2020
DOI: 10.1111/jnc.14960
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Sleep deprivation regulates availability of PrPC and Aβ peptides which can impair interaction between PrPC and laminin and neuronal plasticity

Abstract: Abbreviations: 95CI, 95% confidence interval; AD, Alzheimer's disease; APP, amyloid precursor protein; Aβo, amyloid-beta oligomers; BACE1, β-secretase 1; BPTI, bovine pancreatic trypsin inhibitor; CTact, control group of activity period; CTrest, control group of rest period; ERK, extracellular signal-regulated kinases; FBS, fetal bovine serum; LN, laminin; mGLuR1, metabotropic glutamate receptor 1; NMDAR, N-methyl-D-aspartate receptor; PrP C , cellular prion protein; rPrP, recombinant prion protein; RRID, rese… Show more

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Cited by 9 publications
(4 citation statements)
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“…The results suggest that sleep deprivation has a regulatory influence on the levels of PrP c and Aβ peptides. According to the assays, these changes induced by this process may have adverse effects on the interaction between laminin and PrP c , a relationship known for its involvement in neuronal plasticity [ 112 ].…”
Section: The Function Of the Prion Protein (Prp C ...mentioning
confidence: 99%
“…The results suggest that sleep deprivation has a regulatory influence on the levels of PrP c and Aβ peptides. According to the assays, these changes induced by this process may have adverse effects on the interaction between laminin and PrP c , a relationship known for its involvement in neuronal plasticity [ 112 ].…”
Section: The Function Of the Prion Protein (Prp C ...mentioning
confidence: 99%
“…However, the longer Aβ oligomers induce sleep through a pharmacologically tractable prion protein (PrP) signaling cascade . SD might disrupt the binding between PrP and laminin, which leads to accumulation of Aβ and low cognitive performance . Among the people with poor sleep, the higher Aβ usually means stronger forgetting .…”
Section: Sleep–wake Disorder Is Involved In Ad Pathogenesismentioning
confidence: 99%
“…Creutzfeldt-Jakob disease (CJD) is characterized by the same mutation and accumulation of protease-resistant prion protein plaques, but differs from FFI regarding a polymorphism at codon 129, which is common and leads to either incorporation of a methionine or valine and further to protein isoforms differing in size and glycosylation pattern. While in FFI-affected individuals the mutated allele encodes for methionine, those with CJD express valine on the mutated PRNP allele [125][126][127][128][129][130].…”
Section: Slc6a3(dat)mentioning
confidence: 99%