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Biomedical subjects

M W Jacobson

Publications and source records attributed to M W Jacobson.

13 recordsLinked to original sources
PubMed2004

In vivo evidence of cerebellar atrophy and cerebral white matter loss in Huntington disease.

OBJECTIVE: To investigate the regional pattern of white matter and cerebellar changes, as well as subcortical and cortical changes, in Huntington disease (HD) using morphometric analyses of structural MRI. METHODS: Fifteen individuals with HD and 22 controls were studied; groups were similar in age and education. Primary analyses defined six subcortical regions, the gray and white matter of primary cortical lobes and cerebellum, and abnormal signal in the cerebral white matter. RESULTS: As expected, basal ganglia and cerebral cortical gray matter volumes were significantly smaller in HD. The HD group also demonstrated significant cerebral white matter loss and an increase in the amount of abnormal signal in the white matter; occipital white matter appeared more affected than other cerebral white matter regions. Cortical gray and white matter measures were significantly related to caudate volume. Cerebellar gray and white matter volumes were both smaller in HD. CONCLUSIONS: The cerebellum and the integrity of cerebral white matter may play a more significant role in the symptomatology of HD than previously thought. Furthermore, changes in cortical gray and cerebral white matter were related to caudate atrophy, supporting a similar mechanism of degeneration.

Adult↗
PubMed2004

Rate and correlates of weight change in Huntington's disease.

OBJECTIVE: To determine the rate and correlates of weight change in a large, well characterised sample of patients with Huntington's disease followed at 44 sites by the Huntington Study Group. PARTICIPANTS AND METHODS: Weight change was assessed in 927 adults with a definite diagnosis of Huntington's disease who were followed prospectively for (mean (SD)) 3.4 (1.4) years. The unified Huntington's disease rating scale was used to assess weight, motor dysfunction (including chorea and dystonia), depressive symptoms, and functional decline. RESULTS: Random effects modelling determined that patients gained an average of 0.11 (1.7) kg/year and their chorea scores increased by 0.36 (0.78) points/year. There were significant but weak relations between weight loss and increasingly severe chorea (r = -0.13), worse baseline motor performance (r = -0.12), less severe baseline depressed mood (r = 0.14), and poorer baseline independence ratings (r = 0.07). Patients who were within 0 to 2 years of symptom onset at the time of the baseline visit gained more weight than those with longer disease duration. CONCLUSIONS: Weight loss following symptom onset is not a consistent feature of Huntington's disease. The mechanisms contributing to weight change in this condition are unclear and probably multifactorial. Future studies examining asymptomatic carriers of the mutation could be helpful in identifying incipience of low body weight and may be better suited for identifying clinical correlates of weight loss than studies in symptomatic patients.

Chorea↗
PubMed2003

Behavioural abnormalities contribute to functional decline in Huntington's disease.

The independent and relative contributions of motor, cognitive, and behavioural deficits to functional decline in patients with Huntington's disease are examined. Twenty two patients with Huntington's disease were assessed with rating scales for motor dysfunction, cognitive measures of executive functions, and behavioural measures of apathy, executive dysfunction, and disinhibition. Their functional status was assessed with informant based and clinician based ratings of activities of daily living (ADL). A composite apathy/executive dysfunction behavioural index was strongly related to decline in ADL independently and after controlling for motor and cognitive deficits. These results suggest that behavioural dysfunction contributes to functional decline in patients with Huntington's disease and may impede their ability to utilise motor or cognitive skills that remain available in the early stages of the disease.

Activities of Daily Living↗
PubMed1999

Neuropsychological deficits associated with antiphospholipid antibodies.

Neurologic events associated with antiphospholipid antibodies (aPAs) include transient ischemic attack, stroke, and vascular dementia in individuals much younger than is typically observed with these disorders. The present study evaluated 27 non-elderly adults with aPAs but without concurrent disease processes or history of neurologic event and 27 age- and education-matched controls. MANOVA (p <.01) indicated group differences in executive functioning, verbal learning and memory, and visuospatial ability. In contrast, gross attentional processes and fine motor skills appeared unaffected by the <?Pub Caret>syndrome. Moreover, the frequency of impaired neuropsychologic performance was greater among individuals with aPAs than among controls (p <.01). The presence of cognitive deficits in otherwise asymptomatic patients with aPAs indicates a preclinical phase of neurologic involvement and may prove to be the most sensitive markers of the syndrome.

Antibodies, Antiphospholipid↗
PubMed1996

The effect on memory of chronic prednisone treatment in patients with systemic disease.

There have been no systematic investigations of the effects of glucocorticoid treatment on memory in a clinical population despite experimental and clinical evidence that such treatment could cause memory disturbance. We conducted both cross-sectional and longitudinal studies. In Study 1, we administered tests of both hippocampal-dependent explicit memory and hippocampal-independent implicit memory to twenty-five prednisone-treated patients with systemic disease without CNS involvement and 25 matched clinical controls. All treated patients were taking doses of 5 to 40 mg of prednisone daily for at least 1 year. The glucocorticoid-treated group performed worse than the controls on tests of explicit memory, but the groups did not differ on the implicit memory task. Multiple regression analyses suggested that elderly patients are more susceptible to memory impairment with less protracted treatment. The results of Study 2, a prospective, longitudinal study of the effects of prednisone on memory across 3 months of therapy, suggest that even acute treatment can adversely affect memory. The observed alteration in memory was not secondary to inattention, affective disturbance, generalized global cognitive decline, or severity of disease. Results reported here, combined with previous clinical and experimental reports, indicate that the risk of memory impairment should be carefully considered before initiating treatment with glucocorticoids. Conversely, use of glucocorticoids should be considered in the differential diagnosis of memory loss. Finally, the potential benefit of anti-inflammatory treatment in Alzheimer's disease might be counterbalanced by possible iatrogenic memory impairment, at least when synthetic glucocorticoids are considered.

Adult↗
PubMed1994

Visuoperceptual-spatial ability and visual memory in vascular dementia and dementia of the Alzheimer type.

This study investigated the relationship between visuoperceptual ability and visual memory in dementia. Twenty individuals with probable dementia of the Alzheimer type, 24 individuals with probable vascular dementia, and 20 healthy, elderly adults underwent neuropsychological evaluation. Hierarchical multiple regression analyses suggested that perceptual organization skills contributed to a significant amount of the variance in novel, but not famous, face recognition. This finding was most robust in the clinical groups. Causality cannot be attributed from this regression model. Results suggest, however, that visual processing deficits are more strongly related to the memory process at the time of encoding rather than during recognition of remote information.

Aged↗
PubMed1977

Selective activation of human suppressor cells by a nonproliferative stimulus.

The eliciting of suppressor cell activity by heat-treated stimulating cells demonstrates that suppression can be induced by an antigenic but non-effective mixed lymphocyte culture (MLC) stimulus in vitro. Simultaneous or prior MLC or cytotoxic T lymphocyte activity is not required for alloantigen-induced suppressor cell activation.

Antigens↗
PubMed1975

Pre-emption of human cell-mediated lympholysis by a suppressive mechanism activated in mixed lymphocyte cultures.

The regulation of B-cell and T-cell immune responses has been extensively examined and in the experimental animal appears to involve regulatory or "suppressor" T cells (1-4). The limitations of in vitro experimentation have made comparable study of nonpathological human suppression quite difficult (5). We report here an in vitro method that generates and quantitates suppressor activity in man after antigen-specific activation in mixed leukocyte culture (MLC). The one-way MLC induces both a proliferative response (6) and the generation of cytotoxic T lymphocytes (CTLs) (7). Both of these responses are mediated by antigen-specific T-cell subpopulations (8,9) and have been correlated with recognitive and destructive phases of allograft rejection. Recent reports have examined the antigen reactivity of mouse (10,11), rat (12), or human (13,14) lymphocytes obtained after proliferation in MLC. In all cases, after the primary MLC proliferative peak, the recovered lymphocytes rapidly differentiate upon re-exposure to the initial stimulating population, but do so only weakly when exposed to a presumably noncross-reactive third-party stimulating population. Velocity sedimentation separation studies have shown that the blast cells produced in a primary MLC revert to small lymphocytes that rapidly differentiate into proliferating and/or cytotoxic T lymphocytes upon restimulation with the initial antigen (15). These findings demonstrate that positive selection for the responding population in primary MLC does exist and may account for at least part of the specificity of the secondary response. However, this positive selection does not preclude possible involvement of a suppressor mechanism. In fact we have detected suppressor activity in primary MLC sensitization cultures at a time when the proliferation responsible for positive selection does not preclude possible involvement of a suppressor mechanism. In fact we have detected suppressor activity in primary MLC sensitization cultures at a time when the proliferation responsible for positive selection in not yet significant, suggesting that suppression may be overriding importance in the specificity of MLC-activated secondary responses.

Antigen-Antibody Reactions↗
PubMedDate not supplied

Biomedical publishing and the internet: evolution or revolution?

The Internet is challenging traditional publishing patterns. In the biomedical domain, medical journals are providing more and more content online, both free and for a fee. Beyond this, however, a number of commentators believe that traditional notions of copyright and intellectual property ownership are no longer suited to the information age and that ownership of copyright to research reports should be and will be wrested from publishers and returned to authors. In this paper, it is argued that, although the Internet will indeed profoundly affect the distribution of biomedical research results, the biomedical publishing industry is too intertwined with the research establishment and too powerful to fall prey to such a copyright revolution.

Authorship↗