Application of antiphenylalanine hydroxylase antibodies to the study of the serotonergic system in the human brain.
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Animals↗
Biomedical subjects
G M Halliday
Publications and source records attributed to G M Halliday.
Neurofibrillary degeneration and cell loss in the nucleus basalis in comparison to cortical Alzheimer pathology.
Neurofibrillary tangle staging was compared in the nucleus basalis and cerebral cortex of Alzheimer's disease patients with and without Lewy body disease. In pure Alzheimer's disease, cholinergic nucleus basalis cell number, as determined from counts in serial forebrain sections, was 22-60% of control mean, with the majority of residual cells containing tangles. A comparison between control cell number and the combined number of tangles plus tangle-free neurons in pure Alzheimer's disease suggests that the majority of nucleus basalis neurons were lost through neurofibrillary degeneration. The staging of neurofibrillary degeneration in the nucleus basalis was discordant with cortical changes as some controls had more extensive tangle formation in the nucleus basalis than in the cerebral cortex. Patients having both Alzheimer's disease and Lewy body pathology had few or no tangles in the nucleus basalis despite greater loss of neurons than purely demented patients. The presence of concomitant pathology had a greater effect on nucleus basalis tangle burden than did cortical disease stage, suggesting dichotomous disease processes in the cerebral cortex and forebrain.
Aged↗
A review of the neuropathology of schizophrenia.
1. Research on the structural basis for schizophrenia was considered a graveyard for neuropathologists, largely because its aetiology has remained obscure. However, there have been several recent major reviews and studies in leading journals on the neuropathology of schizophrenia highlighting the alterations found in the brains of schizophrenic patients. 2. It is clear from the evidence that schizophrenia can no longer be considered a purely functional psychosis with no structural basis. Multiple and possibly widespread neural systems are likely to participate, because diffuse ventricular enlargement and decreased cortical volume are common in schizophrenia. Interestingly, these features do not herald neuronal loss, findings similar to those obtained in alcoholic and aged populations. Impairment in judgement is common to all these subject groups. 3. The frontal and temporal lobes and their thalamic relays appear particularly affected in schizophrenia and there is some evidence for significant asymmetries. These regions are also consistently affected in patients with neurodegenerative cognitive impairment, although patients with schizophrenia can be distinguished by a lack of classical tissue pathology. 4. The cellular phenotypes that must be structurally compromised have yet to be definitively identified and the relationship between any neurochemical and structural abnormality remains unclear. The subtlety of these changes and their diffuse nature have evoked a consistent chorus that schizophrenia is a neurodevelopmental abnormality; however, this is hard to prove at a structural level using cross-sectional post-mortem analyses.
Atrophy↗
Regional brain atrophy in idiopathic parkinson's disease and diffuse Lewy body disease.
This study measured brain atrophy in patients with idiopathic Parkinson's disease and diffuse Lewy body disease, all of whom had equivalent loss of midbrain dopammergic neurons and absence of Alzheimer's disease. Characteristic patterns of volume loss were found throughout the brain, depending on the age of onset and clinical signs. An equivalent loss of medial temporal lobe structures occurred in all parkinsonian patients. This atrophy was similar in magnitude to that seen in Alzheimer's disease and is likely to be the anatomical substrate for the memory deficits found in each of these patients groups. Frontal lobe atrophy was a feature of both late-onset Parkinson's disease (mild atrophy) and diffuse Lewy body disease (significant atrophy) groups, with all cases analyzed having dementia. Atrophy of frontal lobes correlated with the duration of motor symptoms in these patients and may suggest an association between dopammergic deafferentation, frontal atrophy and dementia.
Aged↗
Topical retinoic acid inhibits changes in Langerhans cell density during carcinogenesis.
Ultraviolet radiation (UVR), chemical carcinogens and contact sensitisers all reduce the density of Langerhans cells (LC) in murine epidermis; UVR also lowers the number of Thy-1 dendritic epidermal cells (Thy-1+ dEC). Topical application of all-trans retinoic acid (RA) renders these cells insensitive to UVR and the tumour promoter 12-0-tetradecanoylphorbol 13-acetate (TPA) but does not inhibit LC migration from the epidermis in response to a contact sensitiser. Additionally, when the diet of mice was supplemented with the retinoid temarotene, UVR was unable to reduce the number of LC or Thy-1+ dEC. Hence one of the anti-carcinogenic mechanisms of retinoids may be to protect LC from carcinogens.
Administration, Cutaneous↗