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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: The authors' results using common marmoset brain corresponded with the observation that the α-synuclein aggregations were first occurred from olfactory bulb in human normal aged and PD brain, therefore, common Marmoset is expected as useful model for α- synuclein pathology.
7 citations
01 Jan 2017
TL;DR: Findings provide evidence that aerobic exercise could ameliorate learning and memory deficits of aging rats induced by D-gal, which is related to aerobic exercise’ promoting hippocampal BNDF and SYP expression.
Abstract: The aim of this study was to explore the effects of aerobic exercise on learning and memory of aging brain and the underlying potential mechanism. We adopted the method of intraperitoneal administration for 6 weeks to induce aging rat model and gave rats swimming exercise intervention in the process of aging modeling. Then the Morris Water Maze test, immunofluorescence, western blotting and real time PCR technology were adopted to estimate rats’ learning and memory abilities and the expression levels of BDNF and SYP in hippocampus respectively. Compared with the aging model rats induced by D-gal administration, the rats subjected to swimming exercise in the process of aging modeling showed not only faster acquisition and better retention of the maze but also higher expression levels of BDNF and SYP in hippocampus. These findings provide evidence that aerobic exercise could ameliorate learning and memory deficits of aging rats induced by D-gal, which is related to aerobic exercise’ promoting hippocampal BNDF and SYP expression.
7 citations
TL;DR: OCMM reduced amyloid β levels, activated astrocytes, and improved neurotransmission in the aged rat brains, demonstrating the molecular mechanism of OCMM in aged rats.
Abstract: Context In the aging brain, reduction in the pulsation of cerebral vasculature and fluid circulation causes impairment in the fluid exchange between different compartments and lays a foundation for the neuroinflammation that results in Alzheimer disease (AD). The knowledge that lymphatic vessels in the central nervous system play a role in the clearance of brain-derived metabolic waste products opens an unprecedented capability to increase the clearance of macromolecules such as amyloid β proteins. However, currently there is no pharmacologic mechanism available to increase fluid circulation in the aging brain. Objective To demonstrate the influence of an osteopathic cranial manipulative medicine (OCMM) technique, specifically, compression of the fourth ventricle, on spatial memory and changes in substrates associated with mechanisms of metabolic waste clearance in the central nervous system using the naturally aged rat model of AD. Results Significant improvement was found in spatial memory in 6 rats after 7 days of OCMM sessions. Live animal positron emission tomographic imaging and immunoassays revealed that OCMM reduced amyloid β levels, activated astrocytes, and improved neurotransmission in the aged rat brains. Conclusion These findings demonstrate the molecular mechanism of OCMM in aged rats. This study and further investigations will help physicians promote OCMM as an evidence-based adjunctive treatment for patients with AD.
7 citations
TL;DR: In this article, the authors discuss the principles of the nuclear calcium hypothesis in the context of human brain function and its role in controlling diverse forms of neuroadaptation and neuroprotection.
Abstract: Nuclear Ca2+ has emerged as one of the most potent mediators of the dialogue between neuronal synapses and the nucleus that regulates heterochromatin states, transcription factor activity, nuclear morphology and neuronal gene expression induced by synaptic activity. Recent studies underline the importance of nuclear Ca2+ signaling in long-lasting, activity-induced adaptation and maintenance of proper brain function. Diverse forms of neuroadaptation require transient nuclear Ca2+ signaling and cyclic AMP-responsive element-binding protein (CREB1, referred to here as CREB) as its prime target, which works as a tunable switch to drive and modulate specific gene expression profiles associated with memory, pain, addiction and neuroprotection. Furthermore, a reduction of nuclear Ca2+ levels has been shown to be neurotoxic and a causal factor driving the progression of neurodegenerative disorders, as well as affecting neuronal autophagy. Because of its central role in the brain, deficits in nuclear Ca2+ signaling may underlie a continuous loss of neuroprotection in the aging brain, contributing to the pathophysiology of Alzheimer's disease. In this Review, we discuss the principles of the 'nuclear calcium hypothesis' in the context of human brain function and its role in controlling diverse forms of neuroadaptation and neuroprotection. Furthermore, we present the most relevant and promising perspectives for future studies.
7 citations
TL;DR: It is shown that exercise serves as a behavioral intervention to prevent cognitive decline as well as neurodegenerative diseases, and long-term regular exercise in parallel with various learning experiences will be required to prepare successful aging.
Abstract: Arapid increase in the elderly population has raised social awareness for maintaining the health of the elderly and initiated intense research in neurodegenerative diseases. Exercise can improve not only cardiovascular and musculoskeletal fitness, but also suppresses the symptoms of depression and anxiety, suggesting a possible role of exercise in the regulation of brain function. Based on a substantial body of literature, here we introduce the effects of exercise on the structural and functional changes in the aging brain, and also discuss the molecular and cellular effects of exercise and motor learning. Studies show that regular exercise in the elderly promotes neurocognitive function, prevents loss of brain tissue, and reduces the risk for neurodegenerative diseases and brain injury. Although the molecular mechanisms, by which exercise regulates brain function, has not been fully understood, recent cell biological and biochemical studies reveal that exercise increases neurogenesis in the hippocampus, elevates the levels of neurotrophins such as BDNF and IGF-1 to promote the survival of newly generated neurons. Exercise also induces angiogenesis in the motor cortex and cerebellum to enhance delivery of glucose and oxygen to neurons. Furthermore, complex motor skill learning increases the number of synapses to improve cognitive and motor function. Taken together, these findings clearly demonstrate that exercise serves as a behavioral intervention to prevent cognitive decline as well as neurodegenerative diseases. Thus long-term regular exercise in parallel with various learning experiences will be required to prepare successful aging. This study will provide fundamental insights into research in neurodegenerative diseases and a better understanding of the exercise effects in brain function.
7 citations