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C Q Mountjoy

Publications and source records attributed to C Q Mountjoy.

At least 19 recordsLinked to original sources
PubMed2000

Augmentation with sulpiride for a schizophrenic patient partially responsive to clozapine.

OBJECTIVE: Schizophrenic patients who are only partially responsive to clozapine pose a therapeutic challenge. In these circumstances some clinicians would consider adding in a second antipsychotic. We present a case report and review evidence for the efficacy of such augmentation strategies. METHOD: Single case report and literature review. RESULTS: The total number of patients in studies and case reports of combining clozapine with other antipsychotics is small. There has been only one randomized controlled trial. This found the addition of sulpiride to clozapine resulted in clinical improvement in some patients. CONCLUSION: Further randomized controlled studies of augmentation of clozapine therapy are needed to provide scientific justification for this clinical practice.

Antipsychotic Agents↗
PubMed1998

Olanzapine.

Explore the source record for details and available documents.

Antipsychotic Agents↗
PubMed1996

Moclobemide in elderly patients with cognitive decline and depression: an international double-blind, placebo-controlled trial.

BACKGROUND: The new reversible MAOl moclobemide was compared with placebo in the treatment of elderly patients with DSM-III diagnosis of dementia and/or of major depression. METHOD: Six hundred and ninety-four elderly patients with symptoms of depression and cognitive decline entered an international, multi-centre, double blind trial in which they were randomly allocated to treatment with either moclobemide 400 mg daily or placebo for 42 days. Five hundred and eleven patients met DSM-III criteria for dementia and were also depressed (DEM+D); 183 did not meet DSM-III criteria for dementia but met the criteria for DSM-III major depressive episode and also suffered from cognitive decline (MDE+CD). RESULTS: Analysis of the 17 and 24-item Hamilton Depression Scale scores showed that moclobemide, compared with placebo, produced significantly greater improvement in both the demented and depressed groups (P = 0.001 both diagnostic groups). There was an improvement in cognitive function as measured by the SCAG Factor 1 in moclobemide treated patients (P = 0.005 DEM+D; P = 0.02 MDE+CD). There was no evidence of decline in cognitive function as the result of treatment. Clinical global assessment of tolerance was 'excellent' and 'good' in 88% of the moclobemide and in 92% of the placebo treated patients. The proportion of patients discontinuing treatment prematurely was similar in both treatment groups. There were no significant differences in side-effects between treatment groups. There were no significant changes in vital signs, ECG or laboratory findings in either treatment group. There were no dietary restrictions and no report of any tyramine reaction. CONCLUSIONS: Moclobemide was shown to be a safe, well tolerated and effective antidepressant, which did not cause impairment of cognitive function in elderly patients with a DSM-III diagnosis of dementia and/or DSM-III major depression.

Aged↗
PubMed1993

Evidence of subtypes of Alzheimer's disease and implications for etiology.

OBJECTIVE: Because age of onset does not reliably define two subtypes of Alzheimer's disease, classification based on the severity of neuronal degeneration was tested. DESIGN: Numbers of extracellular tangles and pyramidal neurons in the hippocampus were used to group patients. PATIENTS: The study population consisted of 46 elderly patients satisfying DSM-III criteria for dementia and NINCDS-ADRDA criteria for definite Alzheimer's disease after death. RESULTS: Univariate logistic regression analysis showed the numbers of neurofibrillary tangles and pyramidal neurons and the duration of dementia were significantly associated with grouping based on the presence of abundant extracellular tangles. Ninety-one percent of patients were correctly classified as compared with 85% correctly classified by age of onset data. Odds ratios showed that increasing numbers of neurofibrillary tangles predicted greater severity of neuronal loss. CONCLUSION: The results of the study indicate the importance of neurofibrillary degeneration, not the deposition of amyloid, in the pathogenesis of Alzheimer's disease. They support a classification of Alzheimer's disease related more closely to the severity of neurofibrillary degeneration than to age at onset.

Age Factors↗
PubMed1990

Cerebral cortical calbindin D28K and parvalbumin neurones in Down's syndrome.

Anti-calbindin D28K (CaBP) and anti-parvalbumin (PVA) antibodies were used to study the number and size of neurones containing these two calcium binding proteins in post-mortem brains from 7 neurologically normal controls and from 4 elderly patients with clinically diagnosed Down's syndrome (DS) and whose brains contained numerous senile plaques and neurofibrillary tangles. The possible co-existence of these two calcium binding proteins in human cerebral cortex was also examined. In the controls, CaBP immunoreactive neurones were mainly non-pyramidal neurones although some pyramidal neurones were also CaBP immunoreactive. All the PVA immunoreactive neurones were non-pyramidal cells. CaBP and PVA did not apparently co-exist with each other in cortical neurones. When compared with the neurologically normal controls, the number and size of CaBP and PVA immunoreactive neurones were significantly reduced in the cortex of patients with DS. These findings show that CaBP and PVA containing cortical neurones are affected in elderly persons with DS.

Aged↗
PubMed1989

Calbindin-immunoreactive cholinergic neurones in the nucleus basalis of Meynert in Alzheimer-type dementia.

An antibody to the calcium binding protein, calbindin D28K (CaBP), was used to study the number and size of CaBP-immunoreactive neurones in the nucleus basalis of Meynert (nbM) of postmortem human brains from neurologically normal controls and from patients with neuropathologically diagnosed Alzheimer-type dementia (ATD). In controls, almost all the large neurones and their processes in the nbM were CaBP immunoreactive. Compared to neurologically normal controls the number of CaBP-immunoreactive neurones in the nbM in patients dying with ATD was significantly reduced and there was a clear loss of the majority of CaBP immunoreactive neurones. The few remaining nbM CaBP immunoreactive neurones in the ATD cases were smaller than those in the neurologically normal controls. Double-staining experiments revealed that many of the nbM CaBP-immunoreactive neurones contained choline acetyltransferase immunoreactivity, so that CaBP is an alternative marker for the nbM cholinergic neurones in the human fore-brain. These findings suggest that a disturbance in calcium homeostasis may be a possible factor contributing to the loss of these cholinergic/CaBP-containing neurones.

Adult↗
PubMed1989

Vicia villosa lectin-positive neurones in human cerebral cortex. Loss in Alzheimer-type dementia.

Frontal and temporal sections of 4 normal human brains and 3 brains from patients with a diagnosis of Alzheimer-type dementia (ATD) were stained with Vicia villosa lectin conjugated to biotin to localize glycoproteins containing terminal N-acetylgalactosamine. These lectin binding sites were localized at the surface of a population of non-pyramidal interneurones. Examination of the co-existence of calbindin D28K or parvalbumin (PVA) with the lectin-binding material revealed that in the human cerebral cortex the lectin labelled only the PVA-immunoreactive neurones. Cell counts of the number of lectin-staining cells revealed that these cells are lost in ATD. The few remaining lectin-staining cells in ATD are shrunken and showed reduced expression of the lectin-staining material.

Acetylgalactosamine↗
PubMed1989

The substantia nigra and ventral tegmental area in Alzheimer's disease and Down's syndrome.

Degenerative changes in the substantia nigra and ventral tegmental area were investigated in 104 cases of Alzheimer's disease and 13 cases of Down's syndrome. Frequencies of tangles in three groups of patients with Alzheimer's disease were 86%, 44% and 46% (54% overall) respectively. About half of those with tangles, but no Lewy bodies, had excess nigral cell loss, and 16% had moderate or severe neuronal fallout, but none had a Parkinsonian syndrome. Cases with nigral tangles were younger, tended to have more hippocampal and cortical tangles and plaques, and lower activities of cortical choline acetyltransferase. In most cases of Alzheimer's disease degeneration in nigral and tegmental areas was greater than controls, and tangles were evenly distributed. All the cases of Down's syndrome had tangles in the nigra and eight showed mild cell loss. Mild degenerative changes accompanied by tangles in the substantia nigra and ventral tegmental area are common in Alzheimer's disease, but severe cell loss is rare. When a Parkinsonian syndrome occurs in Alzheimer's disease it is likely to be due to Lewy body pathology.

Adult↗
PubMed1989

A pathological study of the association between Lewy body disease and Alzheimer's disease.

The possibility of an association between Parkinson's disease and Alzheimer's disease has been examined by studying the age-specific prevalence of Lewy bodies in the substantia nigra in a group of 273 control cases without Parkinson's disease and 121 cases of Alzheimer's disease. The substantia nigra was also studied in 14 cases of Down's syndrome, 13 of which had cortical Alzheimer pathology. Twelve (7.8%) of the controls aged over 60 years showed nigral Lewy bodies. There was mild nerve cell degeneration and/or an extranigral distribution of Lewy bodies, suggestive of presymptomatic Parkinson's disease. Twenty five (22.5%) of the Alzheimer's disease cases over 60 years showed Lewy bodies, but only 14 (14.0%) of these had mild nigral cell loss consistent with presymptomatic Parkinson's disease. No case of Down's syndrome had Lewy bodies. Counts of tangles and plaques in hippocampus, frontal and temporal cortex were lower in cases of Alzheimer's disease with Lewy bodies compared with those without, but cortical choline acetyltransferase (ChAT) activities were similar. This suggests that Lewy body degeneration in the nucleus basalis of Meynert contributes to the deficit of cortical ChAT, but not to the cortical Alzheimer pathology. The relatively small difference in the prevalence of Lewy bodies between controls and Alzheimer's disease could be explained by the additive effects of Lewy body and tangle pathology causing dementia, rather than a greater than chance association between Parkinson's disease and Alzheimer's disease.

Adult↗
PubMed1988

Loss of calbindin-28K immunoreactive neurones from the cortex in Alzheimer-type dementia.

An antibody raised against chick intestinal calbindin D28K was used to study the number and size of calbindin immunoreactive neurones in postmortem human brains from neurologically normal controls and from patients with neuropathologically diagnosed Alzheimer-type dementia (ATD). In the controls, calbindin immunoreactive neurones were observed in all cerebral cortex areas examined including the frontal, temporal and parietal cortices. When compared with the controls, the number and size of calbindin immunoreactive neurones were significantly reduced in the cortices of patients with ATD. These findings suggest that calbindin containing neurones are affected in ATD.

Aged↗
PubMed1988

Loss of matrix calcium-binding protein-containing neurons in Huntington's disease.

In post-mortem brain specimens from patients dying with a clinical diagnosis of Huntington's disease (HD) immunohistochemistry showed a substantial loss from the neostriatum of neurons containing the calcium-binding protein calbindin 28K. These calbindin neurons, and the straital compartment in which they are sited, are particularly damaged in HD, suggesting that a failure of calcium buffering or homeostasis may contribute to cell death in HD.

Adult↗
PubMed1987

Loss of parvalbumin-immunoreactive neurones from cortex in Alzheimer-type dementia.

The type and cell size of parvalbumin-immunoreactive (PV-Ir) neurones were examined in 14 postmortem brains from elderly control and Alzheimer-type dementia (ATD) patients with the aid of an image analyser. Morphological features of PV-Ir neurones suggested the existence of PV in the non-pyramidal interneurones in the cerebral cortex. A significant loss of PV-Ir cells was found in the frontal and temporal cortex in ATD. A significant reduction in the size of PV-Ir cells was also noted in the temporal cortex in ATD. These findings suggested that PV-Ir neurones in the cortex are affected in ATD.

Aged↗
PubMed1987

Age and histopathologic heterogeneity in Alzheimer's disease. Evidence for subtypes.

In support of heterogeneity in Alzheimer's disease (AD), the existence of clinical and biologic subtypes has been claimed. We have investigated this claim by a statistical analysis of the relationships between the number of neurons in nucleus locus ceruleus (nLC), cortical levels of neurotransmitters, number of cortical plaques and tangles, and age. We separated AD patients into two groups: AD-1, with a less severe loss of nLC neurons; and AD-2, with a greater loss. The AD-2 cases were associated with less choline acetyltransferase activity, smaller concentrations of somatostatin and norepinephrine, and more plaques and tangles in the cerebral cortex. Although the mean age at death was less and the duration of dementia was greater in AD-2 patients than in AD-1 patients, the differences in these age-related variables were not significant. Further evidence of heterogeneity came from discriminant function analyses based on nLC neuronal counts and age at death. These findings, suggesting two subtypes of AD, suggest heterogeneity.

Age Factors↗
PubMed1987

Neuronal degeneration in locus ceruleus and cortical correlates of Alzheimer disease.

Relationships were examined between neuronal degeneration in the nucleus locus ceruleus (nLC), a parameter of central noradrenergic impairment, and neocortical markers of Alzheimer disease (AD). The loss of nLC neurons was found to correlate significantly with norepinephrine concentration, choline acetyltransferase (ChAT) activity, and numbers of plaques and tangles on Brodmann area 24 (cingulate); ChAT and plaque counts in area 21 (temporal); and with ChAT activity in area 10 (frontal). In addition, nLC neuronal counts were correlated significantly with the severity and estimated duration of dementia. The number of neurofibrillary tangles in nLC, which did not correlate significantly with neocortical markers of AD, correlated with the estimated duration and severity of dementia. These data suggest that changes in central noradrenergic pathways are related to the pathophysiology of AD.

Aged↗