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MIR-19A-3P INHIBITION IMPROVES MEMORY AND SYNAPTIC FUNCTION IN ALZHEIMER’S DISEASE
Mireia Millet Sigalatand 8 co-authors
Department of Pharmacology, Toxicology and Therapeutic Chemistry, Faculty of Pharmacy and Food Science, Universitat de Barcelona
FENS Forum 2026 (2026)
Barcelona, Spain
Board PS03-08AM-097
Presentation
Date TBA
Board: PS03-08AM-097
Event Information
Poster Board
PS03-08AM-097
Poster
View posterAbstract
Alzheimer's disease (AD) is a neurodegenerative disorder characterized by progressive cognitive decline and memory loss. It is hallmarked by amyloid plaque deposition, and neurofibrillary tangles, while neuroinflammation and oxidative stress play key roles in its pathophysiology, suggesting its multifactorial etiology. Thus, multitarget pharmacological approach could constitute an effective strategy. In recent studies, dysregulation of microRNA (miRNA) expression has been reported in differents tissues of AD patients, highlighting miRNAs as potential biomarkers and therapeutic targets. Previous studies from our group analyzed the expression of several miRNAs in SH-SY5Y cells and demonstrated that miR-19a-3p is overexpressed following β-amyloid exposure. Based on these results, the present study aimed to evaluate the expression of miR-19a-3p and to investigate its potential role in AD development in vitro and in vivo.
To perform this study, protective role of anti-miR-19a-3p in SH-SY5Y was determined. For in vivo studies, 5-months-old APPswe/PS1dE9 (APP/PS1) male mice were treated with vehicle (CT), anti-miR-19a-3p (A-19a-3p) or miRNA inhibitor negative control (CT-mir) for a month. Behavioral tests were conducted to assess learning and memory capacity and several molecular pathways involved in AD pathology were also analyzed.
Preliminary results indicated that modulation of mir-19a-3p is associated with an improvement in cognitive performance, ameliorating memory impairments in APP/PS1 treated with A-19a-3p. Moreover, these animals exhibited preserved synaptic structures and a restoration of additional pathways associated with AD.
Overall, these results support a potential role for miR-19a-3p in AD development and highlights its relevance as a possible therapeutic target.
To perform this study, protective role of anti-miR-19a-3p in SH-SY5Y was determined. For in vivo studies, 5-months-old APPswe/PS1dE9 (APP/PS1) male mice were treated with vehicle (CT), anti-miR-19a-3p (A-19a-3p) or miRNA inhibitor negative control (CT-mir) for a month. Behavioral tests were conducted to assess learning and memory capacity and several molecular pathways involved in AD pathology were also analyzed.
Preliminary results indicated that modulation of mir-19a-3p is associated with an improvement in cognitive performance, ameliorating memory impairments in APP/PS1 treated with A-19a-3p. Moreover, these animals exhibited preserved synaptic structures and a restoration of additional pathways associated with AD.
Overall, these results support a potential role for miR-19a-3p in AD development and highlights its relevance as a possible therapeutic target.
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