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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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Journal ArticleDOI
TL;DR: The data indicate that the co-occurrence of aging-associated neuropathologies with reduced quantitative susceptibility mapping measures of cortical iron load constitutes a lower vulnerability to cognitive loss.

17 citations

Journal ArticleDOI
TL;DR: The present synopsis of recent studies at the molecular, cellular, and functional levels emphasizes the idea that the normal aging brain should be viewed as an example of adaptation and plasticity rather than as an obligatory decline.
Abstract: Tissues and organs change over time, regulated by intrinsic (genetic) determinants and environmental (and microenvironmental) adaptation. Brain changes during lifetime are especially critical, as the brain is the effector of cognition and the vast majority of neurons live throughout the life of the individual. In addition, brain aging mechanisms are especially critical for disease vulnerability, given the aging­related prevalence of pathologies that include neurodegenerative diseases. In this context, the present contribution concisely highlights data yielded by recent trends of research on the normal aging brain, and specifically: the occurrence of synaptic changes (rather than neuronal loss) and the altered regulation of adult neurogenesis (which represents a novel exciting field of knowledge); the development of a low­grade chronic inflammatory state which primes glial cells and may lead to changes in intercellular crosstalk, thus playing a potential role in the brain susceptibility to neurodegeneration; changes occurring in state­dependent behavior, sleep and wake, which are products of global brain functioning and underlie consciousness and cognitive performance; changes in the biological clock, the hypothalamic suprachiasmatic nucleus, which regulates sleep­wake alternation and other endogenous rhythms. Altogether, the present synopsis of recent studies at the molecular, cellular, and functional levels emphasizes the idea that the normal aging brain should be viewed as an example of adaptation and plasticity rather than as an obligatory decline.

17 citations

Journal ArticleDOI
TL;DR: An overview of AN in the SVZ-OB and olfactory epithelium in mice and humans is presented followed by a comprehensive update of the distinct roles played by cell cycle proteins including major tumors suppressor genes in various steps during neurogenesis to provide a novel approach to the modeling of neurodegenerative diseases in humans.
Abstract: Adult neurogenesis (AN) is an ongoing developmental process that generates newborn neurons in the olfactory bulb (OB) and the hippocampus (Hi) throughout life and significantly contributes to brain plasticity. Adult neural stem and progenitor cells (aNSPCs) are relatively limited in number and fate and are spatially restricted to the subventricular zone (SVZ) and the subgranular zone (SGZ). During AN, the distinct roles played by cell cycle proteins extend beyond cell cycle control and constitute key regulatory mechanisms involved in neuronal maturation and survival. Importantly, aberrant cell cycle re-entry (CCE) in post-mitotic neurons has been strongly linked to the abnormal pathophysiology in rodent models of neurodegenerative diseases with potential implications on the etiology and progression of such diseases in humans. Here, we present an overview of AN in the SVZ-OB and olfactory epithelium (OE) in mice and humans followed by a comprehensive update of the distinct roles played by cell cycle proteins including major tumors suppressor genes in various steps during neurogenesis. We also discuss accumulating evidence underlining a strong link between abnormal cell cycle control, olfactory dysfunction and neurodegeneration in the adult and aging brain. We emphasize that: (1) CCE in post-mitotic neurons due to loss of cell cycle suppression and/or age-related insults as well as DNA damage can anticipate the development of neurodegenerative lesions and protein aggregates, (2) the age-related decline in SVZ and OE neurogenesis is associated with compensatory pro-survival mechanisms in the aging OB which are interestingly similar to those detected in Alzheimer's disease and Parkinson's disease in humans, and (3) the OB represents a well suitable model to study the early manifestation of age-related defects that may eventually progress into the formation of neurodegenerative lesions and, possibly, spread to the rest of the brain. Such findings may provide a novel approach to the modeling of neurodegenerative diseases in humans from early detection to progression and treatment as well.

16 citations

Book
01 Jan 2006
TL;DR: The aim of this work was to clarify the role of reorganization in the development of cortical plasticity in the aging brain and to propose novel cell therapy approaches for brain repair.
Abstract: I Basis for Cortical Re-Wiring Visual activity and cortical rewiring: activity-dependent plasticity of cortical networks II Molecular Basis for Signaling in CNS and Memory TrkB mediated excitatory synaptogenesis Signal transduction mechanisms in memory disorders III The Aging Brain Altered brain activity in healthy seniors: what does it mean? Cortical re-organization in the aging brain Brain plasticity and functional losses in the aged: scientific bases for a novel intervention Cortical plasticity and rehabilitation Neural mechanisms of prefrontal cortical function: implications for cognitive rehabilitation IV Brain Injury Recovery from aphasia following brain injury: the role of reorganization Relocation of specific visual functions following damage of mature posterior parietal cortex A SPECT study of language and brain reorganization three years after pediatric brain injury Activation of neural stem and progenitor cells after injury Cognitive neural plasticity during learning and recovery from brain damage Novel cell therapy approaches for brain repair Recovery of motor function after stroke V Spinal Cord Functional plasticity following spinal cord lesions The education and re-education of the spinal cord VI Prostheses and Plasticity Cochlear implants: cortical plasticity in congenital deprivation Disrupting the brain to guide plasticity and improve behavior VII Pain and Tinnitus Plasticity in brain processing and modulation of pain Plasticity of pain-related neuronal activity in the human thalamus Neural platicity in Tinnitus

16 citations

Journal ArticleDOI
TL;DR: Significant age‐related changes in the expression of several proteins that play critical roles in the proliferation and survival of neural stem/progenitor cells in the SVZ are found and likely underlie the diminishing proliferative capacity of stem/ Progenitor Cells in the aging brain.
Abstract: In the mammalian central nervous system, generation of new neurons persists in the subventricular zone (SVZ) throughout life. However, the capacity for neurogenesis in this region declines with aging. Recent studies have examined the degree of these age-related neurogenic declines and the changes of cytoarchitecture of the SVZ with aging. However, little is known about the molecular changes in the SVZ with aging. In this study, we dissected the SVZs from rats aged postnatal day 28, 3 months, and 24 months. The SVZ tissues were processed for 2-D gel electrophoresis to identify protein changes following aging. Protein spots were subsequently subjected to mass spectrometry analysis to compare age-related alterations in the SVZ proteome. We also examined the level of cell proliferation in the SVZ in animals of these three age groups by using bromodeoxyuridine labeling. We found significant age-related changes in the expression of several proteins that play critical roles in the proliferation and survival of neural stem/progenitor cells in the SVZ. Among these proteins, glial fibrillary acidic protein, ubiquitin carboxy terminal hydrolase 1, glutathione S-transferase omega, and preproalbumin were increased with aging, whereas collapsin response-mediated protein 4 (CRMP-4), CRMP-5, and microsomal protease ER60 exhibited declines with aging. We have also observed a significant decline of neural stem/progenitor cell proliferation in the SVZ with aging. These alterations in protein expression in the SVZ with aging likely underlie the diminishing proliferative capacity of stem/progenitor cells in the aging brain.

16 citations


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