Masashi Kitazawa

About

Masashi Kitazawa is an Associate Professor at the University of California, Irvine, affiliated with the Center for Occupational and Environmental Health (COEH) in the School of Medicine, the Joe C. Wen School of Population & Public Health, and the Institute for Memory Impairments and Neurological Disorders (UCI MIND). He earned his Ph.D. in Toxicology from Iowa State University in 2003, following an M.S. in Environmental Toxicology from the University of California, Irvine, and a B.S. in Chemistry from California State University, San Bernardino. His research primarily focuses on understanding the molecular pathogenesis of neurodegenerative diseases, particularly Alzheimer's disease (AD), with an emphasis on the role of neuroinflammation triggered by both endogenous factors such as aging and exogenous environmental factors including chronic exposure to environmental chemicals and toxicants. Kitazawa's laboratory employs multiple experimental platforms, including transgenic mouse models, primary and established cell cultures, and organotypic slices, to investigate dysregulated cellular signaling cascades in microglia and astrocytes during the early phases of AD. His work explores how environmental risk factors like air pollution and inflammation contribute to disease progression, aiming to elucidate mechanisms underlying microglial and astrocyte dysfunction in neurodegeneration. Throughout his career, Kitazawa has been recognized with several awards, including the 2019…

Research topics

• Neuroscience
• Biology
• Medicine
• Genetics
• Pathology
• Internal medicine
• Immunology
• Cell biology

Selected publications

• Metal Toxicity Links to Alzheimer's Disease and Neuroinflammation

  Journal of Molecular Biology · 2019-01-18 · 459 citations

  reviewOpen access
  PublisherOA PDFDOI

• Generation of a humanized Aβ expressing mouse demonstrating aspects of Alzheimer’s disease-like pathology

  Nature Communications · 2021 · 113 citations

  The majority of Alzheimer's disease (AD) cases are late-onset and occur sporadically, however most mouse models of the disease harbor pathogenic mutations, rendering them better representations of familial autosomal-dominant forms of the disease. Here, we generated knock-in mice that express wildtype human Aβ under control of the mouse App locus. Remarkably, changing 3 amino acids in the mouse Aβ sequence to its wild-type human counterpart leads to age-dependent impairments in cognition and syna…

  PublisherDOI

• Impaired <scp>AMPA</scp> signaling and cytoskeletal alterations induce early synaptic dysfunction in a mouse model of Alzheimer's disease

  Aging Cell · 2018-06-06 · 63 citations

  articleOpen access

  Alzheimer's disease (AD) is a devastating neurodegenerative disorder that impairs memory and causes cognitive and psychiatric deficits. New evidences indicate that AD is conceptualized as a disease of synaptic failure, although the molecular and cellular mechanisms underlying these defects remain to be elucidated. Determining the timing and nature of the early synaptic deficits is critical for understanding the progression of the disease and for identifying effective targets for therapeutic inte…

  PublisherDOI

• miR‐181a negatively modulates synaptic plasticity in hippocampal cultures and its inhibition rescues memory deficits in a mouse model of Alzheimer’s disease

  Aging Cell · 2020 · 62 citations

  Senior authorCorresponding

  MicroRNAs play a pivotal role in rapid, dynamic, and spatiotemporal modulation of synaptic functions. Among them, recent emerging evidence highlights that microRNA-181a (miR-181a) is particularly abundant in hippocampal neurons and controls the expression of key plasticity-related proteins at synapses. We have previously demonstrated that miR-181a was upregulated in the hippocampus of a mouse model of Alzheimer's disease (AD) and correlated with reduced levels of plasticity-related proteins. Her…

  PublisherOA PDFDOI

• Copper-Induced Upregulation of MicroRNAs Directs the Suppression of Endothelial LRP1 in Alzheimer’s Disease Model

  Toxicological Sciences · 2019-03-27 · 34 citations

  articleOpen accessSenior authorCorresponding

  Chronic exposure to copper and its dyshomeostasis have been linked to accelerated cognitive decline and potentially increasing risk for Alzheimer's disease (AD). We and others have previously demonstrated that exposure to copper through drinking water significantly increased parenchymal amyloid-beta (Aβ) plaques and decreased endothelial low-density lipoprotein receptor-related protein 1 (LRP1) in mouse models of AD. In this study, we determined the underlying mechanisms that microRNA critically…

  PublisherOA PDFDOI

Recent grants

• Environmental copper exposure and its impact on microglial Abeta clearance

  NIH · $2.7M · 2014–2020

• Mechanisms of particulate matter-induced neurotoxicity and cognitive decline in mice

  NIH · $414k · 2018–2021

• NIH Grant R00AR054695

  NIH · $714k · 2016

Frequent coauthors

• Frank M. LaFerla

  University of California, Irvine

  44 shared

• Carlos J. Rodríguez‐Ortiz

  Center for Environmental Health

  36 shared

• Masaki Tanemura

  Nagoya Institute of Technology

  36 shared

• Rodrigo Medeiros

  University of California, Irvine

  26 shared

• David Baglietto‐Vargas

  22 shared

• Ryo Ohta

  22 shared

• Sharon Lim

  Broomfield Hospital

  17 shared

• Shuichi Takeda

  Okayama University

  15 shared

Education

• Ph.D., Environmental Health Sciences

  University of California, Los Angeles

  1995

• M.S., Environmental Health Sciences

  University of California, Los Angeles

  1991

• B.S., Environmental Health Sciences

  University of California, Los Angeles

  1989

Similar researchers at University of California, Irvine

• Charles Limolih-66
• Stephen Bondyh-58
• Jun Wuh-51