Dr. Iijima-Ando Kanae Iijima-Ando, Ph.D.

Contact Dr. Iijima-Ando

900 Walnut St.
Suite 410
Philadelphia, PA 19107

215-503-9897
215-955-4949 fax

Graduate School
Ph. D., The University of Tokyo, Tokyo, Japan

Fellowship
Postdoctoral fellow, Cold Spring Harbor Laboratory

Board Certification
Ph. D., The University of Tokyo, Tokyo, Japan

University Appointment
Assistant Professor (2006)

Research and Clinical Interests
Microtubule-associated protein tau is thought to play a central role in the pathogenesis of neurodegenerative diseases including Alzheimer disease and tauopathies. Abnormally phosphorylated tau is accumulated in the patient brains, and tau gene mutations and polymorphisms are associated with tauopathies. Overexpression of tau causes neuronal dysfunction and degeneration in animal models. However, the molecular mechanisms that promote tau toxicity in the disease progression are not fully understood. We study the mechanisms underlying neuronal dysfunction and degeneration induced by tau. Elucidation of the mechanisms that enhances tau toxicity will increase our understanding of AD and tauopathies and may provide insights into potential therapeutic interventions.

Also, we investigate the biological function of, and regulatory mechanisms underlying, circadian oscillation of the cAMP responsive element binding protein (CREB) in flies. CREB is an evolutionarily conserved transcription factor that plays a pivotal role in neuronal functions. In vivo reporter assays utilizing transgenic flies revealed that CREB activity cycles in a 24 hour rhythm. Elucidation of the mechanisms underlying oscillation of CREB activity may lead to understanding of the mechanisms by which circadian rhythms regulate physiological processes.

Publications

Most recent Peer-reviewed Publications

  1. Loss of Axonal Mitochondria Promotes Tau-Mediated Neurodegeneration and Alzheimer's Disease-Related Tau Phosphorylation Via PAR-1
  2. Membrane-microdomain localization of amyloid β-precursor protein (APP) C-terminal fragments is regulated by phosphorylation of the cytoplasmic Thr668 residue
  3. Transgenic drosophila models of Alzheimer's amyloid-β 42 toxicity
  4. Tau Ser262 phosphorylation is critical for Aβ42-induced tau toxicity in a transgenic Drosophila model of Alzheimer's disease
  5. Transgenic drosophila models of Alzheimer's disease and tauopathies
  6. A DNA damage-activated checkpoint kinase phosphorylates tau and enhances tau-induced neurodegeneration
  7. Mitochondrial mislocalization underlies aβ42-induced neuronal dysfunction in a drosophila model of alzheimer's disease
  8. Mitochondrial mislocalization underlies Abeta42-induced neuronal dysfunction in a Drosophila model of Alzheimer's disease.
  9. Regulation of energy stores and feeding by neuronal and peripheral CREB activity in Drosophila
  10. JNK/FOXO-mediated neuronal expression of fly homologue of peroxiredoxin II reduces oxidative stress and extends life span
  11. Drosophila models of Alzheimer's amyloidosis: The challenge of dissecting the complex mechanisms of toxicity of amyloid-β 42
  12. Overexpression of neprilysin reduces alzheimer amyloid-β42 (Aβ42)-induced neuron loss and intraneuronal Aβ42 deposits but causes a reduction in cAMP-responsive element-binding protein-mediated transcription, age-dependent axon pathology, and premature death in Drosophila
  13. Aβ42 mutants with different aggregation profiles induce distinct pathologies in Drosophila
  14. Synthesis and characterization of Mg-containing nano-apatite
  15. Structural characterization and protein adsorption property of hydroxyapatite particles modified with zinc ions
  16. Physiological mouse brain Aβ levels are not related to the phosphorylation state of threonine-668 of Alzheimer's APP
  17. Synthesis and structural characterization of silica-hybridized hydroxyapatite with gas adsorption capability
  18. Synthesis and structural characterization of nanoapatite ceramics powders for biomedical applications
  19. cAMP-response element-binding protein and heat-shock protein 70 additively suppress polyglutamine-mediated toxicity in Drosophila
  20. Transgenic cAMP response element reporter flies for monitoring circadian rhythms

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