Topic
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: The present finding suggests that E2 along with NKB reverse aging and Aβ (25 - 35) induced toxicity as well as AChE and LPO levels.
Abstract: The brain experiences structural, molecular and functional alterations during aging. In aging brain tissue, the oxidative stress increases due to decreased activity of antioxidant enzymes and increased oxidative stress leading to neurodegeneration associated with excitotoxicity. In the present study, we observed the effect of tachykinin neuropeptide Neurokinin B (NKB) and amyloid beta fragment Aβ (25 - 35) on the activity of Acetylcholine esterase (AChE) and Lipid peroxidation (LPO) in brains of 17β estradiol (E2) treated aging female rat synaptosomes of different age groups. An in-vitro incubation of E2 treated brain synaptosomes with Aβ (25 - 35) showed toxic effects on all the parameters. The treatment of NKB and combined NKB and Aβ (25 - 35) increased the AChE enzyme activity and decreased the level of LPO in E2 treated aging rats. The treatment of NKB and combined NKB and Aβ (25 - 35) in a concentration dependent manner reversed the effects of aging and Aβ (25 - 35) on AChE and LPO. The present finding suggests that E2 along with NKB reverse aging and Aβ (25 - 35) induced toxicity as well as AChE and LPO levels. The results of the current study showed a possible beneficial role of NKB with E2 inthe age related neurological diseases.
5 citations
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25 Jan 2019
TL;DR: Cognitive reserve refers to the many ways that neural, cognitive, and psychosocial processes can adapt and change in response to brain aging, damage, or disease, with the overarching effect of preserving cognitive function as discussed by the authors.
Abstract: Cognitive reserve refers to the many ways that neural, cognitive, and psychosocial processes can adapt and change in response to brain aging, damage, or disease, with the overarching effect of preserving cognitive function. Cognitive reserve therefore helps to explain why cognitive abilities in late life vary as dramatically as they do, and why some individuals are brittle to degenerative pathology and others exceptionally resilient. Historically, the term has evolved and at times suffered from vague, circular, and even competing notions. Fortunately, a recent broad consensus process has developed working definitions that resolve many of these issues, and here the evidence is presented in the form of a suggested Framework: Contributors to cognitive reserve, which include environmental exposures that demand new learning and intellectual challenge, genetic factors that remain largely unknown, and putative G × E interactions; mechanisms of cognitive reserve that can be studied at the biological, cognitive, or psychosocial level, with a common theme of plasticity, flexibility, and compensability; and the clinical outcome of (enriched) cognitive reserve that can be summarized as a compression of cognitive morbidity, a relative protection from incident dementia but increased rate of progression and mortality after diagnosis. Cognitive reserve therefore has great potential to address the global challenge of aging societies, yet for this potential to be realized a renewed scientific, clinical, and societal focus will be required.
5 citations
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TL;DR: In this article , the authors describe the transcriptional landscape of young and middle-aged mouse median eminence at single-cell resolution, revealing the common and cell type-specific transcriptional changes with age.
5 citations
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TL;DR: It is shown that age-dependent reduction in neurotransmitter plasticity is robust at 1 and at 3 months but reduced in TH+ neurons at 12 months and completely abolished in both TH+ and SST+ neurons by 18 months, which indicates the importance of studying epigenetic regulation at the circuit level for identified cell phenotypes.
Abstract: Neuroplasticity has classically been understood to arise through changes in synaptic strength or synaptic connectivity. A newly discovered form of neuroplasticity, neurotransmitter switching, involves changes in neurotransmitter identity. Chronic exposure to different photoperiods alters the number of dopamine (tyrosine hydroxylase, TH+) and somatostatin (SST+) neurons in the paraventricular nucleus (PaVN) of the hypothalamus of adult rats and results in discrete behavioral changes. Here we investigate whether photoperiod-induced neurotransmitter switching persists during aging and whether epigenetic mechanisms of histone acetylation and DNA methylation may contribute to this neurotransmitter plasticity. We show that this plasticity is robust at 1 and at 3 months but reduced in TH+ neurons at 12 months and completely abolished in both TH+ and SST+ neurons by 18 months. De novo methylation and histone 3 acetylation were observed following short-day photoperiod exposure in both TH+ and SST+ neurons at 1 and 3 months while an overall increase in methylation of SST+ neurons paralleled neuroplasticity reduction at 12 and 18 months. Histone acetylation increased in TH+ neurons and decreased in SST+ neurons following short-day exposure at 3 months while the total number of acetylated PaVN neurons remained constant. Reciprocal histone acetylation in TH+ and SST+ neurons suggests the importance of studying epigenetic regulation at the circuit level for identified cell phenotypes. The association of age-dependent reduction in neurotransmitter plasticity and changes in DNA methylation and acetylation patterns in two neuronal phenotypes known to switch transmitter identity suggests mechanistic insights into transmitter plasticity in the aging brain. SIGNIFICANCE Neurotransmitter switching, like changes in synaptic strength, formation of new synapses and synapse remodeling, declines with age. This age-dependent reduction in transmitter plasticity is associated with changes in levels of DNA methylase and histone deacetylase that imply epigenetic regulation of transcription. A reciprocal pattern of histone acetylation in a single population of neurons that depends on the transmitter expressed emphasizes the value of studying epigenetic mechanisms at the level of cell phenotypes rather than cell genotypes or whole tissue. The findings may be useful for developing approaches for non-invasive treatment of disorders characterized by neurotransmitter dysfunction.
4 citations
01 Jan 2012
TL;DR: A new hypothesis is proposed that tooth loss and changes in the functionality of teeth may cause brain damage due to recurrent remapping of the brain, and may even be a triggering and aggravating factor in the onset and progression of Alzheime r's disease.
Abstract: Basic biomedical knowledge of the neurobiological mechanisms of the deafferentation o f stomatognathic systems has expanded greatly in recent decades. In both human and animal experimental trials, there are indications that the deafferentation of stomatognathic systems may be a critical factor in triggering and aggravating neurodegenerative diseases. This review explores basic neurobiological mechanisms associated with the deafferentation of stomatognathic systems; further include d is a discussion on tooth loss and other oral-maxillofacial deafferentation (OMFD) mechanisms, with a focus on dental and periodontal apparatus that are associated with brain function and that may underlie the changes observed in the aging brain. A new hypothesis is proposed that tooth loss and changes in the functionality of teeth may cause brain damage due to recurrent remapping of the brain, and may even be a triggering and aggravating factor in the onset and progression of Alzheime r's disease. A growing understanding of the association of OMFD with brain aging may lead to solutions in treating and preventing cognitive decline a nd A lzheime r's disease.
4 citations