Free intracellular calcium concentration in the aging brainCalcium homeostasis in aged neurones
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Cited by (73)
The aging mouse brain: cognition, connectivity and calcium
2021, Cell CalciumCitation Excerpt :Taken together, the available evidence in mice does not yield a uniform picture of age-related changes in basal [Ca2+]i. This resembles the lack of agreement in studies involving rats (cf. [308,312,317]). However, recent data suggests that Ca2+ homeostasis impairments might emerge in late adult animals (∼12 m), before the conventional definition of old age [221].
Regulation of intrinsic excitability: Roles for learning and memory, aging and Alzheimer's disease, and genetic diversity
2019, Neurobiology of Learning and MemoryCitation Excerpt :Generally, these currents are initiated upon an increase in intracellular calcium following neuronal activity. However, in both normal aging and AD, Ca2+ homeostasis is disrupted and intracellular Ca2+ concentrations may be elevated (Hölscher, 2005; Khachaturian, 1987; Landfield, 1987; Thibault, Mazzanti, Blalock, Porter, & Landfield, 1995), particularly in cells that are in close proximity to amyloid plaques in AD (Hermes, Eichhoff, & Garaschuk, 2010; Kirischuk & Verkhratsky, 1996). The precise mechanisms underlying Ca2+ dyshomeostasis in aging and AD have not been fully elucidated, though several components that maintain calcium homeostasis are disrupted.
Cellular calcium signaling in the aging brain
2019, Journal of Chemical NeuroanatomyInhibition of PMCA activity by tau as a function of aging and Alzheimer's neuropathology
2015, Biochimica et Biophysica Acta - Molecular Basis of DiseaseCitation Excerpt :Thus, the presence of these tau aggregates, known as neurofibrillary tangles (NFTs), is a hallmark of different tauopathies [4]. Neural aging is also well associated to Ca2+ dyshomeostasis [5–9]. That would involve alteration of Ca2+-mediated signaling pathways that may affect critical activities as membrane excitability, synaptic plasticity or cytoskeleton reorganization [10].
Calcium dysregulation, and lithium treatment to forestall Alzheimer's disease - a merging of hypotheses
2014, Cell CalciumCitation Excerpt :During the past three decades, dysregulated intracellular Ca2+ has been linked to aging, and to Alzheimer's disease [14–16] (for history – see the Annals of the New York Academy of Sciences, Volume 568–1989, Volume 747–1994). Increased intracellular Ca2+ concentrations have been observed in neurons from aging mice and rats [64–67], and in neurons from 3xTg-AD transgenic mice [68]. Presenilins (PSs) are integral membrane proteins that form part of the gamma secretase multimeric enzyme complex that cleaves of APP into Aβ; and PSs are located primarily in the ER, Golgi complex, and the plasma membrane [15].