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Biomedical subjects

J C Morris

Publications and source records attributed to J C Morris.

At least 235 records · Page 13Linked to original sources
PubMed1991

Clinical diagnosis and course of Alzheimer's disease.

Alzheimer's disease can be accurately diagnosed by clinical methods alone in about 90% of cases. The adoption of uniform diagnostic criteria and assessment procedures, such as those developed by the Consortium to Establish a Registry for Alzheimer's Disease (CERAD), will likely improve the characterization of the disease across a variety of clinical settings. In general, Alzheimer's disease is a relentlessly progressive disorder; however, it also is clinically heterogeneous. This is underscored by its diverse cognitive deficits, neurologic features, behavioral pathology, and rates of progression.

Alzheimer Disease↗
PubMed1990

Tyrosine hydroxylase-like (TH) immunoreactivity in human mesolimbic system.

A practical methodology has been described for the use of human postmortem brain tissue in both tyrosine hydroxylase and dopamine beta-hydroxylase immunohistochemistry in which in situ perfusion with paraformaldehyde is followed by immersion fixation in Bouin's fixative. These studies indicate that TH-like immunoreactive fibers and terminals are not uniformly distributed in the human hippocampal complex. A distinctive lesser innervation is noted for the structures that compose the perforant pathway and may be important for the predilection of these areas for pathological change particularly as occurs in Alzheimer's disease.

Adult↗
PubMed1990

Pulmonary carcinoid presenting as multiple subcutaneous nodules.

A 60-year-old female presented with a one-year history of multiple enlarging tender subcutaneous nodules. Initial biopsy demonstrated a poorly differentiated adenocarcinoma. Mammography showed multiple nodular breast lesions. After the patient failed to respond to tamoxifen, a second biopsy demonstrated a metastatic carcinoid tumor. Further search revealed a single small pulmonary nodule, which on aspiration biopsy proved to be a carcinoid tumor. The patient failed to respond to treatment with streptozotocin and 5'-fluorouracil. Therapy with leucovorin calcium and 5'-fluorouracil then produced a partial response.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1990

Inhibition of thyrotropin binding to receptor by synthetic human thyrotropin beta peptides.

In order to study the structure and function relationships of the thyrotropin (TSH)-specific beta-subunit, we produced 11 synthetic overlapping peptides containing the entire 112-amino acid sequence of human beta TSH and tested them for activity in TSH radioreceptor assay using both human and porcine thyroid membranes. Synthetic peptides representing four regions of the beta-subunit demonstrated the ability to inhibit binding of 125I-bovine TSH to crude thyroid membranes. The peptide representing the -COOH terminus of the subunit (beta 101-112) possessed highest binding activity, inhibiting binding of labeled TSH with an EC50 of 80 microM. The remaining active peptides were: beta 71-85 (104 microM), beta 31-45 (186 microM), beta 41-55 (242 microM), and beta 1-15 (331 microM). Specificity of the binding activity was shown by the inability of the peptides representing the remainder of the subunit to inhibit binding of label and by the inability of any of the peptides to inhibit binding of 125I-epidermal growth factor to the same thyroid membranes. The low affinity of the peptides as compared with native hormone is in agreement with previous studies of synthetic alpha-subunit peptides and, further, suggests that the interaction of beta TSH with receptor is multifaceted, requiring cooperative binding of these sites for the observed high affinity of the whole hormone. These studies are in agreement with previous predictions of active regions by chemical modification but add two regions to the list, showing the utility of the synthetic peptide strategy in the study of peptide hormone structure-activity relationships.

Amino Acid Sequence↗
PubMed1990

Advanced Alzheimer's disease is a risk factor for late-onset seizures.

To determine the role of Alzheimer's disease as a causative factor for late-onset epilepsy, 44 subjects with mild senile dementia of the Alzheimer type and 58 healthy control subjects were examined over a 90-month period for the development of focal or generalized seizure activity (excluding myoclonus). At entry, all subjects were free of prior seizures and other neurologic, medical, and psychiatric disorders with the potential to impair cognition. Although no control subject developed seizures during the study period, 7 subjects with senile dementia of the Alzheimer type had at least one documented seizure. All 7 subjects had progressed to the severe stage of dementia by the time of the first seizure. Seizures were generalized tonic-clonic in type and were unassociated with clinical or (in 3 subjects) neuropathologic evidence for epileptogenic factors other than Alzheimer's disease. We conclude that advanced Alzheimer's disease alone may be an important risk factor for new-onset seizures in older adults.

Aged↗
PubMed1990

Mild senile dementia of the Alzheimer type: 3. Longitudinal and cross-sectional assessment.

Sixty-six subjects diagnosed by validated criteria as having senile dementia of the Alzheimer type (SDAT) were assessed with clinical measures commonly used to study dementia. The severity of the SDAT was mild in 24, moderate in 24, and severe in 18. The data from these three groups in a cross-sectional study were compared with results in our earlier study of 43 subjects enrolled with mild SDAT and followed longitudinally. We concluded that the cross-sectional method underestimates the severity of progression as indicated by some of the clinical measures. Additionally, the 24 new subjects with mild SDAT were assessed longitudinally. This replication study confirmed our earlier conclusions that four of six clinical measures showed similar patterns over time and were useful throughout the study, global measures being more informative than brief individual measures with ceiling or floor effects.

Aged↗
PubMed1990

Polymerase chain reaction for detection of Toxoplasma gondii.

A DNA-based assay has been developed for the detection of Toxoplasma gondii. The assay makes use of the polymerase chain reaction (PCR) to amplify part of the P30 gene on the parasite's DNA. Following gel electrophoresis, the amplified DNA can be detected either directly on the gel or by Southern hybridisation with radioactive or non-radioactive DNA probes. The assay has been used to detect the DNA from different isolates of T. gondii in a background of human or mouse DNA. Together with other information such as clinical data, CT scans and serology, the PCR assay should improve the diagnosis of toxoplasmosis in immunosuppressed and immunocompromised patients as well as in fetal tissues.

Animals↗
PubMed1990

Brief screening tests versus clinical staging in senile dementia of the Alzheimer type.

Several brief screening tests of cognitive function were compared with a reliable and valid global rating of the presence and severity of senile dementia of the Alzheimer type, the Washington University Clinical Dementia Rating (CDR). The six-item Short Blessed Test, the Short Portable Mental Status Questionnaire, the 26-item Blessed Information-Memory-Concentration Test, the Blessed Dementia Scale, and the Blessed Dementia Scale-Cognitive were able to discern both the presence of dementia and its severity. The six-item Short Blessed Test is preferred as a screening test because of its brevity, administration to the subject only, inclusion of a learning task, reliability, and neuropathologic validity. Evidence is presented for the convergent validity of the Initial Subject Protocol, used to derive the Clinical Dementia Rating.

Aged↗
PubMed1990

Progressive aphasia: a precursor of global dementia?

We studied 8 subjects longitudinally in whom isolated language dysfunction had developed gradually at a mean age of 62.8 years. The language deficits initially displayed by the subjects were characteristic of the syndrome of "progressive aphasia without dementia." By 5 years after onset of progressive aphasia, however, 7 of the 8 subjects additionally had developed mild dementia as diagnosed by clinical means, and the remaining subject demonstrated declining performance in both verbal and nonverbal psychometric measures. Thus, generalized cognitive impairment occurred in all. Neuropathologic evidence of a diffuse dementing disorder was present in the 2 subjects studied postmortem. One had Alzheimer's disease with disproportionate involvement of the left inferior parietal cortex, and the other displayed widespread neocortical neuronal loss and microvacuolation in the absence of specific histopathologic markers. In this series, progressive aphasia was a precursor of global dementia.

Aged↗
PubMed1989

Very mild senile dementia of the Alzheimer type. I. Clinical assessment.

We report a longitudinal study of 16 subjects originally enrolled in the Washington University (St Louis, Mo) Memory and Aging Project with Clinical Dementia Rating (CDR) of "questionable" dementia (CDR 0.5). A 0.5 rating was intended to characterize subjects in whom mild cognitive impairment due to senile dementia of the Alzheimer type was suspected but was insufficient in degree to warrant a diagnosis of definite dementia. Over an 84-month follow-up period, 11 of the 16 subjects either had Alzheimer's disease verified post mortem or had clinically progressed to a more advanced CDR stage in which the dementia was clearly evident. These results suggest that the CDR 0.5 stage likely represents the incipient clinical manifestation of Alzheimer's disease and that the majority of subjects with CDR 0.5 have "very mild senile dementia of the Alzheimer type." Performance on several standard clinical scales was significantly different when comparing a larger sample of controls (n = 83), subjects with CDR 0.5 (n = 41), and subjects with mild senile dementia of the Alzheimer type (score of 1; n = 68).

Aged↗
PubMed1989

Clinical and pathological aspects of parkinsonism in Alzheimer's disease. A role for extranigral factors?

To examine the natural history and pathogenesis of parkinsonism in Alzheimer's disease, 44 subjects with clearly established senile dementia of the Alzheimer type were studied during a 66-month period. Sixteen subjects (36%) developed idiopathic parkinsonism, and 12 subjects (27%) developed drug-induced parkinsonism; the chief clinical features of both types were bradykinesia and rigidity, but not resting tremor. The presence of parkinsonism was associated with global (rather than selective) cognitive impairment, as determined by psychometric testing, and with more rapid progression to advanced stages of dementia. The pathological correlates of clinical parkinsonism were heterogeneous in 10 subjects with Alzheimer's disease who were examined post mortem. Coexistent Parkinson's disease was observed in five cases and nonspecific nigral degenerative lesions were present in another three; however, two cases had neither histological changes nor reduced neuronal densities in the substantia nigra. These two cases suggested that extranigral lesions, possibly involving mesocortical dopaminergic pathways, may contribute to the development of parkinsonism in subjects with Alzheimer's disease.

Alzheimer Disease↗
PubMed1989

Reliability of clinical nurse specialists in the staging of dementia.

We studied the reliability of master's-prepared clinical nurse specialists for the identification and staging of dementia, using videotapes of physician assessments of both healthy older persons and those with senile dementia of the Alzheimer type. The Washington University (St Louis, Mo) Clinical Dementia Rating system was the staging instrument. The results from three nurses, each reviewing 25 videotaped assessments, indicate that agreement is high between clinical nurse specialists and physicians for the presence and severity of dementia (kappa = .75). This study suggests that clinical nurse specialists can use the Clinical Dementia Rating scale effectively, and thus reliably identify and stage dementia.

Aged↗
PubMed1989

Vascular glycosaminoglycans in periventricular leukoencephalopathy.

Three cases of adult dementia with periventricular leukoencephalopathy demonstrated staining with alcian blue dye (alcianophilia) in thickened cerebral arteries and arterioles of the abnormal white matter. The property of alcianophilia identifies glycosaminoglycans (GAGs); retention of alcian blue staining at high MgCl2 concentrations (0.7 M) in these cases indicates that the GAGs are highly sulfated and are likely to represent heparan sulfate. Arteriosclerotic risk factors (including hypertension) were absent in all cases, suggesting that GAG deposition occurred as part of a separate cerebral vasculopathic process. These findings suggest that cerebral white matter changes associated with dementia do not always represent Binswanger's disease.

Adult↗
PubMed1989

The Consortium to Establish a Registry for Alzheimer's Disease (CERAD). Part I. Clinical and neuropsychological assessment of Alzheimer's disease.

The Consortium to Establish a Registry for Alzheimer's Disease (CERAD) has developed brief, comprehensive, and reliable batteries of clinical and neuropsychological tests for assessment of patients with the clinical diagnosis of Alzheimer's disease (AD). We administered these batteries in a standardized manner to more than 350 subjects with a diagnosis of AD and 275 control subjects who were enrolled in a nationwide registry by a consortium of 16 university medical centers. The tests selected for this study measured the primary cognitive manifestations of AD across a range of severity of the disorder, and discriminated between normal subjects and those with mild and moderate dementia. The batteries also detected deterioration of language, memory, praxis, and general intellectual status in subjects returning for reassessment 1 year later. Interrater and test-retest reliabilities were substantial. Long-term observations of this cohort are in progress in an effort to validate the clinical and neuropsychological assessments and to confirm the diagnosis by postmortem examinations. Although information on validation is limited thus far, the CERAD batteries appear to fill a need for a standardized, easily administered, and reliable instrument for evaluating persons with AD in multicenter research studies as well as in clinical practice.

Alzheimer Disease↗