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Aging brain

About: Aging brain is a research topic. Over the lifetime, 1255 publications have been published within this topic receiving 66405 citations.


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TL;DR: Understanding mitochondrial function and regulation should be the first line of research to know how neurogenesis is regulated, because melatonin is an endogenous indoleamine take up by the mitochondria; once inside, melatonin promotes energy production and reduces free radical generation, thus preventing mitochondrial damage.
Abstract: Aging is an irreversible process affecting all living organisms. During aging, all organs and tissues of the body reduce their functional capabilities, leading to a progressive loss of physical and cognitive performances. The loss of cells with age is directly related to apoptosis, a mechanism of cell death linked to mitochondrial failure. Attempting to understand the aging process, several theories have been proposed; among them, the mitochondrial free radical theory of aging is the one with more experimental evidence to date. Mitochondria are the source but also the target of these radicals, which produce their age-dependent slow and continuous damage. It is now recognized that mitochondrial impairment underlies not only the aging process but also many other age- associated pathologies, including neurodegenerative diseases, cancer, metabolic alteractions, etc. These diseases, mainly neurodegeneration, share mitochondrial dysfunction, oxidative/nitrosative stress and apoptosis in particular brain areas as a final common pathway. Consequently, neuronal loss may be associated to mitochondrial dysfunction in those disorders. Although the vast majority of cells in the adult brain are generated during the embryonic and early postnatal period, it is now apparent that some proportion of neurogenesis is also happening during adulthood. The functional significance of the adult neurogenesis is not fully understood and recent data point to a role of mitochondria in the process of stem cell differentiation. Thus, understanding mitochondrial function and regulation should be the first line of research to know how neurogenesis is regulated. Melatonin is an endogenous indoleamine take up by the mitochondria; once inside, melatonin promotes energy production and reduces free radical generation, thus preventing mitochondrial damage. These functions of melatonin seem to be related to the neurogenesis promoting role of the indoleamine. The physiological and pathophysiological meanings of these functions of melatonin are also revised here.

6 citations

27 Jun 2018
TL;DR: In this paper, individual differences in visual processing speed are examined in association with the coherence of the brain's spontaneous activity and how this coherence is affected by normal aging, and evidence is presented for an association of a slowed visual processing with decreased coherent activity of a frontoinsular network in healthy aging and simultaneous object perception deficits in patients at risk of Alzheimer's dementia.
Abstract: Either reading a text in the office or looking for an apple in the supermarket, we are continuously flooded with visual stimuli. But how does the human brain support the efficient processing of those stimuli? And, if pathological changes occur in the brain, how do these changes lead to reductions in such efficient processing? In the present dissertation, aging is used as a model to address these two questions. First, individual differences in visual processing speed are examined in association with the coherence of the brain’s spontaneous activity and how this coherence is affected by normal aging. Second, individual differences in visual processing speed are studied in association with behavior in tasks that measure complex visual object perception in patients at risk of Alzheimer’s dementia and healthy aging adults. Based on these two approaches, evidence will be presented for an association of a slowed visual processing with (a) decreased coherent activity of a frontoinsular network in healthy aging and (b) simultaneous object perception deficits in patients at risk of Alzheimer’s dementia. This evidence provides critical insights into the particular link between visual processing speed and the coherence of the brain’s spontaneous activity and reveals perceptual deficits in patients whose clinically most apparent impairments lie in memory.

5 citations

Book
01 Jan 1997
TL;DR: In this article, the Neuronal Cytoskeleton: Changes Associated with Age, Neurodegenerative Disease, and Neural Insult (J.W.Geddes and A.I. Matus).
Abstract: Contents. List of Contributors. Preface (M.P. Mattson and J.W. Geddes). Toward a Cognitive Neuroscience of Normal Aging (P.R. Rapp and M. Gallagher). The Neuronal Cytoskeleton: Changes Associated with Age, Neurodegenerative Disease, and Neuronal Insult (J.W. Geddes and A.I. Matus). Structural Changes in the Aged Brain (D.W. Dickson). Cerebrovascular Changes in the Aging Brain (J.C. de la Torre). Metabolism of the Aging Brain (J.P. Blass, G.E. Gibson, and S. Hoyer). Contribution of Mitochondrial Alterations to Brain Aging (G. Benzi and A. Moretti). Protein Oxidation Processes in Aging Brain (D.A. Butterfield and E.R. Stadtman). Neuroendocrine Aspects of the Aging Brain (P.M. Wise, J.P. Herman, and P.W. Landfield). Changes in Neurotransmitter Signal Transduction Pathways in the Aging Brain (J.F. Kelly and G.S. Roth). Food Restriction and Brain Aging (C.E. Finch and T.E. Morgan). Neurotrophic Factors and the Aging Brain (M.P. Mattson and O. Lindvall). Index.

5 citations

Journal ArticleDOI
TL;DR: In this paper, the effects of caloric restriction, physical exercise and their pharmacological mimetics on synaptic homeostasis and cognitive function were investigated in the animal models of neurodegenerative diseases and autophagy impairment.
Abstract: Enhanced mental and physical activity can have positive effects on the function of aging brain, both in the experimental animals and human patients, although cellular mechanisms underlying these effects are currently unclear. There is a growing evidence that pre-clinical stage of many neurodegenerative diseases involves changes in interactions between astrocytes and neurons. Conversely, astrocytes are strategically positioned to mediate the positive influence of physical activity and diet on neuronal function. Thus, development of therapeutic agents which could improve the astroglia-neuron communications in ageing brain is of crucial importance. Recent advances in studies of cellular mechanisms of brain longevity suggest that astrocyte-neuron communications have a vital role in the beneficial effects of caloric restriction, physical exercise and their pharmacological mimetics on synaptic homeostasis and cognitive function. In particular, our recent data indicate that noradrenaline uptake inhibitor atomoxetine can enhance astrocytic Ca2+-signaling and astroglia-driven modulation of synaptic plasticity. Similar effects were exhibited by caloric restriction-mimetics metformin and resveratrol. The emerged data also suggest that astrocytes could be involved in the modulatory action of caloric restriction and its mimetics on neuronal autophagy. Still, the efficiency of astrocyte-targeting compounds in preventing age-related cognitive decline is yet to be fully explored, in particular in the animal models of neurodegenerative diseases and autophagy impairment.

5 citations

Journal ArticleDOI
TL;DR: Comparative data on epigenetic brain ageing for chimpanzees and humans is added to help understand which aspects of human ageing are evolutionarily conserved or specific to the authors' species, especially given that humans are distinguished by a long lifespan, large brain, and, potentially, more severe neurodegeneration with age.
Abstract: ABSTRACT Epigenetic age has emerged as an important biomarker of biological ageing. It has revealed that some tissues age faster than others, which is vital to understanding the complex phenomenon of ageing and developing effective interventions. Previous studies have demonstrated that humans exhibit heterogeneity in pace of epigenetic ageing among brain structures that are consistent with differences in structural and microanatomical deterioration. Here, we add comparative data on epigenetic brain ageing for chimpanzees, humans’ closest relatives. Such comparisons can further our understanding of which aspects of human ageing are evolutionarily conserved or specific to our species, especially given that humans are distinguished by a long lifespan, large brain, and, potentially, more severe neurodegeneration with age. Specifically, we investigated epigenetic ageing of the dorsolateral prefrontal cortex and cerebellum, of humans and chimpanzees by generating genome-wide CpG methylation data and applying established epigenetic clock algorithms to produce estimates of biological age for these tissues. We found that both species exhibit relatively slow epigenetic ageing in the brain relative to blood. Between brain structures, humans show a faster rate of epigenetic ageing in the dorsolateral prefrontal cortex compared to the cerebellum, which is consistent with previous findings. Chimpanzees, in contrast, show comparable rates of epigenetic ageing in the two brain structures. Greater epigenetic change in the human dorsolateral prefrontal cortex compared to the cerebellum may reflect both the protracted development of this structure in humans and its greater age-related vulnerability to neurodegenerative pathology.

5 citations


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Performance
Metrics
No. of papers in the topic in previous years
YearPapers
202328
202256
202179
202072
201978
201872