Kanae Iijima-Ando, PhD
Philadelphia, PA 19107
(215) 955-4949 fax
Most Recent Peer-reviewed Publications
- Loss of Axonal Mitochondria Promotes Tau-Mediated Neurodegeneration and Alzheimer's Disease-Related Tau Phosphorylation Via PAR-1
- Membrane-microdomain localization of amyloid β-precursor protein (APP) C-terminal fragments is regulated by phosphorylation of the cytoplasmic Thr668 residue
- Transgenic drosophila models of Alzheimer's amyloid-β 42 toxicity
- Tau Ser262 phosphorylation is critical for Aβ42-induced tau toxicity in a transgenic Drosophila model of Alzheimer's disease
- Transgenic drosophila models of Alzheimer's disease and tauopathies
Research and Clinical Interests
Drosophila Neurobiology, neurodegenerative diseases,Synucleopathy
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.