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ANALYSIS OF THE EFFECT OF A MUTANT VARIANT OF E2F4 IN OLIGODENDROCYTES IN A MOUSE MODEL OF ALZHEIMER´S DISEASE
Cristina González Bragadoand 2 co-authors
Cajal Neurosciences Center
FENS Forum 2026 (2026)
Barcelona, Spain
Board PS07-10AM-193
Presentation
Date TBA
Board: PS07-10AM-193
Event Information
Poster Board
PS07-10AM-193
Poster
View posterAbstract
Alzheimer’s disease (AD) is the most common age-related neurodegenerative disease and the leading cause of dementia. In addition to neuronal dysfunction, increasing evidence highlights the contribution of non-neuronal cells to disease progression. Oligodendrocytes (OLs) are generated throughout life from oligodendrocyte progenitor cells (OPCs), making OPCs a potential source to repair myelin defects in AD. Previous studies in our laboratory have shown that neuronal expression of a dominant negative form of the transcription factor E2F4 (E2F4DN), unable to become phosphorylated at a conserved threonine motif, reduces microgliosis and astrogliosis in homozygous 5xFAD (h5xFAD) mice. However, the impact of E2F4DN on the oligodendrocyte lineage has not been addressed yet. This study aims to characterize the oligodendrocyte lineage in this AD model and assess the effect of E2F4DN on these cells. The analysis of these populations reveals an increase in the number of OPCs in the cortex and corpus callosum of h5xFAD animals. Moreover, the number of OPCs in the CA1 region of the hippocampus, another well-known area involved in AD, tends to increase in the h5xFAD animals. In contrast, mature OL population is decreased in cortex, while similar tendency in CA1 of h5xFAD mice is observed. Notably, the expression of E2F4DN in these animals attenuates significantly the alterations of OPCs and OLs in these regions to control levels. These findings, together with previous evidence from our laboratory, support E2F4DN as a promising multifactorial therapeutic strategy for AD.
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