2023
DOI: 10.1007/s11010-023-04872-3
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Neuroprotection elicited by taurine in sporadic Alzheimer-like disease: benefits on memory and control of neuroinflammation in the hippocampus of rats

Fernanda Huf,
Jessié Martins Gutierres,
Gabrielle N. da Silva
et al.
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Cited by 6 publications
(6 citation statements)
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“…Taurine has been linked to the mitigation of neuroinflammation in rat models of Alzheimer's disease, where a notable increase in disease markers was observed. It has been identified as a partial agonist of glycine receptors, leading to the reduction of glutamatergic currents and a decrease in pro-inflammatory cytokines such as interleukins [54]). In the realm of neurodegenerative disorders, taurine supplementation has shown efficacy in decreasing the secretion of inflammatory markers including TNFα, IL-1α, IL-1β, IL-6, and IL-17 [35], thereby reducing senescence and extending lifespan.…”
Section: Discussionmentioning
confidence: 99%
See 1 more Smart Citation
“…Taurine has been linked to the mitigation of neuroinflammation in rat models of Alzheimer's disease, where a notable increase in disease markers was observed. It has been identified as a partial agonist of glycine receptors, leading to the reduction of glutamatergic currents and a decrease in pro-inflammatory cytokines such as interleukins [54]). In the realm of neurodegenerative disorders, taurine supplementation has shown efficacy in decreasing the secretion of inflammatory markers including TNFα, IL-1α, IL-1β, IL-6, and IL-17 [35], thereby reducing senescence and extending lifespan.…”
Section: Discussionmentioning
confidence: 99%
“…However, excessive taurine levels in the cerebrospinal fluid can induce cognitive retardation, particularly during sensitive developmental periods. This review examines taurine's role in various cognitive impairments and its effects on cognition in aging, Alzheimer's disease, streptozotocin-induced brain damage [54], ischemia, mental disorders, genetic diseases, and drug/toxin-induced cognitive deficits. Evidence suggests that taurine may enhance cognitive function through diverse mechanisms, underscoring its potential as a therapeutic agent for cognitive disorders [38].…”
Section: Discussionmentioning
confidence: 99%
“…Taurine has been linked to the mitigation of neuroinflammation in rat models of Alzheimer’s disease, where a notable increase in disease markers was observed. It has been identified as a partial agonist of glycine receptors, leading to the reduction of glutamatergic currents and a decrease in pro-inflammatory cytokines such as interleukins [ 71 ]. In the realm of neurodegenerative disorders, taurine supplementation has shown efficacy in decreasing the secretion of inflammatory markers including TNFα, IL-1α, IL-1β, IL-6, and IL-17 [ 23 ], thereby reducing senescence and extending lifespan.…”
Section: Discussionmentioning
confidence: 99%
“…Administration of high doses of taurine in rat models of intracerebral hemorrhage (ICH) has been demonstrated to ameliorate white matter injury and neuronal damage by suppressing inflammatory mediators, glial activation, and neutrophil infiltration while concurrently enhancing CBS expression [ 72 , 73 ]. Huf and co-workers revealed that the effect of taurine supplementation shows promise in alleviating cognitive impairment across diverse conditions and examined taurine’s role in various cognitive impairments and its effects on cognition in aging, Alzheimer’s disease, streptozotocin-induced brain damage, ischemia, mental disorders, genetic diseases, and drug/toxin-induced cognitive deficits [ 71 ]. The evidence suggests that taurine may enhance cognitive function through diverse mechanisms, underscoring its potential as a therapeutic agent for cognitive disorders [ 74 ].…”
Section: Discussionmentioning
confidence: 99%
“…Various animal models are available to study AD characteristics, such as intracerebroventricular streptozotocin administration (ICV-STZ). ICV-STZ is a chemical-induced model of sporadic Alzheimer’s disease that has been extensively explored [ 39 , 40 , 41 ], but the use of STZ in in vitro models has been little explored, especially in astrocytes [ 42 ]. The mechanism by which STZ induces AD is not entirely understood, but it is known that the compound can enter CNS cells via glucose transporter 2 (GLUT2) and interfere with the insulin receptor (IR), compromising the glycogen synthase kinase 3 (GSK3) pathway and affecting the metabolism of Aβ peptide and tau phosphorylation.…”
Section: Introductionmentioning
confidence: 99%