Takashi Saito

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Nagoya University

Japan

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Professor Takashi Saito is a faculty member at Nagoya City University in Japan. His research primarily focuses on Alzheimer's disease, with recent publications addressing topics such as the phenotyping of APP knock-in mouse models, neurodegeneration mechanisms, and the impacts of diet on cerebral cholesterol accumulation. Professor Saito's work also explores the effects of various treatments and environmental factors on cognitive function related to amyloid pathology.

Recent Grants

Grant: Close

Elucidation for role of intracellular/extracellulra quality control system in pathogenesis of Alzheimer's disease

Open Date: 2014-04-01

Close Date: 2017-03-31

Grant: Close

Establishment and application of novel type of Alzheimer's disease model mouse

Open Date: 2011-04-01

Close Date: 2014-03-31

Grant: Close

Establishment of the diagnostics of Alzheimer' s disease using A・43

Open Date: 2011-01-01

Close Date: 2012-12-31

Grant: Close

ネプリライシンを中軸とするアルツハイマー病予防・治療のための創薬標的の探索

Open Date: 2009-01-01

Close Date: 2010-12-31

Grant: Close

Generation and application of the novel mouse model for Alzheimer's disease

Open Date: 2007-01-01

Close Date: 2009-12-31

Articles (20)

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2021

Collaborators (23)

Millicent Ekwudo

Florey Institute of Neuroscience and Mental Health

AUSTRALIA

Takashi Saito

Research Interests

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About

Recent Grants

Articles (20)

High-Fat Diet-Induced Excessive Accumulation of Cerebral Cholesterol Esters and Microglial Dysfunction Exacerbate Alzheimer's Disease Pathology in APPNL−G−F mice

Impaired Cognitive Flexibility With Preserved Learning in an Amyloid Precursor Protein Knock‐In Mouse Model of Amyloidopathy

A decade progress in the phenotyping of App knock-in mouse model of Alzheimer’s disease

Fingolimod treatment exacerbates tau phosphorylation and neurodegeneration in a mouse model of tauopathy with accumulated brain CD8+ T cells

High Affinity Staining for Histological Immunoreactivity revealed phosphorylated tau within amyloid-cored plaques in the brain of AD model mice

Progressive amyloid-β accumulation in the brain leads to altered protein expressions in the liver and kidneys of APP knock-in mice

Cognitive Effects of Simulated Galactic Cosmic Radiation Are Mediated by ApoE Status, Sex, and Environment in APP Knock-In Mice

The NRF2 inducer CDDO-2P-Im provokes a reduction in amyloid β levels in Alzheimer’s disease model mice

GLP-1 receptor signaling restores aquaporin 4 subcellular polarization in reactive astrocytes and promotes amyloid β clearance in a mouse model of Alzheimer's disease

The dopaminergic system promotes neprilysin-mediated degradation of amyloid-β in the brain

Correction: Hoshi et al. High Correlation among Brain-Derived Major Protein Levels in Cerebrospinal Fluid: Implication for Amyloid-Beta and Tau Protein Changes in Alzheimer’s Disease. <i>Metabolites</i> 2022, <i>12</i>, 355

Multifactorial glial responses and their contributions to Alzheimer's disease continuum

Corrigendum to “MUTYH Actively Contributes to Microglial Activation and Impaired Neurogenesis in the Pathogenesis of Alzheimer’s Disease”

G protein–biased GPR3 signaling ameliorates amyloid pathology in a preclinical Alzheimer’s disease mouse model

Genetic Mapping of APP and Amyloid-β Biology Modulation by Trisomy 21

AAV‐mediated delivery of an anti‐BACE1 VHH alleviates pathology in an Alzheimer's disease model

Deficiency of MTH1 and/or OGG1 increases the accumulation of 8-oxoguanine in the brain of the AppNL-G-F/NL-G-F knock-in mouse model of Alzheimer’s disease, accompanied by accelerated microgliosis and reduced anxiety-like behavior

High Correlation among Brain-Derived Major Protein Levels in Cerebrospinal Fluid: Implication for Amyloid-Beta and Tau Protein Changes in Alzheimer&rsquo;s Disease

MUTYH Actively Contributes to Microglial Activation and Impaired Neurogenesis in the Pathogenesis of Alzheimer’s Disease

Author Correction: Comparative profiling of cortical gene expression in Alzheimer’s disease patients and mouse models demonstrates a link between amyloidosis and neuroinflammation

Collaborators (23)

Millicent Ekwudo

Per Nilsson

Takeshi Masuda

Aya Goto

Yusaku Nakabeppu

Cynthia Lemere

Cécile Vincke

Elizabeth Fisher

Motoko Maekawa

Satoko Hattori

R. J. Rylett

Maarten Dewilde

Shuhan Yang

Marco Antonio Maximo Prado

Masanori HIJIOKA

Tim Bussey

Hiroki Fujita

Akira Uruno

Yuji Owada

Yoshiki Yamaguchi

Tatsuya Manabe

Laura Cox

Toru Iwaki

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High Correlation among Brain-Derived Major Protein Levels in Cerebrospinal Fluid: Implication for Amyloid-Beta and Tau Protein Changes in Alzheimer’s Disease