Non-steroidal anti-inflammatory drugs (NSAIDs) and neuroprotection in the elderly: a view from the mitochondria.
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TLDR
Significant evidence suggests that the prolonged use of non-steroidal anti-inflammatory drugs (NSAIDs) may reduce the incidence of Alzheimer's disease (AD) and protect against the cognitive decline associated to healthy aging in humans.About:
This article is published in Neural Regeneration Research.The article was published on 2015-09-01 and is currently open access. It has received 19 citations till now. The article focuses on the topics: Neuroprotection & Excitotoxicity.read more
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Journal ArticleDOI
Aging and amyloid β oligomers enhance TLR4 expression, LPS-induced Ca2+ responses, and neuron cell death in cultured rat hippocampal neurons.
Maria Calvo-Rodriguez,Carmen de la Fuente,Mónica García-Durillo,Carmen García-Rodríguez,Carlos Villalobos,Lucía Núñez,Lucía Núñez +6 more
TL;DR: Aging and amyloid β oligomers, the neurotoxin involved in Alzheimer’s disease, enhance TLR4 expression as well as LPS-induced Ca2+ responses and neuron cell death in rat hippocampal neurons aged in vitro.
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In vitro aging promotes endoplasmic reticulum (ER)-mitochondria Ca2 + cross talk and loss of store-operated Ca2 + entry (SOCE) in rat hippocampal neurons
TL;DR: This work found that short-term cultured neurons show large SOCE, low Ca2+ store content and no functional coupling between ER and mitochondria, and suggests that neuronal aging is associated to increased ER-mitochondrial cross talking and loss of SOCE.
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Role of serum albumin as a nanoparticulate carrier for nose-to-brain delivery of R-flurbiprofen: implications for the treatment of Alzheimer's disease
Ling Rong Wong,Paul C. Ho +1 more
TL;DR: The potential of serum albumin as nanoparticulate carriers for nose‐to‐brain delivery of R‐FP to improve its brain accumulation is investigated.
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Aging enables Ca2+ overload and apoptosis induced by amyloid-β oligomers in rat hippocampal neurons: Neuroprotection by non-steroidal anti-inflammatory drugs and r-flurbiprofen in aging neurons
TL;DR: Long-term cultures of rat hippocampal neurons, a model of neuronal in vitro aging, are used to investigate the contribution of aging to Ca2+ dishomeostasis and neuron cell death induced by Aβ42 oligomers and to test whether non-steroidal anti-inflammatory drugs (NSAIDs) and R-flurbiprofen prevent apoptosis acting on subcellular Ca2+.
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Quality by Design Based Formulation Study of Meloxicam-Loaded Polymeric Micelles for Intranasal Administration.
Bence Sipos,Piroska Szabó-Révész,Ildikó Csóka,Edina Pallagi,Dorina Gabriella Dobó,Péter Bélteky,Zoltán Kónya,Ágota Deák,László Janovák,Gábor Katona +9 more
TL;DR: The developed formulation resulted in more than 20 times faster MEL dissolution rate and five-fold higher nasal permeability compared to starting MEL, and the prediction of IVIVC confirmed the great potential for in vivo brain distribution of MEL.
References
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Neuroprotection by Aspirin and Sodium Salicylate Through Blockade of NF-κB Activation
TL;DR: At concentrations compatible with amounts in plasma during chronic anti-inflammatory therapy, acetylsalicylic acid and its metabolite sodium salicylate were found to be protective against neurotoxicity elicited by the excitatory amino acid glutamate in rat primary neuronal cultures and hippocampal slices.
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Anti-inflammatory drugs and risk of Alzheimer's disease: an updated systematic review and meta-analysis.
TL;DR: Observational studies support the use of NSAIDs for prevention of AD, but RCT do not; well-designed studies and innovative approaches are required to illuminate the exact relationship between NSAID use and AD risk.
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Mitochondrial Ca2+ overload underlies Aβ oligomers neurotoxicity providing an unexpected mechanism of neuroprotection by NSAIDs
TL;DR: It is found that a series of non-steroidal anti-inflammatory drugs (NSAIDs) including salicylate, sulindac sulfide, indomethacin, ibuprofen and R-flurbiprofen depolarize mitochondria and inhibit mitochondrial Ca2+ overload, cytochrome c release and cell death induced by Aβ oligomers.
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Excitotoxic Calcium Overload in a Subpopulation of Mitochondria Triggers Delayed Death in Hippocampal Neurons
Natalia B. Pivovarova,Huy V. Nguyen,Christine A. Winters,Christine A. Brantner,Carolyn L. Smith,S. Brian Andrews +5 more
TL;DR: A mechanism in which delayed excitotoxic death involves apoptogen release from a subpopulation of calcium-overloaded mitochondria, whereas other, undamaged mitochondria maintain normal function is supported, supported by measured concentrations of total Ca in individual mitochondria.
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Increased vulnerability of hippocampal neurons with age in culture: temporal association with increases in NMDA receptor current, NR2A subunit expression and recruitment of L-type calcium channels.
Lawrence D. Brewer,Olivier Thibault,Jeanise Staton,Veronique Thibault,Justin T. Rogers,Gisela García-Ramos,Susan D. Kraner,Philip W. Landfield,Nada M. Porter +8 more
TL;DR: Enhanced excitotoxic vulnerability with age in culture was associated with a substantial increase in NMDA-R current, concomitant increases in NR2A and NR1 but not NR2B subunit expression, and with apparent recruitment of L-VGCCs into the excitOToxic process.