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W Bondareff

Publications and source records attributed to W Bondareff.

At least 37 records · Page 2Linked to original sources
PubMed1986

Comparison of counts of neurons in the locus coeruleus made from serial sections and from a single section at the centre of the nucleus.

This paper describes the comparability of counts in the locus coeruleus made from serial sections and those made from a single section at the point of greatest density of neurons. Samples of the locus coeruleus neuronal population derived from single section counts though not exactly comparable, are of comparable utility to those obtained from more laborious total neuronal counts. The simpler method was used to examine the hypothesis that there are subtypes of senile dementia of the Alzheimer type. Separation into two groups was achieved when independent variables of cortical neuronal counts and tangle estimates were used. This finding adds to the growing evidence that Alzheimer's disease of the senile type is not a unitary disorder.

Alzheimer Disease↗
PubMed1984

Stability of neuronal number in the human nucleus basalis of Meynert with age.

Numbers of neurons in the nucleus basalis of Meynert were estimated in seventeen non-demented patients who died of chronic hepatic or cardiopulmonary disease. Neurons were counted at the site of maximal neuronal density (SMND). This site was chosen by reviewing serial sections around the decussation of the anterior commissure and appeared to be comparable in different individuals. No correlation between numbers of neurons and age could be found. It appears that no uniform neuronal loss occurs in the nucleus basalis with age. Taken together with biochemical studies of cerebral cortical choline acetyltransferase activity, these findings suggest that there is no overall change in cholinergic input to cerebral cortex with age.

Adult↗
PubMed1982

Loss of neurons of origin of the adrenergic projection to cerebral cortex (nucleus locus ceruleus) in senile dementia.

To examine the possibility that senile dementia may be associated with a loss of noradrenergic neurons that innervate the cerebral cortex, we used a Quantimet 720 image analyzer to estimate the number of neurons in the nucleus locus ceruleus in elderly patients with the clinical diagnosis of senile dementia. In all but one case, the diagnosis was established histopathologically as senile dementia of the Alzheimer type (SDAT). In a subgroup characterized by a high dementia score and relatively young age at death, there was a loss of about 80% of locus ceruleus neurons. This loss of neurons indicates a deficit of noradrenergic innervation to cerebral cortex in a group of patients which may represent a variant of SDAT.

Adrenergic Fibers↗
PubMed1981

Quantitative computed tomography in senile dementia.

Mean computed tomography (CT) numbers or Hounsfield units (HU) were computed in 15 regions of the brain in routine CT scans of 25 patients with senile dementia and 29 normal community volunteer controls. Mean HU values were significantly lower bilaterally in the medial temporal lobe, anterior frontal lobe, and head of the caudate in the group of patients with senile dementia. There was no correlation between mean HU values and age, and covariate analysis showed that the differences between patients and controls were not attributable to the size of the ventricles. These data suggest that the determination of mean HU values from selected technically suitable regions of CT scans of the brain may have clinical applications of the diagnosis of senile dementia and provide a reliable means of monitoring changes in brain tissue density during the course of senile dementia.

Aged↗
PubMed1980

Compensatory loss of axosomatic synapses in the dentate gyrus of the senescent rat.

A portentous reorganization of the dentate gyrus occurs characteristically in senescent rats. This reorganization includes atrophy of dendrites, hypertrophy of astrocytes and a 27% loss of axodendritic synapses in the molecular layer of the dentate gyrus. A coincident loss of axosomatic synapses is now reported. These synapses on granule cell somata were counted in electron micrographs of representative coronal sections through the dentate gyri of five 3-month-old and five 25-month-old Fischer-344 male rats. A 15% decrease in the number of axosomatic synapses per 100 micron length of granule cell plasma membrane and a 22% decrease in the amount of neuronal surface covered by synapses were found in the senescent, as compared with the young adult, animals. These differences were statistically significant. As synapses on granule cell somata are inhibitory terminals of GABAergic interneurons it is suggested that their loss in senescence may be compensatory for the loss of axodendritic synapses, which are excitatory. By means of a compensatory loss of synapses it may be possible for the aging animal to maintain a reasonably adaptive level of function in spite of ongoing changes in the level of granule cell excitation resulting from the reorganization of the dentate gyrus in senescence.

Adaptation, Physiological↗
PubMed1979

Synaptic atrophy in the senescent hippocampus.

Quantitative analyses of electron micrographs have shown a decrease in the number of synapses in the dentate gyrus of the senescent Fischer-344 rat. The loss of synapses, involving both dendritic spines and shafts and axon terminals of more than one population of presynaptic neurons, did not depend upon the antecedent loss of postsynaptic neurons or their dendrites. These findings suggest that the age-related loss of synapses in the dentate gyrus may depend upon an inability of presynaptic elements to maintain the structural integrity of synapses in senescence. It is proposed that a change in the glycoprotein component of presynaptic plasma membranes resulting from a deficiency in axonal transport mechanisms in the septo-hippocampal pathway may underly this presynaptic malfunction. The resulting partial deafferentation of neurons in the dentate gyrus in senescence appears to be associated with a secondary atrophy of dendrites, which results in a loss of postsynaptic membranes before a loss of postsynaptic neurons can be documented.

Aging↗
PubMed1979

Loss of synapses in the cerebellar cortex of the senescent rat.

Numbers of synapses were compared in the cerebellar cortex of adult (12 months of age) and senescent (25 months of age) male rats of the Fisher-344 strain. The total number of axodendritic synapses was found to be 24% lower in the senescent rats as compared with adults. A differential analysis of synapses involving dendritic shafts and spines showed no significant change in numbers of synapses involving shafts, but a highly sigificant 33% decrease in numbers involving spines in senescent rats. These data suggest that the selective age-related loss of synapses involving dendritic spines (but not shafts) in the cerebellar cortex results from the impairment with advanced age of specific afferent neurons and/or a selective age-related vulnerability of dendritic spines.

Aging↗
PubMed1978

Dendritic atrophy in the dentate gyrus of the senescent rat.

Quantitative electron microscopic analysis of the supragranular zone of the dentate gyrus molecular layer has shown that the number, volume fraction and surface area of dendritic shaft profiles are significantly decreased in senescent rats, relative to young adults. These modifications of dendritic morphology, which are not associated with age-related changes in dimensions of the molecular layer or in numbers of granule cells, may result from a decrease in the number and/or length of dendrites. In either case, the decreases in the number, volume fraction and surface area of dendritic shaft profiles found in the dentate gyrus of senescent rats signify an age-related atrophy of dendrites. Comparison of changes in the number and volume fraction of dendritic shaft profiles has demonstrated that age-related dendritic atrophy involves predominantly dendritic branches.

Aging↗
PubMed1978

Hypertrophy of astroglial processes in the dentate gyrus of the senescent rat.

Quantitative electron microscopic analysis of the supragranular zone of the dentate gyrus molecular layer has shown that the number and volume fraction of profiles of astroglial processes are significantly increased in senescent rat relative to young adults. These ultrastructural modifications, which are not associated with significant age-related changes in the number of astrocytes or in the width of the molecular layer, may result from a formation of new astroglial processes and/or elongation of existing ones. In either case, the increase in the number and volume fraction of astroglial process profiles is an indicator of age-related astroglial hypertrophy. Hypertrophy of astroglial procecesses, which seems to develop with advanced age as a response to partial deafferentation of neurons, may compensate for a decrease in the dendritic volume fraction, thereby preventing changes in the dimensions of the dentate gyrus molecular layer in senescence.

Aging↗
PubMed1977

Age-related change in the neuronal microenvironment: penetration of ruthenium red into extracellular space of brain in young adult and senescent rats.

The volume of the extracellular space, which contributes to the microenvironment of neurons, is diminished in the brains of senescent (as compared to adult) rats and an age-related change in its composition has been hypothesized. To test this hypothesis we have compared the penetration of ruthenium red, a polyanion selectively distributed in the extracellular space, into the dentate gyri of young adult and senescent Fischer 344 rats. Slices of hoppocampal formation were fixed by immersion, first in a glutaraldehyde solution containing ruthenium red, then in a solution of osmium tetroxide containind examined by electron microscopy. Dense particles of ruthenium red reaction product were readily localized in intercellular channels and synaptic clefts and the depth of penetration of ruthenium red in 25-month-old rats, as compared with 3-month-old animals, was found. These data indicate an age-related change in the charge density of the intercellular channels in the dentate gyrus of 25-month-old rats. They suggest a primary age-related change in the charg density of extracellular macromoledules, presumed to be primarily glycosaminoglycans, with a consequent change in water binding capacity and volume of the extracellular space.

Aging↗
PubMed1977

Age related differences in binding of concanavalin A to plasma membranes of isolated neurons.

Neurons isolated from the lateral vestibular nucleus of young adult and senescent Fischer-344 rats were incubated with fluorescamine-labelled Concanavalin A (fl-Con A) alone, or following incubation in trypsin or Vibrio cholerae neuraminidase. They were then observed and photographed. Microdensitometric analysis of fluorescence micrographs showed that senescent rat neurons were significantly more fluorescent than those from young adult rats. Additionally, either patches or caps of fl-Con A were seen on the surface of neurons from senescent rats, while most young adult rat neurons bound fl-Con A uniformly. Pretreatment with trypsin or neuraminidase had no effect on the amount of fluorescence on the surface of senescent rat neurons, and only a slight effect on the surface distribution. Trypsin and neuronal plasma membranes of young adult rats and a rearrangement of the binding pattern in the majority of neurons observed.

Aging↗
PubMed1976

Loss of synapses in the dentate gyrus of the senescent rat.

Synapses were counted in electron micrographs of the middle third of the molecular layer of the dentate gyrus of Fischer 344 rats, 3 months and 25 months of age. A 27% decrease in the number of synapses was found in senescent animals compared with young adults. This loss of synapses could not be correlated with changes in synaptic size. tissue volume or number of postsynaptic granule cells.

Aging↗