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Takashi Saito

Professor

Nagoya University

Japan

Has grant

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Research Interests

Neurology

20%

Neuropsychology

30%

Neurodegenerative Disease

60%

Neuroinflammation

40%

Neuroprotection

40%

Alzheimer's Disease

40%

Mouse Genetics

30%

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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

Articles20

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

Article Link

Year:

2025

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

Article Link

Year:

2025

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

Article Link

Year:

2025

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

Article Link

Year:

2025

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

Article Link

Year:

2025

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

Article Link

Year:

2025

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

Article Link

Year:

2024

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

Article Link

Year:

2024

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

Article Link

Year:

2024

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

Article Link

Year:

2024

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

Article Link

Year:

2023

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

Article Link

Year:

2023

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

Article Link

Year:

2023

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

Article Link

Year:

2022

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

Article Link

Year:

2022

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

Article Link

Year:

2022

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

Article Link

Year:

2022

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

Article Link

Year:

2022

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

Article Link

Year:

2021

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

Article Link

Year:

2021

Collaborators23

Millicent Ekwudo

Florey Institute of Neuroscience and Mental Health

AUSTRALIA

Per Nilsson

Team leader, Assoc Prof

Karolinska Institutet

SWEDEN

Takeshi Masuda

Kumamoto University

JAPAN

Aya Goto

Professor

Fukushima Medical University

JAPAN

Yusaku Nakabeppu

Professor Emeritus

Kyushu University

JAPAN

Cynthia Lemere

Professor of Neurology

Brigham and Women's Hospital and Harvard Medical School

UNITED STATES

Cécile Vincke

Vrije Universiteit Brussel

BELGIUM

Elizabeth Fisher

University College London

UNITED KINGDOM

Motoko Maekawa

Tohoku University

JAPAN

Satoko Hattori

Aichi Medical University

JAPAN

R. J. Rylett

CANADA

Maarten Dewilde

Professor

KU Leuven

BELGIUM

Shuhan Yang

Tohoku University

JAPAN

Marco Antonio Maximo Prado

Professor

University of Western Ontario

CANADA

Masanori HIJIOKA

Assistant Professor

Nagoya University

JAPAN

Tim Bussey

Professor and Western Research Chair in Behavioural Neuroscience

University of Western Ontario

CANADA

Hiroki Fujita

Akita University

JAPAN

Akira Uruno

Tohoku University

JAPAN

Yuji Owada

Professor

Tohoku University

JAPAN

Yoshiki Yamaguchi

Tohoku Medical and Pharmaceutical University

JAPAN

Tatsuya Manabe

Assistant Professor

Nagoya University

JAPAN

Laura Cox

Assistant Professor

Brigham and Women's Hospital and Harvard Medical School

UNITED STATES

Toru Iwaki

Professor

Kyushu University

JAPAN

How do I reach out?

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Takashi Saito

Professor

How do I reach out?

Contact this professor

Research Interests

Ask ApplyKite AI

Recent Grants

Articles20

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

Collaborators23

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

How do I reach out?

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