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ASSESSING CELLULAR SENESCENCE, INFLAMMATION AND NEURODEGENERATION IN TWO MOUSE MODELS OF DOWN SYNDROME
Hira Nizamand 4 co-authors
Universitat Pompeu Fabra
FENS Forum 2026 (2026)
Barcelona, Spain
Board PS05-09AM-185
Presentation
Date TBA
Board: PS05-09AM-185
Event Information
Poster Board
PS05-09AM-185
Poster
View posterAbstract
Down syndrome (DS) produced by the partial or complete trisomy of human chromosome 21 (HSA21), is the most common cause of intellectual disability with individuals showing many shared features such as cognitive impairment, neuroinflammation, early onset Alzheimer’s dementia and accelerated aging. The early aging is associated with cellular mechanisms such as cellular senescence and neuroinflammation, the focus of our study. We used two mouse models of DS, Ts65Dn and Ts66Yah, that reproduce to some extent the HSA21 trisomy, to characterize the expression of the endocannabinoid system, and specific biomarkers of cellular senescence and neuroinflammation that later could be assessed as efficacy biomarkers in experimental treatments. In Ts65Dn middle-aged (8 months old) male mice, we identified the enhanced activity of β-galactosidase, a marker of cellular senescence, in CA3 and subgranular region of hippocampus, areas relevant for memory encoding and neurogenesis, respectively. On the other hand, we used immunoblots to measure the components of the endocannabinoid system, markers of synaptic content and cellular senescence in young (5 months old) Ts66Yah mice both in cortex and hippocampus. We found no significant changes in cortex of these mice, but significant alterations were found in pre and postsynaptic markers in hippocampus, while senescence markers showed an increasing trend. Both models showed reduced expression of neurotrophin receptor p75NTR in hippocampus. Overall, in this study we explored molecular features in two mouse models of DS associated with cellular phenotypes including synaptic function, cellular senescence and neuroinflammation that could help test the efficacy of alleviating treatments.
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