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Biomedical subjects

P O Yates

Publications and source records attributed to P O Yates.

At least 19 recordsLinked to original sources
PubMed1992

Cerebral vasculopathy in divers.

Brains from 12 amateur and 13 professional divers, all but one of whom died accidentally, were examined neuropathologically. Grossly distended, empty vessels (presumably caused by gas bubbles) were found in the brains of 15 out of 22 divers who died from diving accidents. Perivascular lacuna formation was found in cerebral and/or cerebellar white matter in three amateurs and in five professionals. In addition to lacuna formation, hyalinization of vessel walls was present in the brains of three amateurs and five professionals. Necrotic foci in grey matter occurred in seven cases and perivascular vacuolation of white matter occurred in seven cases. The vascular changes probably arose from intravascular gas bubble formation. In one professional diver, there was also unilateral necrosis of the head of the caudate nucleus.

Adult↗
PubMed1988

Topography of nerve cell loss from the locus caeruleus in middle aged persons with Down's syndrome.

A topographical analysis of nerve cell loss from the locus caeruleus in middle aged patients with Down's syndrome (whose brains show the pathological changes of Alzheimer's disease), has shown that cell loss is confined to dorsal areas, being least most rostrally and greatest caudally. By contrast, there is no significant cell loss from ventral parts of the locus, at any point along its rostrocaudal length. Dorsally located neurones of the locus project to cerebral cortex; ventrally located neurones to non-cortical areas such as basal ganglia, cerebellum and spinal cord. These data suggest that the damage to nerve cells of the locus caeruleus in Down's syndrome at middle age, like that seen in Alzheimer's disease itself, relates to primary pathological events within the cortical projection fields of affected cells with perikaryal loss following on as a later change.

Adult↗
PubMed1988

Alzheimer's disease: an olfactory connection?

The density and distribution of senile plaques and neurofibrillary tangles were examined in the olfactory bulbs and tracts, amygdala and hippocampus of 28 patients with Alzheimer's disease, 13 with Down's syndrome and 60 non-demented patients of age range 6-84 years. In all three patient groups comparisons of incidence and severity over the three areas showed the amygdala to be the most commonly and most severely affected area by senile plaques, the hippocampus by neurofibrillary tangles, and the olfactory bulbs and tracts to be the least affected by both. These findings are discussed in relationship to the possibility that the olfactory tracts might provide a portal of entry to the brain for any putative pathogenic agent(s) that might be responsible for the induction of senile plaques and/or neurofibrillary tangles.

Adolescent↗
PubMed1987

Glycogen accumulations in the cerebral cortex in Alzheimer's disease.

The fine structure of granular glycogen bodies (GGB) within the grey matter of the temporal cortex of 11 patients with Alzheimer's disease is described. GGB measure up to 50 microns in diameter and consist of densely packed alpha or beta glycogen granules (never both), neither of which are membrane bound. They were noted in axons, both myelinated and unmyelinated (sometimes close to the dystrophic neurites of senile plaques), and also in other processes of indeterminate origin. Their appearance may relate to disturbances of axonal transport resulting from damage to terminals within evolving senile plaques.

Aged↗
PubMed1987

A quantitative morphometric analysis of the neuronal and synaptic content of the frontal and temporal cortex in patients with Alzheimer's disease.

A quantitative morphometric analysis was used to estimate neurone and synapse densities in cerebral cortical biopsy tissues from patients with dementia under 65 years of age and pathologically verified as suffering from Alzheimer's disease. Estimates of the numerical density of neurones and synapses were made in layers II-III and V of both frontal and temporal cortex. A greater loss of synapses than that of neurones was found in Alzheimer's disease, amounting to a minimum (uncorrected for atrophy) of 25% in layers II-III and 36% in layer V of the temporal cortex, and 27% in layer V of the frontal cortex. Values of synapse to neurone ratio also demonstrated this greater loss of synapses, there being on average 38% fewer synapses associated with each surviving neurone in layers II-III of the temporal cortex, 30% fewer in layer V, and a deficit of 14% in layer V of the frontal cortex. It is concluded that a major loss of synapses occurred in this group of patients with Alzheimer's disease, probably at an early stage of the disease, and that the loss is likely to form a fundamental part of the pathological process that underlies the cortical damage of this condition.

Aged↗
PubMed1987

Loss of neurones from cortical and subcortical areas in Down's syndrome patients at middle age. Quantitative comparisons with younger Down's patients and patients with Alzheimer's disease.

Brains were examined after autopsy from 12 patients over 53 years of age with Down's syndrome (in whose brains plaques and tangles were numerous in many areas of cortex and subcortex), 3 patients under 53 years of age with Down's syndrome (in whose brains plaques and tangles were minimal or absent), 10 patients, of age range similar to the older Down's group but with Alzheimer's disease and 5 control patients of age range similar to the younger Down's group. The number of plaques and tangles in the hippocampus and their density within the temporal cortex, the thickness of the temporal cortex, the cross-sectional area of the hippocampus and the relative number and mean nucleolar volume of nerve cells in these cortical and in some subcortical areas were estimated and compared in each of the 4 groups. The relative loss of nerve cells and the decrease in mean nucleolar volume were calculated in percentage terms for the older Down's syndrome patients by reference to data from the younger Down's syndrome patients, whereas such losses in Alzheimer's disease were calculated by reference to the younger control patients. While in qualitative terms, all areas of brain found to be damaged in Alzheimer's disease were also damaged in Down's syndrome at middle age, quantitative differences emerged with the reductions in relative nerve cell number and mean nucleolar volume being significantly less in many areas in Down's syndrome. Conversely plaques and tangles were more numerous in the hippocampus in Down's syndrome though in the temporal cortex plaques were less numerous. It seems, therefore, that although the same pathological process is likely to operate in the two conditions, additional biological and mortality differences between Down's syndrome and the general population may account for the observed quantitative variations.

Adult↗
PubMed1987

Dopaminergic neurotransmitter systems in Alzheimer's disease and in Down's syndrome at middle age.

In 15 patients with Alzheimer's disease and in 10 with Down's syndrome at middle age, there was severe atrophy, neurofibrillary degeneration and loss of pigmented dopaminergic nerve cells from ventral tegmental area (A10) whereas nerve cells in neighbouring substantia nigra (A9) were much less affected in all three respects. It is suggested that these findings may represent different patterns of damage within the two systems in these conditions which may relate to the presence of Alzheimer type changes (senile plaques) within their respective projection fields.

Aged↗
PubMed1986

Loss of nerve cells from locus coeruleus in Alzheimer's disease is topographically arranged.

Serial sectioning of the locus coeruleus (LC) was employed to determine a topographic loss of nerve cells in patients with Alzheimer's disease (AD). Heaviest loss of nerve cells occurred in the central part of the LC which is thought to project to the temporal cortex and hippocampus, whereas least loss of cells occurred in the most rostral and caudal parts, thought to project to frontal and occipital regions of cortex, respectively. Such changes suggest that the primary damage to these nerve cells in AD occurs within their terminal fields and that perikaryal loss follows as a secondary retrograde change.

Aged↗
PubMed1986

The nucleus basalis of Meynert in multi-infarct (vascular) dementia.

The number and nucleolar volume of nerve cells within the nucleus basalis of Meynert were estimated in 10 patients with Alzheimer's disease, 12 with multi-infarct dementia, 9 with a mixed Alzheimer/multi-infarct dementia and in 10 age-matched controls. As reported previously in Alzheimer's disease, both the number and nucleolar volume of surviving cells was reduced, whereas in multi-infarct dementia no significant change in either measure was noted. In patients with Alzheimer's disease/multi-infarct dementia the loss of nerve cells and reduction in nucleolar volume varied greatly in severity from patient to patient according to the relative balance of Alzheimer and vascular type pathological changes present within each patient.

Aged↗
PubMed1986

The topography of cell loss from locus caeruleus in Alzheimer's disease.

A topographical analysis of nerve cell loss from locus caeruleus in Alzheimer's disease has shown that cell loss is confined to the dorsal areas and occurs uniformly throughout the rostrocaudal length of the locus. By contrast there is no significant cell loss from ventral parts of the locus, at any point along its rostrocaudal length. Dorsally located neurones of the locus project to cerebral cortex; ventrally located neurones to non-cortical areas such as basal ganglia, cerebellum and spinal cord. These data suggest that damage to nerve cells of locus caeruleus in Alzheimer's disease relates primarily to pathological events within their terminal fields, with perikaryal loss following as a secondary retrograde change. The senile plaque may represent the actual site of the damage to nerve terminals.

Aged↗
PubMed1986

Cerebral biopsy in the investigation of presenile dementia due to cerebral atrophy.

Investigation by cerebral biopsy of patients with dementia associated with cerebral atrophy permits the examination of clinico-pathochemical relationships, and provides a means of distinguishing and classifying forms of cerebral atrophy. Benefits of the procedure must however be weighed against possible adverse effects of surgical intervention. The study examines the outcome following biopsy of 24 patients with presenile dementia. No major operative complications were encountered, and recovery was uneventful in all but a single patient. The relevance of the findings to the study of dementia by cerebral biopsy is discussed.

Aged↗
PubMed1986

Neuropsychological syndromes in presenile dementia due to cerebral atrophy.

In a prospective study of 24 patients with presenile dementia associated with cerebral atrophy, clinical and psychological characteristics of patients' disorder were examined in relation to pathological and chemical findings obtained from tissue analysis following cerebral biopsy. The histological features of Alzheimer's disease were found in 75% of cases, but not in 25%. Distinctive patterns of neuropsychological breakdown emerged allowing clinical grouping of patients. While clinical patterns were helpful in differentiating Alzheimer's disease from non-Alzheimer's disease, there was not an absolute concordance between clinical and patho-chemical groupings. The findings, which support the notion that the "cerebral atrophies" represent a heterogeneous group of conditions, have relevance for the clinical diagnosis of presenile dementia.

Aged↗
PubMed1986

Alzheimer's disease: a correlative study.

In a study of 17 patients with histologically proven Alzheimer's disease the relationship between psychological, pathological and chemical measures of disorder was examined. Severity of dementia, determined by mental test performance, correlated highly with pathological change in large cortical neurons (cell loss and reduction in nuclear and nucleolar volume and cytoplasmic RNA content), to a lesser extent with cortical senile plaque and neurofibrillary tangle frequency and reduction in acetylcholine (ACh) synthesis, and not with reduction in choline acetyltransferase (CAT) activity. A strongly significant relationship was demonstrated between cell loss and reductions in nuclear and nucleolar volume and cytoplasmic RNA content. Reduction in CAT activity and senile plaque frequency were significantly correlated, thereby linking changes in the sub-cortical projection system of the nucleus basalis with the cortical pathology. The pattern of correlations suggests that the dementia of Alzheimer's disease is largely a reflection of the state of large cortical neurons, and it is argued that abnormalities in the latter may not be directly related to primary loss of cholinergic neurons in the subcortex.

Acetylcholine↗
PubMed1986

Neurotransmitter deficits in Alzheimer's disease and in other dementing disorders.

The evidence for deficiencies in neurotransmitters in Alzheimer's disease is reviewed. Major losses occur in the subcortical afferent projection systems based on acetylcholine, noradrenaline and serotonin. Within the cortex, somatostatin containing neurones and the large pyramidal cells, presumed to use glutamate/aspartate as transmitters, are the most severely damaged cells. The anatomical distribution of cell loss is explainable if the primary site of damage lies within the cortex; nerve cells are damaged by virtue of their presence within or their connections to this region. The senile plaque may represent the site of this damage and neurofibrillary tangle formation and accumulation may lead to cell death. In patients with Down's syndrome who live past 40 years, changes in transmitters apparently identical to those in Alzheimer's disease occur. The dementia of Parkinson's disease appears related to damage to cholinergic, noradrenergic and dopaminergic systems and may reflect a failure of these subcortical regions to sufficiently "activate" an otherwise undamaged cortex.

Acetylcholine↗