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Showing papers on "Aging brain published in 1988"


Journal ArticleDOI
TL;DR: Since approximately half of the elderly population exhibits only negligible brain alterations, MR imaging may facilitate the distinction between usual (no neurologic dysfunction) and successful (no brain or vascular changes) aging.
Abstract: A thorough knowledge of the normal changes that occur in the brain with age is critical before abnormal findings are analyzed. Magnetic resonance (MR) imaging improves the ability to distinguish normal and abnormal findings in the brain. The major changes that may occur in elderly individuals without neurologic deficits include enlargement of the ventricles, cortical sulci, and vermian subarachnoid spaces; multifocal areas of hyperintensity in the white matter and basal ganglia; a progressive prominence of hypointensity on T2-weighted images of the putamen, almost equal to that of the globus pallidus; an increase in the oxygen extraction ratio with normal or mildly decreased neuron metabolism; arteriosclerosis in large and small arteries and amyloid angiopathy in leptomeningeal cortical vessels; and decreased dopamine receptor binding in the corpus striatum. Since approximately half of the elderly population exhibits only negligible brain alterations, MR imaging may facilitate the distinction between usua...

251 citations


Journal ArticleDOI
TL;DR: It is concluded that neuron numbers and sizes may show similar age-related changes in human and animal brains only for sharply defined brain regions, animal species and/or strains, and age ranges.

249 citations


Journal ArticleDOI
TL;DR: The preliminary data suggest that the density of plaques may be related to poor behavioral performance in some aged monkeys, however, behavioral decline begins before the appearance of significant numbers of senile plaques, suggesting that other factors may interfere with cognition.

122 citations


Journal ArticleDOI
TL;DR: Hastened tapping in the elderly supports the hypothesis that Parkinson's disease is a model for premature aging and represents an extrapyramidal motor dysfunction due to the neuroanatomical and neurochemical changes in the nigro-striatal system of the aging brain.
Abstract: A total of 137 healthy participants aged from 20 to 79 years, including 59 over 60 years, were examined using a finger-tapping test. The test requested the participant to respond synchronously with the right middle finger to a periodic sound train with frequencies of 1, 2, 3, 4, and 5 Hz (cycles/sec). Difficulty keeping the rhythmic movement at a given rate was found to be a characteristic of aging. For the participants over 30 years, the mean rate of tapping deviated towards a faster rate for the stimulus frequency at 4 or 5 Hz (hastened tap, HT). The percentage of the participants who exhibited HT increased with decade of age; 0(20s), 11(30s), 13(40s), 17(50s), 30(60s) and 29(70s). HT in aging appears similar to hastened tapping which is typically observed in patients with Parkinson's disease and may be related to extrapyramidal dysfunction. Hastened tapping in the elderly supports the hypothesis that Parkinson's disease is a model for premature aging, suggesting that HT in aging represents an extrapyramidal motor dysfunction due to the neuroanatomical and neurochemical changes in the nigro-striatal system of the aging brain.

40 citations


Journal ArticleDOI
TL;DR: The data indicate that ACTH levels are significantly reduced both in ATD and MID patients, while beta-EP and beta-LPH are significantly reducing only in ATd.
Abstract: We evaluated the CSF levels of β-lipotropin (β-LPH), β-endorphin (β-EP) and ACTH, which are three neuropeptides expressed by the same gene encoding for pro-opiomelanocortin, in various groups of demen

15 citations


Book ChapterDOI
01 Jan 1988
TL;DR: The view taken here is that the plastic capacity of the developing brain does not suddenly cease as some developmental landmark is reached but that some degree of residual plasticity is maintained to the end of the developmental continuum (death).
Abstract: The plastic capacities of the developing brain are well known, and it is the young brain that usually is emphasized when considering neuronal plasticity. The view taken here is that the plastic capacity of the developing brain does not suddenly cease as some developmental landmark is reached but that some degree of residual plasticity is maintained to the end of the developmental continuum (death). Functionally, this residual plasticity may be manifested in a variety of ways, including (1) recovery from strokes and lesions and (2) compensatory responses to the degenerative phenomena of the aging brain. We define neuronal “plasticity” as the adaptive response(s) of neurons to perturbations in their local environment. The perturbations may be in the chemical composition of the neuron’s immediate surround, its afferent supply, its targets, or in its neighboring neurons and glia. The plastic response(s) to such perturbations may include alteration in dendritic and/or axonal morphology, in synapses, receptors, metabolism, even in genetic expression (e.g., Black et al., 1984: Davis et al., 1986).

13 citations


Journal ArticleDOI
TL;DR: Chemical alterations noted both in frontal lobe and in cerebellum were an increase in lysophosphatidylcholine content and a marked decrease in myelin yield, which seem to be a sign of aging and are not connected with atrophy of the Alzheimer type.
Abstract: The studies were performed on autopsy material of 18 patients who died between the ages of 70-89 y, and of 5 patients who died between 23-44 ys of age. White matter of the frontal lobe and of oerebellum was submitted for histological and biochemical analysis. The neuropathological data provided a rationale for dividing the material into two subgroups: one including patients mainly with vascular changes in the brain, and the other consisting of patients with senile atrophy of the Alzheimer type. Chemical alterations noted both in frontal lobe and in cerebellum were an increase in lysophosphatidylcholine content and a marked decrease in myelin yield. Additionally, in cerebellum a decrease in sulphatide content was observed. The chemical results were almost identical in the two subgroups of patients, although they differ in neuropathological patterns of lesions. It is emphasized that the general decrease in myelin yield as well as some minor changes in myelin lipid pattern seem to be a sign of aging and are not connected with atrophy of the Alzheimer type.

8 citations


Journal ArticleDOI
TL;DR: In addition to selectively facilitating transport between blood and brain, the BBB appears to carry out other functions that may be disturbed in the aging brain, but it is not understood well enough to draw any conclusions as yet.

3 citations



Journal ArticleDOI
TL;DR: This study deals with a correlation of cerebral circulation with intellectual impairment in subjects with aging brain syndrome and with measuring the effect of vinpocetine on cerebral circulation, using the Doppler technique.
Abstract: The Doppler ultrasonic technique is useful for the examination of cerebral circulation as well as for the evaluation of cerebral circulation-improving drugs. This study deals with a correlation of cerebral circulation with intellectual impairment in subjects with aging brain syndrome and with measuring the effect of vinpocetine on cerebral circulation, using the Doppler technique. The correlatiion between cerebral circulation and intellectual impairment was first studied in 48 patients with aging brain and intellectual impairment. As a parameter for cerebral ciruclation, the Continuous Index (CI), as calculated from the blood flow pattern recorded at the internal carotid artery, was used together with Hasegawa's Dementia Scale (HDS) for intellectual impairment. Second, blood flow change of the internal carotid and vertebral artery was measured after a single oral dose of 5 mg vinpocetine and after multiple oral doses of 5 mg vinpocetine three times daily for 7 days in six patients with aging brain. The mean correlation coefficient (r) between CI and HDS was 0.391 (P < 0.01) in 48 patients. It was 0.612 (P < 0.01) in 27 patients with moderate to severe intellectual impairment, 0.735 (P < 0.01) in 14 patients with vascular type impairment, and 0.443 (not significant) in 10 patients with the Alzheimer type. The results suggest some correlation between cerebral circulation and intellectual impairment in the aging brain, especially in patients with the vascular type. An increase of blood flow was recognizable after a single oral dose of 5 mg vinpocetine and was more conspicuous after multiple oral doses. Thus, the effect of vinpocetine in improving cerebral circulation was evident, suggesting its clinical efficacy in improving intellectual impairment in patients with aging brain.

2 citations



Journal ArticleDOI
TL;DR: The major pathological changes of the aging brain affect the cerebral hemispheres grossly as mentioned in this paper, including a decrease in the number and size of neurons in selected areas of the brain, and an increase in the volume of parenchyma and a concomitant enlargement of the ventricles.
Abstract: The major pathological changes of the aging brain affect the cerebral hemispheres grossly. There is a decrease in the volume of the parenchyma and a concomitant enlargement of the ventricles. A decrease in the number and size of the neurons is observed in selected areas – superior frontal, superior temporal, precentral and striatum. In addition, intracellular accumulation of lipofuscin qualitative changes is the dendritic trees and formation of the so called senile plaques, are also prominent features. Other characteristic abnormalities include Alzheimer’s neurofibrillary tangles, granulovacuolar degeneration and Hirano bodies. The typical microscopical appearance, the localization and pathogenesis are briefly reviewed. Accumulation off an amyloid – like substance in the small cerebral vessels – Congophilic Angiopathy – may be the cause of repeated lobar haematomas. These abnormalities are part of the «normal» aging process of the brain. They are also encountered, although in a much more pronounced fashion, in cases of senile dementia. The cellular changes are accompanied by alteration of the cerebral neurotransmitters and a correlation between these and the clinical picture may sometimes be established. The extrapyramidal signs are probably due to a decrease of striatal dopamine levels. It has been suggested that the memory troubles are caused by decrease activity of acetylcholine while reduction of noradrenaline and serotonine are considered responsible for the sleep changes. The various theories of aging are reviewed, and the importance of genetic factors is stressed.