Dr. Iijima-Ando Kanae Iijima-Ando, PhD

Contact Dr. Iijima-Ando

900 Walnut St.
Suite 410
Philadelphia, PA 19107

215-503-9897
215-955-4949 fax

How Does α-Synuclein Cause Dopaminergic Neurospecific Toxicity in Parkinson's Disease?

Accumulation of misfolded-synuclein causes neurodegenerative disorders termed "synucleinopathies". It includes diseases with different clinical and pathological manifestations such as Parkinson's disease and Lewy body dementia (LBD). PD is characterized by loss of dopaminergic neurons in the Substantia Nigra, while cholinergic neurons are mainly affected in LBD. It suggests that an accumulation of a-synuclein may induce cell-type specific pathological consequences. My research focus on the mechanism underlying cell-type specificity of - synuclein induced toxicity.

We use fruit flies, Drosophila melanogaster, as a model system to search for genes that suppress neurodegeneration induced by a-synuclein. Fly models of Parkinson's Disease recapitulated some of the pathological features including neurodegeneration and aggregation formation. Flies have highly organized brains, and many genes and basic cellular machineries are conserved in flies. Short life span of the flies enable us to study age-dependent effect more time efficient manner. Furthermore, genetic tools are available for cell-type specific gene expression. We are searching candidate genes and pathways by DNA microarray analysis.

Drosophila can contribute to study of humandiseases as a tool of gene discovery and efficient mean for in vivo functional assessment of candidate genes. I hope my findings will shed light on pathogenesis of PD and other syncleinopathies and open novel therapeutic avenues in future.

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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