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Biomedical subjects

A J Cross

Publications and source records attributed to A J Cross.

154 records · Page 9Linked to original sources

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.

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Characteristics of 125I-Bolton-Hunter labelled cholecystokinin binding in human brain.

The high affinity binding of 125I-Bolton-Hunter labelled CCK-8 (125I-BHCCK) was studied in human brain using ligand binding and autoradiographic techniques. High levels of 125I-BHCCK binding were observed in cortex, striatum and cerebellum. In cerebellar membranes 125I-BHCCK binding was inhibited by CCK analogues with an order of potency, caerulein greater than CCK-8 greater than CCK-33 greater than gastrin 1-17 = CCK-8 non-sulphated. CCK-4 was inactive. It is suggested that in human brain 125I-BHCCK labels a population of CCK receptors similar to those observed in guinea pig brain. The properties and distribution of these receptors differ from those of rat brain.

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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.

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