Neurobehavioral dysfunction in a mouse model of Down syndrome: upregulation of cystathionine β-synthase, H2S overproduction, altered protein persulfidation, synaptic dysfunction, endoplasmic reticulum stress, and autophagy

Theodora Panagaki; Lucia Janickova; Dunja Petrovic; Karim Zuhra; Tamás Ditrói; Eszter Petra Jurányi; Olivier Bremer; Kelly Ascenção; Thilo M. Philipp; Péter Nagy; Miloš R. Filipović; Csaba Szabó

doi:10.1007/s11357-024-01146-8

April 1, 2024GeroScienceOpen Access

Neurobehavioral dysfunction in a mouse model of Down syndrome: upregulation of cystathionine β-synthase, H2S overproduction, altered protein persulfidation, synaptic dysfunction, endoplasmic reticulum stress, and autophagy

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Key Points

Cystathionine β-synthase upregulation and hydrogen sulfide overproduction drive neurobehavioral and synaptic dysfunction in Down syndrome models.
Investigation of Dp(17)3Yey/+ mice carrying chromosome 17 duplications identifies severe endoplasmic reticulum stress alongside altered protein persulfidation.
Altered transsulfuration enzyme signaling highlights pathways linking accelerated aging and autophagy; mouse model requires further preclinical validation.

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Implication

Animal study reveals cystathionine β-synthase upregulation and synaptic dysfunction in Down syndrome mice, suggesting hydrogen sulfide pathway involvement.

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Panagaki et al. (2024) studied this question.

synapsesocial.com/papers/68e70d94b6db643587687275 https://doi.org/10.1007/s11357-024-01146-8

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Neurobehavioral dysfunction in a mouse model of Down syndrome: upregulation of cystathionine β-synthase, H2S overproduction, altered protein persulfidation, synaptic dysfunction, endoplasmic reticulum stress, and autophagy

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Neurobehavioral dysfunction in a mouse model of Down syndrome: upregulation of cystathionine β-synthase, H2S overproduction, altered protein persulfidation, synaptic dysfunction, endoplasmic reticulum stress, and autophagy

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