damage, cognitive impairment, and most salient, hemorrhagic stroke. We used diffusion tensor imaging to evaluate the anatomic distribution of white matter degeneration in participants diagnosed with advanced CAA. METHODS: Diffusion tensor imaging was obtained from 11 participants diagnosed with CAA-related intracerebral hemorrhage and 13 matched healthy control participants. Fractional anisotropy (FA) and diffusivity maps were compared using voxel based t test and region-of-interest analyses. RESULTS: FA was reduced in CAA in temporal white matter and in the splenium of the corpus callosum (P<0.001 with approximately 17% reduction in temporal white matter and 15% reduction in the splenium). FA was marginally increased in CAA in the posterior limb of the internal capsule and subthalamic gray matter regions (approximately 7% increase in subthalamic gray). FA changes were bilateral, remained significant in cluster analysis controlling for multiple comparisons, and did not depend on the hemisphere of the cerebral hemorrhage. Diffusivity was not substantially altered. CONCLUSIONS: These findings suggest that a pattern of regional brain tissue degeneration is a characteristic feature of advanced CAA.

Aged↗

PubMed2006

Diffusion tensor imaging in presymptomatic and early Huntington's disease: Selective white matter pathology and its relationship to clinical measures.

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) to examine the regional nature of WM abnormalities in early HD, including the preclinical period, and to determine whether regional changes correlated with clinical features. We studied individuals in early stages (HD), presymptomatic individuals known to carry the genetic mutation that causes HD (Pre-HD), and matched healthy controls. DTI indices of tissue integrity were obtained from several regions of interest, including the corpus callosum (CC), internal capsule (IC), and basal ganglia, were compared across groups by t tests, and were correlated to cognitive and clinical measures. WM alterations were found throughout the CC, in the anterior and posterior limbs of the IC, and in frontal subcortical WM in HD subjects, supporting the selective involvement of the pyramidal tracts in HD; a similar distribution of changes was seen in Pre-HD subjects, supporting presymptomatic alterations. There was a significant relationship between select DTI measures and cognitive performance. Alterations in diffusion indices were also seen in the striatum that were independent of atrophy. Our findings support that WM alterations occur very early in HD. The distribution of the changes suggests that these changes contribute to the disruption of pyramidal and extrapyramidal circuits and also support a role of compromised cortical circuitry in early cognitive and subtle motor impairment during the preclinical stages of HD.

Adult↗

PubMed2005

Choice reaction time performance correlates with diffusion anisotropy in white matter pathways supporting visuospatial attention.

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 never been demonstrated in cortical projection or association pathways in healthy young adults. Using diffusion tensor MRI (DTI), we sought to test whether diffusion tensor fractional anisotropy (FA), a measure of the orientational coherence of water self-diffusion, is regionally correlated with RT on a visual self-paced choice RT (CRT) task. CRT was found to be significantly correlated with FA in projection and association pathways supporting visuospatial attention including the right optic radiation, right posterior thalamus, and right medial precuneus WM. Significant correlations were also observed in left superior temporal sulcus WM and the left parietal operculum. The lateralization of the CRT-FA correlation to right visual and parietal WM pathways is consistent with the specialization of right visual and parietal cortices for visuospatial attention. The localization of the CRT-FA correlations to predominantly visual and parietal WM pathways, but not to motor pathways or the corpus callosum indicates that individual differences in visual CRT performance are associated with variations in the WM underlying the visuospatial attention network as opposed to pathways supporting motor movement or interhemispheric transmission.

Adult↗

PubMed2005

The therapeutic role of creatine in Huntington's disease.

Huntington's disease (HD) is an autosomal dominant and fatal neurological disorder characterized by a clinical triad of progressive choreiform movements, psychiatric symptoms, and cognitive decline. HD is caused by an expanded trinucleotide CAG repeat in the gene coding for the protein huntingtin. No proven treatment to prevent the onset or to delay the progression of HD currently exists. While a direct causative pathway from the gene mutation to the selective neostriatal neurodegeneration remains unclear, it has been hypothesized that interactions of the mutant huntingtin protein or its fragments may result in a number of interrelated pathogenic mechanisms triggering a cascade of molecular events that lead to the untimely neuronal death observed in HD. One putative pathological mechanism reported to play a prominent role in the pathogenesis of HD is mitochondrial dysfunction and the subsequent reduction of cellular energy. Indeed, if mitochondrial impairment and reduced energy stores play roles in the neuronal loss in HD, then a therapeutic strategy that buffers intracellular energy levels may ameliorate the neurodegenerative process. Sustained ATP levels may have both direct and indirect importance in ameliorating the severity of many of the pathogenic mechanisms associated with HD. Creatine, a guanidino compound produced endogenously and acquired exogenously through diet, is a critical component in maintaining much needed cellular energy. As such, creatine is one of a number of ergogens that may provide a relatively safe and immediately available therapeutic strategy to HD patients that may be the cornerstone of a combined treatment necessary to delay the relentless progression of HD.

Animals↗

PubMed2004

Age-related alterations in white matter microstructure measured by diffusion tensor imaging.

Cerebral white matter (WM) undergoes various degenerative changes with normal aging, including decreases in myelin density and alterations in myelin structure. We acquired whole-head, high-resolution diffusion tensor images (DTI) in 38 participants across the adult age span. Maps of fractional anisotropy (FA), a measure of WM microstructure, were calculated for each participant to determine whether particular fiber systems of the brain are preferentially vulnerable to WM degeneration. Regional FA measures were estimated from nine regions of interest in each hemisphere and from the genu and splenium of the corpus callosum (CC). The results showed significant age-related decline in FA in frontal WM, the posterior limb of the internal capsule (PLIC), and the genu of the CC. In contrast, temporal and posterior WM was relatively preserved. These findings suggest that WM alterations are variable throughout the brain and that particular fiber populations within prefrontal region and PLIC are most vulnerable to age-related degeneration.

Adult↗

PubMed2001

Functional MRI detection of pharmacologically induced memory impairment.

To examine alterations in brain activation associated with pharmacologically induced memory impairment, we used functional MRI (fMRI) to study the effects of lorazepam and scopolamine on a face-name associative encoding paradigm. Ten healthy young subjects were scanned on four occasions, 2 weeks apart; they were administered i.v. saline during two placebo-scanning sessions and then alternately administered i.v. lorazepam (1 mg) or scopolamine (0.4 mg) in a double-blind, randomized, cross-over design. Both the extent and magnitude of activation within anatomic regions of interest (ROIs) were examined to determine the reproducibility of activation in the placebo sessions and the regional specificity of the pharmacologic effects. Activation within all ROIs was consistent across the two placebo scans during the encoding of novel face-name pairs (compared with visual fixation). With the administration of either lorazepam or scopolamine, significant decreases were observed in both the extent and magnitude of activation within the hippocampal, fusiform, and inferior prefrontal ROIs, but no significant alterations in activation in the striate cortex were found. Both medications impaired performance on postscan memory measures, and significant correlations between memory performance and extent of activation were found in hippocampal and fusiform ROIs. These findings suggest that pharmacologic effects can be detected with fMRI by using a reproducible experimental paradigm and that medications that impair memory also diminish activation in specific brain regions thought to subserve complex memory processes.

Adult↗