ArticleHippocampus2017
Whole transcriptome profiling of the human hippocampus suggests an involvement of the KIBRA rs17070145 polymorphism in differential activation of the MAPK signaling pathway.
Article in Hippocampus, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
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Who cites it
15 citing papers in PubMed, 1 synthesis or guideline pooled it, 28 citations in OpenAlex.
- Pooled it
- Age and the Diurnal Oscillatory Features of the Human Chronobiome.medRxiv : the preprint server for health sciences · 2026Article
- Article
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- Investigating the impact of aspartame on Alzheimer's disease through network toxicology and molecular docking.Frontiers in nutrition · 2025Article
- Single-nucleus analysis reveals microenvironment-specific neuron and glial cell enrichment in Alzheimer's disease.BMC genomics · 2024Article
- KIBRA single nucleotide polymorphism is associated with hippocampal subfield volumes and cognition across development.Brain structure & function · 2024Article
- Advances in the role of the GADD45 family in neurodevelopmental, neurodegenerative, and neuropsychiatric disorders.Frontiers in neuroscience · 2024Review
- The role of Gadd45b in neurologic and neuropsychiatric disorders: An overview.Frontiers in molecular neuroscience · 2022Review
- Integrating Transcriptomics, Genomics, and Imaging in Alzheimer's Disease: A Federated Model.Frontiers in radiology · 2021Article
- Concentrations of bile acid precursors in cerebrospinal fluid of Alzheimer's disease patients.Free radical biology & medicine · 2019Article
- Regulatory SNPs and their widespread effects on the transcriptome.Journal of biosciences · 2018Review
- Distinctive phosphoinositide- and CaThe Journal of biological chemistry · 2018Article
- KIBRA is associated with accelerated cognitive decline and hippocampal atrophy in APOE ε4-positive cognitively normal adults with high Aβ-amyloid burden.Scientific reports · 2018Article
- Age-Modulated Associations betweenFrontiers in aging neuroscience · 2017Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
The rs17070145-T variant of the WWC1 gene, coding for the KIBRA protein, has been associated with both increased episodic memory performance and lowered risk for late onset Alzheimer's disease, although the mechanism behind this protective effect has not been completely elucidated. To achieve a better understanding of the pathways modulated by rs17070145 and its associated functional variant(s), we used laser capture microdissection (LCM) and RNA-sequencing to investigate the effect of rs17070145 genotypes on whole transcriptome expression in the human hippocampus (HP) of 22 neuropathologically normal individuals, with a specific focus on the dentate gyrus (DG) and at the pyramidal cells (PC) of CA1 and CA3 sub-regions. Differential expression analysis of RNA-seq data within the HP based on the rs17070145 genotype revealed an overexpression of genes involved in the MAPK signaling pathway, potentially driven by the T/T genotype. The most important contribution comes from genes dysregulated within the DG region. Other genes significantly dysregulated, and not involved in the MAPK pathway (Adj P < 0.01 and Fold Change > |1.00|) were: RSPO4 (HP); ARC, DUSP5, DNAJB5, EGR4, PPP1R15A, WBP11P1, EGR1, GADD45B (DG); CH25H, HSPA1A, HSPA1B, TNFSF9, and NPAS4 (PC). Several evidences suggested that the MAPK signaling pathway is linked with memory and learning processes. In non-neuronal cells, the KIBRA protein is phosphorylated by ERK1/2 (involved in the MAPK signaling) in cells as well as in vitro. Several of the other dysregulated genes are involved in memory and learning processes, as well as in Alzheimer's Disease. In conclusion, our results suggest that the effect of the WWC1 rs17070145 polymorphism on memory performance and Alzheimer's disease might be due to a differential regulation of the MAPK signaling, a key pathway involved in memory and learning processes.
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