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: Modulation of the n DNA damage response by stimulation of nDNA repair processes, or by elimination of neurons with a high amount of unrepaired nDNA damage in the aging brain, may lead to a functional improvement in networks of these types of neurons and to a better functioning of the agingbrain in general.
55 citations
TL;DR: This chapter reviews how inflammation is triggered in PD and which place it occupies in the sequence of events that ultimately leads to the demise of dopaminergic neurons.
Abstract: Publisher Summary Parkinson's disease (PD) is the second most frequent neurodegenerative disorder of the aging brain after Alzheimer's dementia. Its clinical characteristics include resting tremor, slowness of movement, rigidity, and postural instability. This chapter reviews how inflammation is triggered in PD and which place it occupies in the sequence of events that ultimately leads to the demise of dopaminergic neurons. The chapter describes the composition of the inflammatory response in various parkinsonian syndromes, including PD per se as well as in animal models of PD. The potential beneficial and deleterious role of inflammation in PD and how it can be targeted for therapeutic purposes are also reviewed. Inflammation can involve any part of the body, including the brain. In many neurodegenerative diseases, the innate immune cells are activated and produce a variety of inflammatory mediators. There is often T-cell infiltration in affected brain areas in neurodegenerative diseases.
55 citations
TL;DR: Age-induced effects of GPCR signaling via the Gi/o subfamily at the CNS is reviewed, which results in decreased brain functions, impaired neuroregeneration, and increased vulnerability to neuropathologies, such as Alzheimer's and Parkinson diseases.
Abstract: Cells translate extracellular signals to regulate processes such as differentiation, metabolism and proliferation, via transmembranar receptors. G protein-coupled receptors (GPCRs) belong to the largest family of transmembrane receptors, with over 800 members in the human species. Given the variety of key physiological functions regulated by GPCRs, these are main targets of existing drugs. During normal aging, alterations in the expression and activity of GPCRs have been observed. The central nervous system (CNS) is particularly affected by these alterations, which results in decreased brain functions, impaired neuroregeneration, and increased vulnerability to neuropathologies, such as Alzheimer's and Parkinson diseases. GPCRs signal via heterotrimeric G proteins, such as Go, the most abundant heterotrimeric G protein in CNS. We here review age-induced effects of GPCR signaling via the Gi/o subfamily at the CNS. During the aging process, a reduction in protein density is observed for almost half of the Gi/o-coupled GPCRs, particularly in age-vulnerable regions such as the frontal cortex, hippocampus, substantia nigra and striatum. Gi/o levels also tend to decrease with aging, particularly in regions such as the frontal cortex. Alterations in the expression and activity of GPCRs and coupled G proteins result from altered proteostasis, peroxidation of membranar lipids and age-associated neuronal degeneration and death, and have impact on aging hallmarks and age-related neuropathologies. Further, due to oligomerization of GPCRs at the membrane and their cooperative signaling, down-regulation of a specific Gi/o-coupled GPCR may affect signaling and drug targeting of other types/subtypes of GPCRs with which it dimerizes. Gi/o-coupled GPCRs receptorsomes are thus the focus of more effective therapeutic drugs aiming to prevent or revert the decline in brain functions and increased risk of neuropathologies at advanced ages.
55 citations
TL;DR: The possible role of oxidative stress in AD pathogenesis is supported by evaluated membrane fluidity of mitochondria extracted from different areas of normal and AD brains by means of fluorescence polarization technique.
54 citations
TL;DR: The literature on the possible physiological roles of Abeta and its precursor protein AbetaPP during development with special focus on electrophysiological findings is reviewed, suggesting that this putative function can become pathogenic if activated in the aging brain.
Abstract: Pathological hallmarks of Alzheimer's disease (AD) include synaptic and neuronal degeneration and the presence of extracellular deposits of amyloid-beta (Abeta) in senile plaques in the cerebral cortex. Although these brain lesions may be seen also in aged non-demented individuals, the increase in brain Abeta is believed by many to represent the earliest event in the disease process. Accumulating evidence suggests that Abeta, which is highly conserved by evolution, may have an important physiological role in synapse elimination during brain development. An intriguing idea is that this putative function can become pathogenic if activated in the aging brain. Here, we review the literature on the possible physiological roles of Abeta and its precursor protein AbetaPP during development with special focus on electrophysiological findings.
53 citations