about
Calpain Activation in Alzheimer's Model Mice Is an Artifact of APP and Presenilin Overexpression.APP mouse models for Alzheimer's disease preclinical studies.Loss of kallikrein-related peptidase 7 exacerbates amyloid pathology in Alzheimer's disease model mice.Endoplasmic reticulum stress responses in mouse models of Alzheimer disease: overexpression paradigm versus knock-in paradigm.Critical review: involvement of endoplasmic reticulum stress in the aetiology of Alzheimer's disease.Generation of App knock-in mice reveals deletion mutations protective against Alzheimer's disease-like pathology.Circadian and Brain State Modulation of Network Hyperexcitability in Alzheimer's Disease.The intellectual disability gene PQBP1 rescues Alzheimer's disease pathologyNovel Quantitative Analyses of Spontaneous Synaptic Events in Cortical Pyramidal Cells Reveal Subtle Parvalbumin-Expressing Interneuron Dysfunction in a Knock-In Mouse Model of Alzheimer's DiseaseIntroduction of pathogenic mutations into the mouse Psen1 gene by Base Editor and Target-AIDAmyloid-β plaque formation and reactive gliosis are required for induction of cognitive deficits in App knock-in mouse models of Alzheimer's diseaseSIRT3 mediates hippocampal synaptic adaptations to intermittent fasting and ameliorates deficits in APP mutant miceNeuroinflammation in mouse models of Alzheimer's disease.Author Correction: Tau binding protein CAPON induces tau aggregation and neurodegenerationTau binding protein CAPON induces tau aggregation and neurodegenerationβ-amyloid redirects norepinephrine signaling to activate the pathogenic GSK3β/tau cascadeAmyloid β oligomers constrict human capillaries in Alzheimer's disease via signaling to pericytesProgressive changes in sleep and its relations to amyloid-β distribution and learning in single App knock-in mice
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description
researcher
@en
wetenschapper
@nl
name
Takaomi C Saido
@en
Takaomi C Saido
@nl
type
label
Takaomi C Saido
@en
Takaomi C Saido
@nl
prefLabel
Takaomi C Saido
@en
Takaomi C Saido
@nl
P31
P496
0000-0003-1970-6903