2021
DOI: 10.15252/embj.2021109067
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Inactive variants of death receptor p75 NTR reduce Alzheimer’s neuropathology by interfering with APP internalization

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Cited by 11 publications
(7 citation statements)
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“…p75 NTR can bind APP to enable APP trafficking to the endosomal compartment. Hence, in AD mouse models, removal of p75 NTR or disruption of its internalization substantially lowers amyloidogenic processing, Aβ levels, and reduces cognitive decline [78,79]. p75 NTR also promotes amyloid-induced neuritic dystrophy [80], while soluble ectodomain of p75 NTR is neuroprotective against Aβ [73].…”
Section: Ad As Imbalance Between Neurodegeneration and Neuroprotectionmentioning
confidence: 99%
“…p75 NTR can bind APP to enable APP trafficking to the endosomal compartment. Hence, in AD mouse models, removal of p75 NTR or disruption of its internalization substantially lowers amyloidogenic processing, Aβ levels, and reduces cognitive decline [78,79]. p75 NTR also promotes amyloid-induced neuritic dystrophy [80], while soluble ectodomain of p75 NTR is neuroprotective against Aβ [73].…”
Section: Ad As Imbalance Between Neurodegeneration and Neuroprotectionmentioning
confidence: 99%
“…Nevertheless, the structural mechanism of the interaction between these two receptors is completely unknown. Very recently, it was reported that p75 NTR can interact with APP at the plasma membrane and regulate APP internalization and amyloidogenic processing ( Yi et al, 2021 ). Although p75 NTR has a lower affinity for APP than DR6, it is tempting to speculate that p75 NTR , DR6, and the ectodomain of APP could assemble into a tripartite or even larger oligomeric complex to initiate downstream signaling pathways or undergo complex internalization in neuronal cells.…”
Section: Dr6 Signaling Pathwaymentioning
confidence: 99%
“…Neuroinflammation-and immune-related pathways represent major genetic risk factors for AD. ABCA7, BIN1, CR1, SORL1 [6], CX3CR1 [7], NGFR [8],…”
Section: U N C O R R E C T E D a U T H O R P R O O Fmentioning
confidence: 99%
“…Differential methylation levels of specific genes among individuals can be used to explore interactions between genetic and environmental effects on diseases Few studies have focused on the relationship between the methylation of multiple immune-related genes and AD, as well as mild cognitive impairment (MCI). In this study, we concentrated on differential methylation in the promoter regions of seven immune-related AD risk genes: CX3CR1, ABCA7, NGFR, LRRK2, TARDBP, CNR1, and CSF1 R. These genes either act as members of molecular networks involved in microglial activation [22,23], regulation [24], phagocytosis [25], apoptosis [8,[26][27][28], or as signaling molecules for microglia and neurons [7,29], and participate in the neuroinflam-92 matory mechanism of AD, ultimately regulating the maintenance of independent activities of daily living, 126 with a normal ADL score; 4) diagnostic criteria for 127 dementia have not been met. The exclusion criteria units) were used to collect 3-5 ml of whole blood 176 from the elbow vein of the participants.…”
Section: U N C O R R E C T E D a U T H O R P R O O Fmentioning
confidence: 99%