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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: Advances in in-vivo imaging methods are providing the tools for identifying different trajectories of neurocognitive aging, and knowledge about these brain changes may promote opportunities for treatment.
Abstract: Purpose of review Recent research has revealed that the population of older adults is composed not only of individuals who are either healthy or have an age-related disease, most commonly Alzheimer's disease, but also individuals with mild cognitive impairment who are at-risk for or already in the prodromal stage of Alzheimer's disease. These variations in cognitive aging can be related to their neural bases via structural and functional neuroimaging methods. Recent findings Healthy aging appears to primarily affect a frontal-striatal system that undergirds executive control of cognition, while minimally affecting medial temporal lobe structures. Functional imaging studies suggest that enhanced prefrontal engagement may offer compensatory plasticity that minimizes age-related cognitive losses. Mild cognitive impairment appears to affect the entorhinal cortex in particular, with functional consequences in other brain regions. Alzheimer's disease is characterized by severe hippocampal injury, although early-stage Alzheimer's disease may relatively spare some cortical regions. Summary Advances in in-vivo imaging methods are providing the tools for identifying different trajectories of neurocognitive aging, and knowledge about these brain changes may promote opportunities for treatment.

95 citations

Journal ArticleDOI
TL;DR: Alterations in the aging mammalian brain that correlate with a decline in the function of the ubiquitin/proteasome pathway are described and the evidence for age-related changes in specific UPP components are reviewed.
Abstract: Ubiquitinated proteinaceous inclusions are the hallmark of many neurodegenerative diseases. Inefficient proteolysis might lead to the accumulation and ultimate deposition of potentially toxic entities as inclusions within neurons or glial cells. This hypothesis is supported by genetic evidence both from patient populations and from engineered mutations in genes that encode ubiquitin/proteasome components in mice. The appearance of similar inclusions in the brains of elderly individuals of normal and subclinical conditions begs the question of whether there is a general age-related decline in the ability of the ubiquitin/proteasome pathway (UPP) to recognize and eliminate abnormal proteins, and whether such a decline would be reflected by changes in the abundance or activity of some or all components of the UPP. Here we describe alterations in the aging mammalian brain that correlate with a decline in the function of the UPP and review the evidence for age-related changes in specific UPP components. These alterations are discussed within the context of prevalent theories of aging.

95 citations

Journal ArticleDOI
TL;DR: The results of this study suggest that protein carbonyl formation is both a sensitive and a specific marker of brain aging, and decreased nitrotyrosine levels in old rats, in contradiction to the expected, may be due to mechanisms other than oxidative protein damage in the aging rat brain.

95 citations

Journal ArticleDOI
TL;DR: Functional MEG and structural MRI findings shows regionally specific changes due to maturation and may thus be informative for understanding physiological processes of neural development, maturation, and age‐related decline.
Abstract: The gamma band response is thought to be a key neural signature of information processing in the mammalian brain, yet little is known about how age-related maturation influences the γ-band response. Recent MRI-based studies have shown that brain maturation is accompanied by clear structural changes in both gray and white matter, yet the correspondence of these changes to brain function is unclear. The objective of this study was to relate visual cortex (V1) γ-band responses to age-related structural change. We evaluated MEG measured γ-band responses to contrast gratings stimuli and structural MRIs from participants observed from two separate research centers (MEG lab at CUBRIC, Cardiff University, UK, and the Lurie Family Foundations MEG Imaging Center, (CHOP) at the Children's Hospital of Philadelphia). Pooled participant data (N = 59) ranged in age from 8.7 to 45.3 years. We assessed linear associations between age and MEG γ-band frequency and amplitude, as well as between age and MRI volumetric parameters of the occipital lobe. Our MEG findings revealed a significant negative correlation for gamma band frequency versus age. Volumetric brain analysis from the occipital lobe also revealed significant negative correlations between age and the cortical thickness of pericalcarine and cuneus areas. Our functional MEG and structural MRI findings shows regionally specific changes due to maturation and may thus be informative for understanding physiological processes of neural development, maturation, and age-related decline. In addition, this study represents (to our knowledge), the first published demonstration of multicenter data sharing across MEG centers.

94 citations

Journal ArticleDOI
TL;DR: It is proposed that age‐related astrocytic changes result in reduced VEGF and FGF‐2 signaling, which in turn limits NSC and progenitor cell maintenance and contributes to decreased neurogenesis.
Abstract: Astrocytes secrete growth factors that are both neuroprotective and supportive for the local environment. Identified by glial fibrillary acidic protein (GFAP) expression, astrocytes exhibit heterogeneity in morphology and in expression of phenotypic markers and growth factors throughout different adult brain regions. In adult neurogenic niches, astrocytes secrete vascular endothelial growth factor (VEGF) and fibroblast growth factor-2 (FGF-2) within the neurogenic niche, and are also a source of special GFAP-positive multipotent neural stem cells (NSCs). Normal aging is accompanied by a decline in CNS function and reduced neurogenesis. We asked if a decreased availability of astrocyte-derived factors may contribute to the age-related decline in neurogenesis. Determining alterations of astrocytic activity in the aging brain is crucial for understanding CNS homeostasis in aging and for assessing appropriate therapeutic targets for an aging population. We found region-specific alterations in gene expression of GFAP, VEGF and FGF-2 and their receptors in the aged brain corresponding to changes in astrocytic reactivity, supporting astrocytic heterogeneity and demonstrating a differential aging effect. We found that GFAP-positive NSCs uniquely coexpress both VEGF and its key mitotic receptor Flk-1 in both young and aged hippocampus, indicating a possible autocrine/paracrine signaling mechanism. VEGF expression is lost once NSCs commit to a neuronal fate, but Flk-1-mediated sensitivity to VEGF signaling is maintained. We propose that age-related astrocytic changes result in reduced VEGF and FGF-2 signaling, which in turn limits neural stem cell and progenitor cell maintenance and contributes to decreased neurogenesis.

94 citations


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