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001-es BibID:	BIBFORM121344
035-os BibID:	(Scopus)85189160484 (WoS)001194950200001
Első szerző:	Panagaki, Theodora
Cím:	Neurobehavioral dysfunction in a mouse model of Down syndrome: upregulation of cystathionine beta-synthase, H2S overproduction, altered protein persulfidation, synaptic dysfunction, endoplasmic reticulum stress, and autophagy / Theodora Panagaki, Lucia Janickova, Dunja Petrovic, Karim Zuhra, Tamás Ditrói, Eszter P. Jurányi, Olivier Bremer, Kelly Ascenção, Thilo M. Philipp, Péter Nagy, Milos R. Filipovic, Csaba Szabo
Dátum:	2024
ISSN:	2509-2715 2509-2723
Megjegyzések:	Down syndrome (DS) is a genetic condition where the person is born with an extra chromosome 21. DS is associated with accelerated aging; people with DS are prone to age-related neurological conditions including an early-onset Alzheimer's disease. Using the Dp(17)3Yey/ + mice, which overexpresses a portion of mouse chromosome 17, which encodes for the transsulfuration enzyme cystathionine ?-synthase (CBS), we investigated the functional role of the CBS/hydrogen sulfide (H2S) pathway in the pathogenesis of neurobehavioral dysfunction in DS. The data demonstrate that CBS is higher in the brain of the DS mice than in the brain of wild-type mice, with primary localization in astrocytes. DS mice exhibited impaired recognition memory and spatial learning, loss of synaptosomal function, endoplasmic reticulum stress, and autophagy. Treatment of mice with aminooxyacetate, a prototypical CBS inhibitor, improved neurobehavioral function, reduced the degree of reactive gliosis in the DS brain, increased the ability of the synaptosomes to generate ATP, and reduced endoplasmic reticulum stress. H2S levels in the brain of DS mice were higher than in wild-type mice, but, unexpectedly, protein persulfidation was decreased. Many of the above alterations were more pronounced in the female DS mice. There was a significant dysregulation of metabolism in the brain of DS mice, which affected amino acid, carbohydrate, lipid, endocannabinoid, and nucleotide metabolites; some of these alterations were reversed by treatment of the mice with the CBS inhibitor. Thus, the CBS/H2S pathway contributes to the pathogenesis of neurological dysfunction in DS in the current animal model.
Tárgyszavak:	Természettudományok Kémiai tudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk Astrocytes Brain Cognition Gasotransmitters Gliosis Metabolism Persulfidation
Megjelenés:	GeroScience. - 2024 (2024), p. 1-40. -
További szerzők:	Janickova, Lucia Petrovic, Dunja Zuhra, Karim Ditrói Tamás (1989-) (vegyész) Jurányi Eszter Petra Bremer, Olivier Ascenção, Kelly Philipp, Thilo M. Nagy Péter (1976-) (vegyész) Filipovic, Milos R. Szabó Csaba (1967-) (orvos)
Pályázati támogatás:	TKP2021-EGA-44 Egyéb 2022-2.1.1- NL-2022-00010 Egyéb
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