Quantitative evidence for selective dendritic growth in normal human aging but not in senile dementia

Buell, Stephen J.; Coleman, Paul D.

doi:10.1016/0006-8993(81)90436-4

Cited by 210 publications

(65 citation statements)

References 29 publications

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“…The mean (SEM) ages of control and alcoholic groups were 61 (13) years and 60 (10) years respectively. The mean (SEM) postmortem delays (time between death and necropsy) were 26 (9) hours and 24 (10) hours for the control and alcoholic groups respectively.…”

Section: Resultsmentioning

confidence: 99%

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Changes in the basal dendrites of cortical pyramidal cells from alcoholic patients--a quantitative Golgi study.

Harper

Corbett

1990

Journal of Neurology, Neurosurgery & Psychiatry

110

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Although a variety of pathological changes have been described in the brains of chronic alcoholic patients, there have been no studies which have addressed the question of alterations in cortical neuronal dendritic arborisation. Loss of neurons from the superior frontal gyrui and shrinkage of neurons from both the superior frontal gyrus and motor cortex has been documented in chronic alcoholic patients; these areas were chosen for this study. Using a modified rapid Golgi technique the basal dendritic arborisation of layer III pyramidal neurons was compared in 15 male alcoholic patients and 15 age-matched male controls. All parameters measuring basal dendritic arborisation were significantly less in the alcoholic cases for both the superior frontal and motor cortices. Changes in the arbor are in the terminal branches, which is consistent with other models of dendritic plasticity. Such changes may explain both permanent and reversible functional deficits in chronic alcoholic patients. Materials and methodsThe brains of 15 alcoholics and 15 controls were used in this study. These were obtained from necropsies performed in collaboration with the forensic pathologists of the Perth City Coroner's Department. The cases were all males and the controls were matched for age and postmortem delay to the alcoholics. Five of the controls had been teetotal and the remainder drank less than 20 g of alcohol per day. The alcoholic patients drank more than 120 g of alcohol per day. The information to allow categorisation of cases into "control" and "alcoholic" had been obtained from clinical notes available from previous admissions to the teaching hospitals of Perth, the results of detailed questionnaires on alcohol intake and the nutritional state provided by relatives of the deceased, and reports concerning the circumstances of death.Each case had a complete necropsy and microscopic examination of the tissues including the liver and brain. Patients who had a history of, or showed pathological evidence of neurological diseases other than those associated with alcoholism, were excluded. No cases with evidence of brain pathology (for example, infarcts, contusions) were included.

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Section: Resultsmentioning

confidence: 99%

“…The mean (SEM) postmortem delays (time between death and necropsy) were 26 (9) hours and 24 (10) hours for the control and alcoholic groups respectively. There was no significant difference in either of these parameters.…”

Section: Resultsmentioning

confidence: 99%

Changes in the basal dendrites of cortical pyramidal cells from alcoholic patients--a quantitative Golgi study.

Harper

Corbett

1990

Journal of Neurology, Neurosurgery & Psychiatry

110

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“…Neuron size is thought to reflect the extent of the dendritic and axonal arborizations of the cell, as a more extensive cell requires more energy, more protein synthesis and so on, requiring a larger cell body to furnish these. It is therefore no surprise to find that studies of synapses, located mainly, although not exclusively, on dendritic spines in cerebral cortex, have shown overall decreases with age, although the branching patterns of dendrites suggests that there may be compensatory increases in some dendrites to make up for loss of others [35]. A 46% reduction in spine number and density has been reported in humans over 50 years of age [36].…”

Section: Microscopic Brain Changes With Agementioning

confidence: 99%

Ageing and the brain

2007

The Journal of Pathology

176

111

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In this review, the evidence for changes in the human brain with ageing at both the macroscopic and microscopic levels is summarized. Loss of neurons is now recognized to be more modest than initial studies suggested and only affects some neuron populations. Accompanying loss of neurons is some reduction in the size of remaining neurons. This reflects a reduced size of dendritic and axonal arborizations. Some of the likely causes of these changes, including free radical damage resulting from a high rate of oxidative metabolism in neurons, glycation and dysregulation of intracellular calcium homeostasis, are discussed. The roles of genes and environmental factors in causing and responding to ageing changes are explored.

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“…A postmortem comparison of dendrites of layer II pyramidal neurons in the parahippocampal gyrus of adult (aged 51 years) and neurologically healthy aged (80 years) individuals showed that the dendritic trees were longer and more branched in the healthy 80-year-olds. 149 In a population of persons aged 65 years and older, the level of cognitive function is positively related to the frequency and intensity of cognitive activity. 150 However, it has been shown that a head injury in young adulthood, although well compensated for at the time, exacerbates cognitive decline in later years.…”

Section: Age and Plasticitymentioning

confidence: 99%

Brain Plasticity and Stroke Rehabilitation

Johansson

2000

Stroke

485

263

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Abstract-Neuronal connections and cortical maps are continuously remodeled by our experience. Knowledge of the potential capabilityof the brain to compensate for lesions is a prerequisite for optimal stroke rehabilitation strategies. Experimental focal cortical lesions induce changes in adjacent cortex and in the contralateral hemisphere. Neuroimaging studies in stroke patients indicate altered poststroke activation patterns, which suggest some functional reorganization.To what extent functional imaging data correspond to outcome data needs to be evaluated.

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Quantitative evidence for selective dendritic growth in normal human aging but not in senile dementia

Cited by 210 publications

References 29 publications

Changes in the basal dendrites of cortical pyramidal cells from alcoholic patients--a quantitative Golgi study.

Changes in the basal dendrites of cortical pyramidal cells from alcoholic patients--a quantitative Golgi study.

Ageing and the brain

Brain Plasticity and Stroke Rehabilitation

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