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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: It can be concluded that in vivo 1H-MRS can contribute to the knowledge of pathophysiology of AD, giving neurochemical details of both gray and white matter, and the gray matter NAA/ml ratio seems to be able to differentiate normal cerebral aging from Alzheimer's disease.

123 citations

Journal ArticleDOI
TL;DR: The expression of ERα and ERβ mRNAs is differentially modulated in the aging brain and changes are region specific.

123 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: It is shown that SIRT1 expression increases with age, concurrently with increased acetylated p53 levels in all brain regions investigated, and acetylation H3K9 protein expression is increased throughout the brain.
Abstract: Although there are seven mammalian sirtuins (SIRT1-7), little is known about their expression in the aging brain. To characterize the change(s) in mRNA and protein expression of SIRT1-7 and their associated proteins in the brain of "physiologically" aged Wistar rats. We tested mRNA and protein expression levels of rat SIRT1-7, and the levels of associated proteins in the brain using RT-PCR and western blotting. Our data shows that SIRT1 expression increases with age, concurrently with increased acetylated p53 levels in all brain regions investigated. SIRT2 and FOXO3a protein levels increased only in the occipital lobe. SIRT3-5 expression declined significantly in the hippocampus and frontal lobe, associated with increases in superoxide and fatty acid oxidation levels, and acetylated CPS-1 protein expression, and a reduction in MnSOD level. While SIRT6 expression declines significantly with age acetylated H3K9 protein expression is increased throughout the brain. SIRT7 and Pol I protein expression increased in the frontal lobe. This study identifies previously unknown roles for sirtuins in regulating cellular homeostasis and healthy aging.

122 citations

Journal ArticleDOI
TL;DR: Current knowledge of microglia in the aging brain is reviewed and new, unpublished work is presented that further supports the theory that microglial experience an age-related decline in proliferative function as a result of cellular senescence.
Abstract: Neuroinflammation resulting from chronic reactive microgliosis is thought to contribute to age-related neurodegeneration, as well as age-related neurodegenerative diseases, specifically Alzheimer's disease (AD). Support of this theory comes from studies reporting a progressive, age-associated increase in microglia with an activated phenotype. Although the underlying cause(s) of this microglial reactivity is idiopathic, an accepted therapeutic strategy for the treatment of AD is inhibition of microglial activation using anti-inflammatory agents. Although the effectiveness of anti-inflammatory treatment for AD remains equivocal, microglial inhibition is being tested as a potential treatment for additional neurodegenerative disorders including amyotrophic lateral sclerosis and Parkinson's disease. Given the important and necessary functions of microglia in normal brain, careful evaluation of microglial function in the aged brain is a necessary first step in targeting more precise treatment strategies for aging-related neurodegenerative diseases. Studies from our laboratory have shown multiple age-related changes in microglial morphology and function that are suggestive of cellular senescence. In this manuscript, we review current knowledge of microglia in the aging brain and present new, unpublished work that further supports the theory that microglia experience an age-related decline in proliferative function as a result of cellular senescence.

122 citations


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