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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 results in the HT22 cell line indicate that Apo D protein level increases in a concentration-dependent manner specifically at those H2O2 concentrations that caused oxidative damage and apoptotic cell death, which support the idea that oxidative stress-induced apoptosis during aging and AD may be associated with the increment in the expression of ApoD in these situations.
Abstract: Apolipoprotein D (Apo D) is a lipid binding protein whose expression is strongly induced in the mammalian brain during aging and age-dependent neurodegenerative diseases such as Alzheimer's disease (AD), where it can play an important function as a neuroprotective and antioxidant protein. Increasing evidence suggests that the gradual increase in free radicals and oxidative stress with age is the primary determinant to aging brain. The aim of this work is to study the effect of hydrogen peroxide (H2O2) in Apo D expression, in hippocampal cells, in order to investigate the relationship between oxidative stress and elevated levels of Apo D found in hippocampus during aging and AD and also elucidate the possible pathways that lead to this increase. In this study, we demonstrated that Apo D expression in hippocampal neurons of aged and AD brains directly correlates with age-related increase in oxidative stress. More importantly, our results in the HT22 cell line indicate that Apo D protein level increases in a concentration-dependent manner specifically at those H2O2 concentrations that caused oxidative damage and apoptotic cell death. These data support the idea that oxidative stress-induced apoptosis during aging and AD may be associated with the increment in the expression of Apo D in these situations.
34 citations
TL;DR: Human neural stem cells are ideal for ex vivo gene therapy, and may be used in the future as "minipumps" to release GDNF in vivo to protect aging neurons, and delay the effects of aging in the brain, giving a better quality of life.
Abstract: Stem cells have been suggested as a possible "fountain of youth" for replacing tissues lost during aging. In the brain, replacing lost neurons is a challenge, as they have to then be reconnected with their appropriate targets. Perhaps a more realistic and practical strategy for affecting the aging process would be to prevent the loss of neurons from occurring, thus retaining intact circuitry. Glial cell line-derived neurotrophic factor (GDNF) can reverse some aspects of aging in the monkey. Additionally, we have recently shown that GDNF directly infused into the human brain has significant effects on the symptoms of Parkinson disease. Human neural stem cells can be cultured, genetically modified, and transplanted. As such, these cells are ideal for ex vivo gene therapy, and may be used in the future as "minipumps" to release GDNF in vivo to protect aging neurons. Using such an approach could delay the effects of aging in the brain, giving a better quality of life. Stem cells might not be the fountain of youth, but provide a fountain of youth through the release of growth factors such as GDNF.
34 citations
TL;DR: Uric acid could exert a detrimental influence on neuronal biology being this influence further potentiated by the concomitant exposure to neurotoxic stimuli, and is evident for uric acid concentrations close to those achievable in cerebrospinal fluid in presence of mild hyperuricemia thus suggesting a potential role of uric Acid in pathophysiology of cognitive dysfunction.
Abstract: There is still a considerable debate concerning whether uric acid is neuroprotective or neurotoxic agent. To clarify this topic, we tested the effects of uric acid on neuronal cells biology by using differentiated SHSY5Y neuroblastoma cells incubated with amyloid β to reproduce an in vitro model of Alzheimer's disease. The incubation of cells with uric acid at the dose of 40 µM or higher significantly reduced cell viability and potentiated the proapoptotic effect of amyloid β. Finally, uric acid enhanced the generation of 4-hydroxynonenal and the expression of PPARβ/δ promoted by amyloid β, indicating a prooxidant effects. In conclusion, uric acid could exert a detrimental influence on neuronal biology being this influence further potentiated by the concomitant exposure to neurotoxic stimuli. This effect is evident for uric acid concentrations close to those achievable in cerebrospinal fluid in presence of mild hyperuricemia thus suggesting a potential role of uric acid in pathophysiology of cognitive dysfunction. These effects are influenced by the concentrations of uric acid and by the presence of favoring conditions that commonly occur in neurodegenerative disorders and well as in the aging brain, including increased oxidative stress and exposure to amyloid β. J. Cell. Physiol. 232: 1069-1078, 2017. © 2016 Wiley Periodicals, Inc.
34 citations
TL;DR: Results indicate that selenium treatment reverses AD-like memory and neuropsychiatric symptoms by a mechanism involving reduction of aggregated tau and/or reactive astrocytes but not amyloid pathology, and suggest that sodium selenate could be part of a combined therapeutic approach for the treatment of memory and cognitive behavioral symptoms in advanced AD stages.
Abstract: Accumulation of amyloid-β plaques and tau contribute to the pathogenesis of Alzheimer’s disease (AD), but it is unclear whether targeting tau pathology by antioxidants independently of amyloid-β causes beneficial effects on memory and neuropsychiatric symptoms. Selenium, an essential antioxidant element reduced in the aging brain, prevents development of neuropathology in AD transgenic mice at early disease stages. The therapeutic potential of selenium for ameliorating or reversing neuropsychiatric and cognitive behavioral symptoms at late AD stages is largely unknown. Here, we evaluated the effects of chronic dietary sodium selenate supplementation for 4 months in female 3xTg-AD mice at 12–14 months of age. Chronic sodium selenate treatment efficiently reversed hippocampal-dependent learning and memory impairments, and behavior- and neuropsychiatric-like symptoms in old female 3xTg-AD mice. Selenium significantly decreased the number of aggregated tau-positive neurons and astrogliosis, without globally affecting amyloid plaques, in the hippocampus of 3xTg-AD mice. These results indicate that selenium treatment reverses AD-like memory and neuropsychiatric symptoms by a mechanism involving reduction of aggregated tau and/or reactive astrocytes but not amyloid pathology. These results suggest that sodium selenate could be part of a combined therapeutic approach for the treatment of memory and neuropsychiatric symptoms in advanced AD stages.
34 citations
01 Jan 1975
TL;DR: The brain has received increasing attention in neurobiological studies of aging due to its unique role in adaptation to the physical and social environments, and integration of all bodily organs and functions.
Abstract: The brain has received increasing attention in neurobiological studies of aging due to its unique role in adaptation to the physical and social environments, and integration of all bodily organs and functions and because it is composed of neurons and glia that presumably are not replaced after birth throughout the rest of the life span. Such changes as deterioration of sensory processes, decreased mental alertness and loss of fine motor coordination have been noted among old human subjects for many years. Since the brain mediates the environmental input and behavioral adaptation, the functional decline of sensory, cognitive and motor activity with age have been attributed to structural and functional changes in the brain.
34 citations