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Miguel, L., Frebourg, T., Campion, D., Lecourtois, M. (2020). Moderate Overexpression of Tau in Drosophila Exacerbates Amyloid-β-Induced Neuronal Phenotypes and Correlates with Tau Oligomerization.  J. Alzheimers Dis. 74(2): 637--647.
FlyBase ID
FBrf0245295
Publication Type
Research paper
Abstract

Alzheimer's disease (AD) is neuropathologically defined by two key hallmarks: extracellular senile plaques composed primarily of amyloid-β (Aβ) peptide and intraneuronal neurofibrillary tangles, containing abnormally hyperphosphorylated tau protein. The tau protein is encoded by the MAPT gene. Recently, the H1 and H2 haplotypes of the MAPT gene were associated with AD risk. The minor MAPT H2 haplotype has been linked with a decreased risk of developing late-onset AD (LOAD). MAPT haplotypes show different levels of MAPT/Tau expression with H1 being ∼1.5-fold more expressed than H2, suggesting that MAPT expression level could be related to LOAD risk. In this study, we investigated whether this moderate difference in MAPT/Tau expression could influence Aβ-induced toxicity in vivo. We show that modest overexpression of tau protein in Drosophila exacerbates neuronal phenotypes in AβPP/BACE1 flies. The exacerbation of neuronal defects correlates with the accumulation of insoluble dTau oligomers, suggesting that the moderate difference in level of tau expression observed between H1 and H2 haplotypes could influence Aβ toxicity through the production of oligomeric tau insoluble species.

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    Language of Publication
    English
    Additional Languages of Abstract
    Parent Publication
    Publication Type
    Journal
    Abbreviation
    J. Alzheimers Dis.
    Title
    Journal of Alzheimer's disease : JAD
    ISBN/ISSN
    1387-2877
    Data From Reference
    Alleles (4)
    Genes (4)
    Human Disease Models (3)
    Insertions (1)
    Transgenic Constructs (3)