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Biomedical subjects

T J Crow

Publications and source records attributed to T J Crow.

At least 451 records · Page 25Linked to original sources
PubMedDate not supplied

Monoamine metabolism in senile dementia of Alzheimer type.

Monoamine metabolism in senile dementia of the Alzheimer-type (SDAT) was assessed by measuring the concentrations of the dopamine metabolite HVA, the noradrenaline metabolite MHPG and serotonin metabolite 5-hydroxy-3-indoleacetic acid (5-HIAA) in post-mortem brains of SDAT patients, a group of control subjects and a group of chronically depressed patients. Concentrations of MHPG and 5-HIAA were significantly reduced in hippocampus and cortical regions of the SDAT group. These changes did not correlate with clinical assessments of the degree of dementia or neuropathological assessment of the degree of Alzheimer-type changes in the SDAT group. It is suggested that changes in monoamine metabolite concentrations are not primarily involved in the pathogenesis of SDAT, and may be secondary to the well established cholinergic deficits.

Aged↗
PubMedDate not supplied

The selectivity of the reduction of serotonin S2 receptors in Alzheimer-type dementia.

The high-affinity binding of thirteen ligands to putative neurotransmitter receptors was studied in temporal cortex of control and Alzheimer-type dementia (ATD) patients. A selective reduction of serotonin S2 receptors was observed in the ATD patients, to 57% of controls with no change in S1 receptors. Of the other ligand binding sites studied, only 3H-flunitrazepam binding was significantly reduced, to 84% of controls. Ligand binding sites which were unchanged in ATD temporal cortex included those labelled by adrenergic, adenosine, histamine, opiate, GABA, benzodiazepine and cholinergic ligands.

Aged↗
PubMedDate not supplied

The Northwick Park electroconvulsive therapy trial.

70 patients with endogenous depression, defined by strict criteria, who fulfilled the Newcastle indications for electroconvulsive therapy (ECT) were randomly allocated either to a course of eight simulated ECTs or to a course of eight real ECTs. The improvement in terms of psychiatrists' ratings in the group of patients given real ECT was significantly greater (p < 0.01) than that in those given simulated ECT, but the difference between the two groups was small in relation to the considerable improvement of both groups over the 4-week treatment period. No differences were found between the two groups at one-month and six-month follow-up. The therapeutic benefits of electrically induced convulsions in depression were of lesser magnitude and were more transient than has sometimes been claimed. In the real-ECT group memory was impaired during treatment but memory tests revealed no difference between the groups at six-month follow-up.

Adult↗
PubMedDate not supplied

Neuropeptide Y distribution in human brain.

Tatemoto and Mutt recently used the presence of a C-terminal NH2 group to identify and isolate a new peptide, neuropeptide Y (NPY), from porcine brain. This 36 amino acid peptide was subsequently shown to be active on isolated vas deferens, vascular smooth muscle and pancreatic acinar cells in very low molar concentrations. In view of these potent effects we have now investigated its distribution in the human brain by radioimmunoassay and immunocytochemistry. High concentrations of NPY have been found, exceeding those of cholecystokinin and somatostatin, hitherto considered to be the most abundant neuropeptides. The distribution of NPY was different from that of any other peptide system described, being particularly concentrated in the basal ganglia, amygdala and nucleus accumbens. Immunocytochemistry demonstrated a large number of NPY neuronal cell bodies especially in the caudate and putamen. Immunoreactive neuronal cell bodies were also clearly localized in cortical areas, particularly layers V and VI. NPY, a newly discovered peptide with potent biological activity, thus seems to be among the most abundant of human neuropeptides. The massive numbers of NPY neurones in the basal ganglia suggest NPY to be of fundamental importance in the control of human motor function.

Brain Chemistry↗
PubMedDate not supplied

Location of neuronal tangles in somatostatin neurones in Alzheimer's disease.

Senile dementia of the Alzheimer type is a chronic, progressive neuropsychiatric condition characterized clinically by global intellectual impairment and neuropathologically by the presence of numerous argyrophilic plaques and tangles. Neurochemical investigations have established loss of the cholinergic and aminergic projections to the cerebral cortex and a loss of the content of somatostatin, with preservation of cholecystokinin and vasoactive intestinal polypeptide, neuropeptides also located in cells intrinsic to the cortex. We describe here the relationship between cortical somatostatin immunoreactivity and the plaques and tangles of diseased tissue by immunocytochemical and silver impregnation techniques on paraffin-embedded tissue. In sections of Alzheimer's tissue, cortical somatostatin-immunoreactive perikarya exhibited morphological changes consistent with neuronal degeneration. Silver-stained material immunostained subsequently showed that many neurones containing tangles were also somatostatin positive. No such colocalization was observed using antisera to other neuropeptides. Our findings indicate that a subclass of somatostatin-positive neurones are affected selectively in Alzheimer's disease and that these neurones also contain neuronal tangles. Thus, destruction of somatostatin-containing neurones is an early and perhaps critical event in the disease process.

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