RT journal article
T1 Spatiotemporal Dysregulation of Neuron–Glia Related Genes and Pro-/Anti-Inflammatory miRNAs in the 5xFAD Mouse Model of Alzheimer’s Disease
A1 Ianni, M.
A1 Corraliza Gómez,  Miriam
A1 Costa-Coelho, T.
A1 Ferreira-Manso, M.
A1 Inteiro-Oliveira, S.
A1 Alemãn-Serrano, N.
A1 Sebastião, A.M.
A1 Garcia, G
A1 Diógenes, M.J.
A1 Brites, Carlos D. S.
A2 BiomedicinaBiotecnología y Salud Pública
K1 Alzheimer’s disease
K1 5xFAD mouse model
K1 hippocampus
K1 microRNAs;
K1 neurodegeneration;
K1 neuroimmune genes
K1 neuroinflammation
K1 prefrontal cortex
AB Alzheimer’s disease (AD), the leading cause of dementia, is a multifactorial diseaseinfluenced by aging, genetics, and environmental factors. miRNAs are crucial regulators of geneexpression and play significant roles in AD onset and progression. This exploratory study analyzedthe expression levels of 28 genes and 5 miRNAs (miR-124-3p, miR-125b-5p, miR-21-5p, miR-146a-5p,and miR-155-5p) related to AD pathology and neuroimmune responses using RT-qPCR. Analyseswere conducted in the prefrontal cortex (PFC) and the hippocampus (HPC) of the 5xFAD mouse ADmodel at 6 and 9 months old. Data highlighted upregulated genes encoding for glial fibrillary acidicprotein (Gfap), triggering receptor expressed on myeloid cells (Trem2) and cystatin F (Cst7), in the5xFAD mice at both regions and ages highlighting their roles as critical disease players and potentialbiomarkers. Overexpression of genes encoding for CCAAT enhancer-binding protein alpha (Cebpa)and myelin proteolipid protein (Plp) in the PFC, as well as for BCL2 apoptosis regulator (Bcl2) andpurinergic receptor P2Y12 (P2yr12) in the HPC, together with upregulated microRNA(miR)-146a-5pin the PFC, prevailed in 9-month-old animals. miR-155 positively correlated with miR-146a andmiR-21 in the PFC, and miR-125b positively correlated with miR-155, miR-21, while miR-146a in theHPC. Correlations between genes and miRNAs were dynamic, varying by genotype, region, andage, suggesting an intricate, disease-modulated interaction between miRNAs and target pathways.These findings contribute to our understanding of miRNAs as therapeutic targets for AD, given theirmultifaceted effects on neurons and glial cells.
PB Multidisciplinary Digital Publishing Institute (MDPI)
SN 1422-0067
YR 2024
FD 2024
LK http://hdl.handle.net/10498/35517
UL http://hdl.handle.net/10498/35517
LA eng
DS Repositorio Institucional de la Universidad de Cádiz
RD 11-nov-2026