Matches in SemOpenAlex for { <https://semopenalex.org/work/W2980981871> ?p ?o ?g. }
Showing items 1 to 87 of
87
with 100 items per page.
- W2980981871 abstract "α-Synuclein oligomers (a-Syn0) are crucial players in the pathogenesis of Parkinson's disease and Lewy bodies dementia. α-Syn0 might be responsible of neuronal dysfunction and play an important role in the widespread of the diseases. Through in vitro approaches and in vivo acute mouse model we investigated the influence of inflammation on detrimental activities of α-Syn0. Furthermore we verified the existence of a direct cross-talk between α-Syn0 and cellular prion protein (PrPc) as recently suggested. In vitro, we assessed a-Syn0 toxicity by comparing the effect in Prnp+ /+ versus PrPc knockout (Prnp0/0) hippocampal neurons. In addition, PrPc-α-Syn0 direct binding was investigated through surface plasmon resonance. Using novel object recognition test (NORT) we examined the memory deficits induced by intracerebroventricularly (ICV) application of α-Syn0 (5-10 μM in 7.5 μl). The cognitive evaluation has been associated to histopathological examination and Western blot analysis of gliosis by measuring GFAP and IBA1 expression in hippocampus. The effects of a-Syn0 were analyzed in wild type and Prnp0/0 mice. The mice were pre-treated with anti-inflammatory drugs and Tool-like receptor 2 (TLR2) antagonist, the long lasting effect of inflammation by LPS injection (2.5 mg/kg, ip) on the cognitive decline induced by α-Syn0 was also examined. The ICV application of α-Syn0 induced a cognitive decline determined by NORT, the memory impairment was associated with glial activation in hippocampus. The pre-treatment with ibuprofen or indomethacin not only extinguished the gliosis but also completely antagonized the behavioral deficit induced by α-Syn0, similar effect was obtained with TL-R2 antagonist. Conversely, the ICV injection of α-Syn0 at an ineffective concentration in mice controls became toxic when applied to mice pre-treated with a single dose of LPS, one month before. The absence of PrPc did not affect the detrimental effects, in vitro neurotoxicity memory deficit and hippocampal gliosis, induced by α-Syn0. Accordingly surface plasmon resonance analyses ruled out PrPc–α-Syn0 binding. Our findings indicate the important role played by inflammation in neuronal dysfunction induced by α-Syn0 presumably through TLR2 activation, chronic inflammatory state exacerbate α-Syn0 toxicity while PrPc neither binds α-Syn0 nor mediates their detrimental actions. these evidence might orientate future therapeutic approaches to synucleinopathies." @default.
- W2980981871 created "2019-10-25" @default.
- W2980981871 creator A5003169557 @default.
- W2980981871 creator A5007066407 @default.
- W2980981871 creator A5016280779 @default.
- W2980981871 creator A5025482036 @default.
- W2980981871 creator A5028263534 @default.
- W2980981871 creator A5032228291 @default.
- W2980981871 creator A5035922000 @default.
- W2980981871 creator A5039237680 @default.
- W2980981871 creator A5072555597 @default.
- W2980981871 creator A5072575257 @default.
- W2980981871 creator A5089243124 @default.
- W2980981871 creator A5091028669 @default.
- W2980981871 date "2019-07-01" @default.
- W2980981871 modified "2023-09-27" @default.
- W2980981871 title "P1-105: INFLUENCE OF INFLAMMATION ON COGNITIVE DEFICIT INDUCED BY α SYNUCLEIN OLIGOMERS INDEPENDENTLY OF CELLULAR PRION PROTEIN" @default.
- W2980981871 doi "https://doi.org/10.1016/j.jalz.2019.06.660" @default.
- W2980981871 hasPublicationYear "2019" @default.
- W2980981871 type Work @default.
- W2980981871 sameAs 2980981871 @default.
- W2980981871 citedByCount "0" @default.
- W2980981871 crossrefType "journal-article" @default.
- W2980981871 hasAuthorship W2980981871A5003169557 @default.
- W2980981871 hasAuthorship W2980981871A5007066407 @default.
- W2980981871 hasAuthorship W2980981871A5016280779 @default.
- W2980981871 hasAuthorship W2980981871A5025482036 @default.
- W2980981871 hasAuthorship W2980981871A5028263534 @default.
- W2980981871 hasAuthorship W2980981871A5032228291 @default.
- W2980981871 hasAuthorship W2980981871A5035922000 @default.
- W2980981871 hasAuthorship W2980981871A5039237680 @default.
- W2980981871 hasAuthorship W2980981871A5072555597 @default.
- W2980981871 hasAuthorship W2980981871A5072575257 @default.
- W2980981871 hasAuthorship W2980981871A5089243124 @default.
- W2980981871 hasAuthorship W2980981871A5091028669 @default.
- W2980981871 hasBestOaLocation W29809818711 @default.
- W2980981871 hasConcept C104317684 @default.
- W2980981871 hasConcept C126322002 @default.
- W2980981871 hasConcept C148762608 @default.
- W2980981871 hasConcept C169760540 @default.
- W2980981871 hasConcept C2776415932 @default.
- W2980981871 hasConcept C2776914184 @default.
- W2980981871 hasConcept C2777682930 @default.
- W2980981871 hasConcept C2779134260 @default.
- W2980981871 hasConcept C2779483572 @default.
- W2980981871 hasConcept C2779830541 @default.
- W2980981871 hasConcept C2780942790 @default.
- W2980981871 hasConcept C2781161787 @default.
- W2980981871 hasConcept C2984863031 @default.
- W2980981871 hasConcept C55493867 @default.
- W2980981871 hasConcept C71924100 @default.
- W2980981871 hasConcept C86803240 @default.
- W2980981871 hasConceptScore W2980981871C104317684 @default.
- W2980981871 hasConceptScore W2980981871C126322002 @default.
- W2980981871 hasConceptScore W2980981871C148762608 @default.
- W2980981871 hasConceptScore W2980981871C169760540 @default.
- W2980981871 hasConceptScore W2980981871C2776415932 @default.
- W2980981871 hasConceptScore W2980981871C2776914184 @default.
- W2980981871 hasConceptScore W2980981871C2777682930 @default.
- W2980981871 hasConceptScore W2980981871C2779134260 @default.
- W2980981871 hasConceptScore W2980981871C2779483572 @default.
- W2980981871 hasConceptScore W2980981871C2779830541 @default.
- W2980981871 hasConceptScore W2980981871C2780942790 @default.
- W2980981871 hasConceptScore W2980981871C2781161787 @default.
- W2980981871 hasConceptScore W2980981871C2984863031 @default.
- W2980981871 hasConceptScore W2980981871C55493867 @default.
- W2980981871 hasConceptScore W2980981871C71924100 @default.
- W2980981871 hasConceptScore W2980981871C86803240 @default.
- W2980981871 hasIssue "7S_Part_5" @default.
- W2980981871 hasLocation W29809818711 @default.
- W2980981871 hasOpenAccess W2980981871 @default.
- W2980981871 hasPrimaryLocation W29809818711 @default.
- W2980981871 hasRelatedWork W1501306774 @default.
- W2980981871 hasRelatedWork W2010108080 @default.
- W2980981871 hasRelatedWork W2062610934 @default.
- W2980981871 hasRelatedWork W2138730144 @default.
- W2980981871 hasRelatedWork W2419356453 @default.
- W2980981871 hasRelatedWork W2766424950 @default.
- W2980981871 hasRelatedWork W2783633930 @default.
- W2980981871 hasRelatedWork W2896780584 @default.
- W2980981871 hasRelatedWork W3033872672 @default.
- W2980981871 hasRelatedWork W4317939744 @default.
- W2980981871 hasVolume "15" @default.
- W2980981871 isParatext "false" @default.
- W2980981871 isRetracted "false" @default.
- W2980981871 magId "2980981871" @default.
- W2980981871 workType "article" @default.