Advanced search

Filter By:

Journal Check one or more journals to show results from those journals only.

Choose more journals

Article type Check one or more article types to show results from those article types only.
Subject Check one or more subjects to show results from those subjects only.
Date Choose a date option to show results from those dates only.

Custom date range

Clear all filters
Sort by:
Showing 1–8 of 8 results
Advanced filters: Author: Yukio Matsuba Clear advanced filters

  • To date, only one mutation in the gene for amyloid-beta precursor protein APP has been suggested to be protective against Alzheimer’s disease. Here, authors found using gene editing of a mutant App knock-in mouse line that deletion of the 3’UTR region is protective against amyloid-β accumulation in vivo, and subsequently identify a 52-bp element in the 3’UTR region that is responsible for this effect.

    • Kenichi Nagata
    • Mika Takahashi
    • Takaomi C. Saido
    ResearchOpen Access
    Nature Communications
    Volume: 9, P: 1-7

  • CRISPR-guided cytidine deaminases, including BE3 (Base Editor 3) and Target-AID (activation-induced cytidine deaminase), can covert C:G base pairs to T:A at target site. Here, the authors generate missense mutations of mouse Psen1 gene and find BE3 has higher editing efficiency than Target-AID.

    • Hiroki Sasaguri
    • Kenichi Nagata
    • Takaomi C. Saido
    ResearchOpen Access
    Nature Communications
    Volume: 9, P: 1-8

  • To understand the molecular processes that link Aβ amyloidosis, tauopathy and neurodegeneration, the authors screened for tau-interacting proteins. They demonstrated that a novel tau binding protein CAPON accelerates tau pathology and neuronal cell death in an Alzheimer’s disease mouse model.

    • Shoko Hashimoto
    • Yukio Matsuba
    • Takashi Saito
    ResearchOpen Access
    Nature Communications
    Volume: 10, P: 1-16

  • In addition to neurotoxic Aβ42, the Aβ43 variant is also abundant in Aβ plaques in the brains of individuals with sporadic and familial Alzheimer's disease. As the functional difference between the two species of Aβ fragments are not known, Saido et al. used a presenilin-1 (PS1) mutation that increases Aβ43 production over other Aβ fragments and generated a knock-in mouse line mimicking the human PS1 mutation. They report that Aβ43 is highly amyloidogenic in this line of mice and leads to behavioral deficits.

    • Takashi Saito
    • Takahiro Suemoto
    • Takaomi C Saido
    Research
    Nature Neuroscience
    Volume: 14, P: 1023-1032

  • Many mouse models of Alzheimer's disease (AD) rely on overexpression of amyloid precursor (APP) transgenes, which makes it difficult to tease out which effects are truly disease-relevant and which are induced by the overexpression. In this study, the authors describe several new knock-in AD model mice that express mutant APP at near physiological levels.

    • Takashi Saito
    • Yukio Matsuba
    • Takaomi C Saido
    Research
    Nature Neuroscience
    Volume: 17, P: 661-663