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Background  P73 belongs to the p53 family of cell survival regulators with the corresponding locus  Trp73  producing the N-terminally distinct isoforms, TAp73 and DeltaNp73. Recently, two studies have implicated the murine  Trp73  in the modulation in phospho-tau accumulation in aged wild type mice and in young mice modeling Alzheimer’s disease (AD) suggesting that  Trp73 , particularly the DeltaNp73 isoform, links the accumulation of amyloid peptides to the creation of neurofibrillary tangles (NFTs). Here, we reevaluated tau pathologies in the same TgCRND8 mouse model as the previous studies.    Results  Despite the use of the same animal models, our  in vivo  studies failed to demonstrate biochemical or histological evidence for misprocessing of tau in young compound Trp73 +/-  + TgCRND8 mice or in aged Trp73 +/-  mice analyzed at the ages reported previously, or older. Secondly, we analyzed an additional mouse model where the DeltaNp73 was specifically deleted and confirmed a lack of impact of the DeltaNp73 allele, either in heterozygous or homozygous form, upon tau pathology in aged mice. Lastly, we also examined human  TP73  for single nucleotide polymorphisms (SNPs) and/or copy number variants in a meta-analysis of 10 AD genome-wide association datasets. No SNPs reached significance after correction for multiple testing and no duplications/deletions in  TP73  were found in 549 cases of AD and 544 non-demented controls.    Conclusion  Our results fail to support P73 as a contributor to AD pathogenesis.

Role of p73 in Alzheimer disease: lack of association in mouse models or in human cohorts