2020
DOI: 10.1016/j.intimp.2020.106354
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RETRACTED: 5-HT1AR alleviates Aβ-induced cognitive decline and neuroinflammation through crosstalk with NF-κB pathway in mice

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Cited by 16 publications
(6 citation statements)
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“…5-HT 1A R is a well-studied member of this subfamily and shows overexpression under Aβ stimulation ( Verdurand et al, 2011 , 2016 ). Treatment with 5-HT 1A R antagonists (e.g., NAD-299 and WAY-100635) has been shown to reduce amyloid plaque deposition, increase levels of hippocampal BDNF, alleviate neuroinflammation and oxidative stress, and improve cognitive deficits in individual animal models of AD ( Afshar et al, 2018 , 2019 ; Wang et al, 2020 ; Table 3 ). These results imply that 5-HT 1A R, in response to specific ligands, is involved in the regulation of AD pathology through multiple pathways.…”
Section: Serotonergic Systemmentioning
confidence: 99%
“…5-HT 1A R is a well-studied member of this subfamily and shows overexpression under Aβ stimulation ( Verdurand et al, 2011 , 2016 ). Treatment with 5-HT 1A R antagonists (e.g., NAD-299 and WAY-100635) has been shown to reduce amyloid plaque deposition, increase levels of hippocampal BDNF, alleviate neuroinflammation and oxidative stress, and improve cognitive deficits in individual animal models of AD ( Afshar et al, 2018 , 2019 ; Wang et al, 2020 ; Table 3 ). These results imply that 5-HT 1A R, in response to specific ligands, is involved in the regulation of AD pathology through multiple pathways.…”
Section: Serotonergic Systemmentioning
confidence: 99%
“…Tβ4 has been implicated as a potential molecular connection. Raising possibility of Tβ4’s relation to inhibition of inflammation can be linked to the high concentrations of Tβ4 found in peripheral macrophages, which shares morphological and other similarities with microglia [ 79 ] and to our previous research confirming that Tβ4 is expressed both in neurons and microglia in AβOs treated 2-month-old C57/BL mice brain [ 80 ]. In human corneal epithelial cell line HCET, Tβ4 was reported to be colocalized with transcription factor RelA/p65 in the cytoplasm [ 81 ], and in the response to TNF-α stimulation, Tβ4 was translocated into the nucleus with p65, and inhibited p65 from binding to the promoter of interleukin [ 82 ], thus exert anti-inflammatory effect via targeting NF-κB p65.…”
Section: Discussionmentioning
confidence: 90%
“…5-HT, when increased by aerobic exercise, can reduce inflammasome activation and alleviate stress induced mitochondrial damage by decreasing calcium overload through the way inhibiting NF-κB/NLRP3 inflammasome initiation [ 62 ] 5-HT secretion has been shown to significantly elevate NF-κB signaling during hypoxia in gut enterochromaffin cells [ 63 ]. In addition, 5-HT1AR inhibitor can decrease levels of TNF-α, GFAP and Iba1 in the hippocampus and inhibit phospho-NF-κB in the hippocampus of Aβ1-42-injected mice [ 64 ]. Thus, our study results are consistent with the above research findings in that the Iba1, GFAP, phospho-NF-κB, and inflammatory cytokines are increased while 5-HT is decreased in the hippocampi of PPD rats.In this study we further expanded the target of SJF on PPD.…”
Section: Discussionmentioning
confidence: 99%