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Biomedical subjects

G S Zubenko

Publications and source records attributed to G S Zubenko.

At least 73 records · Page 4Linked to original sources
PubMed1990

Risk factors for white matter changes detected by magnetic resonance imaging in the elderly.

We found increased age (p = 0.001) and history or evidence of stroke (p = 0.016) to be significant independent multivariate predictors of the presence and severity of leukoencephalopathy on magnetic resonance imaging brain scans in a mixed population of 35 elderly psychiatric patients and 25 neurologically healthy elderly volunteers. These results suggest that subcortical ischemia, as well as age-related changes that may not be vascular in origin, contribute to the emergence of periventricular and other deep white matter hyperintensities that are commonly seen on the magnetic resonance imaging brain scans of older adults.

Aged↗
PubMed1990

Progression of illness in the differential diagnosis of primary dementia.

The diagnostic utility of determinations of insidious or stepwise progression of illness was examined in 124 geriatric inpatients with primary dementia. Such determinations failed to distinguish patients with primary degenerative dementia of the Alzheimer type from those with multi-infarct dementia. Episodic behavioral complications, especially depression and delusions, in the patients with primary degenerative dementia were associated with stepwise progression. Determinations of stepwise progression were made in only six (15%) of the 40 demented patients with at least two cerebral infarctions, a finding inconsistent with current diagnostic criteria for multi-infarct dementia.

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PubMed1990

Significance of increased platelet membrane fluidity in mental disorders of late-life.

Increased platelet membrane fluidity, as determined by the fluorescence anisotropy of 1,6-diphenyl-1,3,5-hexatriene (DPH), appears to be a stable, inherited trait that identifies a prominent subgroup of patients with Alzheimer's disease with distinct clinical features. Evidence bearing on the clinical and biological significance of this genetic source of clinical heterogeneity in Alzheimer's disease is presented.

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PubMed1989

Cholinergic and noradrenergic toxicity of intraventricular aluminum chloride in the rat hippocampus.

The effects of the intraventricular administration of aluminum chloride (AlCl3) on high affinity choline transport (HAChT) and norepinephrine concentration were examined in the hippocampus of the rat. Controlling for osmolarity and pH, the intraventricular administration of AlCl3 resulted in a dose-related reduction in both variables with relative selectivity for HAChT. Moreover, the neurotoxicity of intraventricular aluminum appeared to be dependent on the forms of the aluminum salt administered.

Aluminum↗
PubMed1989

SOD-1 activity and platelet membrane fluidity in Alzheimer's disease.

An early-onset, familial form of Alzheimer's disease (AD) has been reported to be linked to a locus on the long arm of chromosome 21 (21q21). Furthermore, duplications in the vicinity of this locus involving the beta-amyloid gene and the proto-oncogene ets-2 have been reported in association with AD. The structural gene for Cu,Zn superoxide dismutase, SOD-1, is located between the beta-amyloid gene and ets-2. For this reason and because SOD-1 is a plausible candidate for a gene that might influence the fluidity of cellular membranes, we determined whether or not the subtype of AD with increased platelet membrane fluidity was associated with an increase in Cu,Zn superoxide dismutase activity.

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PubMed1989

A brain regional analysis of morphologic and cholinergic abnormalities in Alzheimer's disease.

In the brains of 21 patients with Alzheimer's disease (AD) and 10 nondemented controls, senile plaques (SPs), neurofibrillary tangles (NFTs), and three indexes of cholinergic function were quantified in the middle frontal (MF) and superior temporal (ST) cortex, the entorhinal cortex (HEN), and the prosubiculum (HPR) of the hippocampus. Control brains contained few SPs without preferential distribution in any of the brain regions examined, while NFTs were found almost exclusively in the HPR. In brains from patients with AD, an inverse relationship of SPs and NFTs was found in the brain regions examined; SPs were preferentially in the neocortex and NFTs preferentially in the hippocampus. The specific activities of choline acetyltransferase and acetylcholinesterase were reduced in all regions examined, while no significant change in the density of muscarinic binding sites was observed in any region. Numerous NFTs were associated with an earlier age at onset, while the presence of SPs was related to the cholinergic deficit in AD. Earlier-onset (less than 67 years) AD was also associated with a qualitative difference in the regional distribution of NFTs compared with cases with a later onset. In the latter group, most NFTs were observed in the hippocampus, a distribution pattern similar to that observed with normal aging. In AD cases with an earlier onset, NFTs were more globally distributed in the neocortex and allocortex.

Acetylcholinesterase↗
PubMed1989

Lateralization of brain morphologic and cholinergic abnormalities in Alzheimer's disease.

The extent of left-right asymmetry in the densities of senile plaques and neurofibrillary tangles and the levels of the cholinergic enzymes choline acetyltransferase and acetylcholinesterase were quantified in the middle frontal and superior temporal cerebral cortex, entorhinal cortex, and prosubiculum of the hippocampus from 21 patients who died with Alzheimer's disease. Morphologic lesions were more asymmetrically distributed than deficits in the cholinergic enzymes. Neither cerebral hemisphere showed consistently higher densities of senile plaques and neurofibrillary tangles, or lower levels of choline acetyltransferase and acetylcholinesterase. Deficits in the cholinergic enzymes tended to colateralize, while asymmetries of senile plaques and neurofibrillary tangles did not. Finally, left-right asymmetry in the density of senile plaques diminished with increasing neuropathologic severity, while similar evidence for diminishing left-right asymmetry of neurofibrillary tangle density or cholinergic enzyme activity with increasing severity was not found.

Acetylcholinesterase↗
PubMed1989

Inheritance pattern of platelet membrane fluidity in Alzheimer disease.

The fluorescence anisotropy of 1,6-diphenyl-1,3,5-hexatriene in labeled platelet membranes, an index of membrane fluidity, is a stable, familial trait that is associated with a clinically distinct subtype of Alzheimer disease. Complex segregation analysis of this continuous variable was performed on 95 members of 14 pedigrees identified through probands who had autopsy-confirmed or clinically diagnosed Alzheimer disease. The results suggest that platelet membrane fluidity is controlled by a single genetic locus, PMF, with two alleles that have additive effects. The PMF locus appears to explain approximately 80% of the total variation in platelet membrane fluidity within the families of patients with Alzheimer disease.

Adolescent↗
PubMed1988

Bilateral symmetry of morphologic lesions in Alzheimer's disease.

We studied 16 brains of patients with Alzheimer's disease for left-right differences, or similarities, in the density of senile plaques (SPs) or neurofibrillary tangles (NFTs). Counts were made of SPs and NFTs on the left and right side of five different brain areas, which included middle frontal, superior temporal, the prosubiculum of the hippocampus (HPR), the entorhinal cortex of the hippocampus (HEN), and the basal nucleus of Meynert. The density of SPs was bilaterally symmetrical in all regions except the basal nucleus of Meynert in which technical problems may have occurred in sampling. In contrast to SPs, the density of NFTs was bilaterally symmetrical in both neocortical regions (middle frontal, superior temporal), but not in either hippocampal region (HPR, HEN). The absence of bilateral symmetry for the density of NFTs in the hippocampus, where the density of SPs was highly symmetrical, suggests that there may be a different pathogenesis for these lesions in Alzheimer's disease. The lack of a significant correlation between SP and NFT density within four of five regions, including HPR and HEN, also supports this suggestion.

Aged↗
PubMed1988

Bilateral symmetry of cholinergic deficits in Alzheimer's disease.

The specific activities of the cholinergic enzymes, choline acetyltransferase and acetylcholinesterase, as well as the density of muscarinic binding sites, were determined in five corresponding left and right regions of 16 brains obtained at autopsy from patients with histologically confirmed Alzheimer's disease. While a significant proportion of the individual specimens exhibited left-right asymmetries in cholinergic deficits, bilateral symmetry was the rule for frontal and temporal cortex, basal nucleus, and the prosubiculum of the hippocampus. In contrast to these four regions, left-right asymmetries in choline acetyltransferase activity and muscarinic receptor density appeared to be typical in the entorhinal cortex of the hippocampus.

Acetylcholinesterase↗
PubMed1988

Electroencephalographic correlates of increased platelet membrane fluidity in Alzheimer's disease.

Increased platelet membrane fluidity is a stable, familial characteristic that describes a clinically distinct subgroup of patients with Alzheimer's disease. In the current study, electroencephalograms (EEGs) from 49 patients with probable Alzheimer's disease were subjected to visual and computerized spectral analysis. Only three (14.3%) of 21 patients in the subgroup with increased platelet membrane fluidity exhibited focal EEG abnormalities, while 12 (42.9%) of 28 of the residual subgroup exhibited focal EEG findings, a threefold difference. This difference in EEG profile provides further validation of these two subgroups and suggests that the subgroup with increased fluidity is less heterogeneous than the residual group.

Alzheimer Disease↗
PubMed1988

Major depression in primary dementia. Clinical and neuropathologic correlates.

Cytopathologic features were quantified in seven brain regions in the brains of 37 demented patients, with or without major depression, and in those of seven controls with no history of dementia or depression. The middle frontal and superior temporal cortex, prosubiculum and entorhinal cortex of the hippocampus, nucleus basalis of Meynert, locus ceruleus, and substantia nigra were the areas evaluated. Patients with major depression had significantly more degenerative findings in the locus ceruleus and substantia nigra than demented patients who were not depressed. In contrast, these groups were similar with respect to other clinical features and indexes of global severity of dementia. A logistic regression model that included the degenerative features of both the locus ceruleus and the substantia nigra was significantly better at predicting the presence of major depression than those employing the characteristics of either pigmented nucleus alone. Our results indicate that the development of major depression in patients with primary dementia is associated with the degeneration of the locus ceruleus and substantia nigra.

Aged↗
PubMed1988

Familial risk of dementia associated with a biologic subtype of Alzheimer's disease.

Increased platelet membrane fluidity is a stable familial trait that identifies a prominent subgroup of patients with Alzheimer's disease. Patients in this subgroup have distinct clinical features, including an early age at symptomatic onset and a rapidly progressive course. The morbid risk of Alzheimer's-type dementia was studied in 421 first-degree relatives of 43 patients who met current consensus criteria for probable Alzheimer's disease and 47 healthy controls. Relatives of patients showed an approximate 50% (90- to 95-year) lifetime risk of dementia, regardless of the platelet membrane phenotype of the respective proband, which was over four times the control value. However, relatives of patients with increased platelet membrane fluidity who developed dementia exhibited symptoms significantly earlier than relatives of patients with normal platelet membrane fluidity. Alternative genetic models that describe the relationship of platelet membrane fluidity and Alzheimer's disease are discussed.

Actuarial Analysis↗
PubMed1988

Monozygotic twins concordant for probable Alzheimer disease and increased platelet membrane fluidity.

This report describes monozygotic twins who were concordant for probable Alzheimer disease, as defined by currently-accepted clinical criteria. Monozygosity was established by blood typing. Their ages of symptomatic onset were 57 and 66 yr, and the times from onset to institutionalization were 8 and 2 yr, respectively. These results suggest that age at onset and rate of progression are clinical features that can be affected by random processes or exposure to environmental factors. The platelet membrane fluidity of both twins was abnormally increased, and the respective values were identical within experimental limits. This result is consistent with published data suggesting that increased platelet membrane fluidity is associated with a clinically distinct subtype of Alzheimer disease and that this platelet membrane characteristic may be genetically determined.

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PubMed1988

Platelet membrane fluidity and treatment response in cognitively-impaired, depressed elderly: initial results.

A prospective study of response to treatment with nortriptyline was carried out in a group of 14 inpatients with mixed symptoms of depression and dementia. Platelet membrane fluidity, as reflected by the fluorescence anisotropy of DPH labeled membranes, was determined for all 14 drug-free subjects prior to treatment by staff who were blind to clinical and demographic data. Patients who exhibited worsening of their cognitive impairment exhibited "increased" platelet membrane fluidity, an abnormally found in approximately 50% of patients with Alzheimer's disease.

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PubMed1988

Longitudinal study of platelet membrane fluidity in Alzheimer's disease.

Increased platelet membrane fluidity identifies a prominent subgroup of patients with Alzheimer's disease who exhibit distinct clinical features. In the current longitudinal study, the stability of this membrane characteristic was determined for 15 patients with Alzheimer's disease and 10 healthy elderly controls over a 1-year follow-up period.

Aged↗
PubMed1988

Cognitive function and platelet membrane fluidity in Alzheimer's disease.

Increased platelet membrane fluidity, as reflected by a decrease in the fluorescence anisotropy of diphenylhexatriene in labeled membranes, identifies a clinically distinct subgroup of approximately 50% of patients at our center who meet NINCDS-ADRDA clinical criteria for Alzheimer's disease. In the current study, we compared the cognitive impairments of patients in this subgroup to those observed in the residual subgroup of patients with Alzheimer's disease who had normal platelet membrane fluidity. No significant differences in the number or distribution of deficits in six cognitive domains were observed between the two subgroups. However, in the subgroup with increased platelet membrane fluidity, there were significantly more patients who exhibited dissociation of deficits on tests related to left and right parietal lobe function than in the residual subgroup. Moreover, the cases with dissociation of deficits consisted almost entirely of patients with deficits on tests reflecting left parietal lobe function and no deficit on tests of right parietal lobe function.

Aged↗