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NR4A2 OVEREXPRESSION REDUCES SYNAPTIC PLASTICITY DYSFUNCTION AND BEHAVIOURAL ALTERATION IN THE APP<SUB >SW,IND</SUB> MICE
José Rodríguez Alvarezand 8 co-authors
Institut de Neurociències and Dpt. Bioquímica i Biología Molecular, Universitat Autònoma de Barcelona
FENS Forum 2026 (2026)
Barcelona, Spain
Board PS05-09AM-150
Presentation
Date TBA
Board: PS05-09AM-150
Event Information
Poster Board
PS05-09AM-150
Poster
View posterAbstract
Alzheimer’s disease AD is associated with disruptions in neuronal communication, especially in brain regions crucial for learning and memory, such as the hippocampus. It has been reported that Nr4a2, a member of the Nr4a family of orphan nuclear receptors, plays a role in hippocampal synaptic plasticity by regulating BDNF and synaptic AMPA receptors. Here, we demonstrate that oAβ inhibits activity-dependent Nr4a2 activation in hippocampal neurons, indicating a potential link between oAβ and Nr4a2 down-regulation. Furthermore, we have observed a reduction in Nr4a2 protein levels in human postmortem hippocampal tissue samples at early AD stages. Pharmacological activation of Nr4a2 prevented oAβ-mediated synaptic depression in the hippocampus. Notably, Nr4a2 overexpression in the hippocampus ameliorates spatial learning and memory deficits and reduced anxiety-related behaviour of the APPSw,Ind mice. Together, our findings suggest that oAβ may contribute to early cognitive impairment in AD by blocking Nr4a2 activation, leading to synaptic dysfunction. Our study highlights that Nr4a2 activation is a potential therapeutic target to mitigate oAβ-induced synaptic and cognitive impairments in the early stages of AD.
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