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Noel Y. Calingasan

Researcher at Cornell University

Publications -  117
Citations -  9869

Noel Y. Calingasan is an academic researcher from Cornell University. The author has contributed to research in topics: Neuroprotection & Oxidative stress. The author has an hindex of 56, co-authored 116 publications receiving 9198 citations. Previous affiliations of Noel Y. Calingasan include Obihiro University of Agriculture and Veterinary Medicine & Washington State University.

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Neural subtype specification of fertilization and nuclear transfer embryonic stem cells and application in parkinsonian mice.

TL;DR: A set of coculture conditions is provided that allows rapid and efficient derivation of most central nervous system phenotypes and transplantation of ES and ntES cell–derived dopaminergic neurons corrected the phenotype of a mouse model of Parkinson disease, demonstrating an in vivo application of therapeutic cloning in neural disease.
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Protein-bound acrolein: a novel marker of oxidative stress in Alzheimer's disease.

TL;DR: The results suggest that protein‐bound acrolein is a powerful marker of oxidative damage to protein and support the hypothesis that lipid peroxidation and oxidativedamage to protein may play a crucial role in the formation of neurofibrillary tangles and to neuronal death in AD.
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Increased plaque burden in brains of APP mutant MnSOD heterozygous knockout mice

TL;DR: In this article, the authors showed that partial deficiency of MnSOD, which is well established to cause elevated oxidative stress, significantly increased brain Aβ levels and plaque burden in Tg19959 mice.

COMMUNICATION Increased plaque burden in brains of APP mutant MnSOD heterozygous knockout mice

TL;DR: Complete deficiency of MnSOD, which is well established to cause elevated oxidative stress, significantly increased brain Aβ levels and Aβ plaque burden in Tg19959 mice, indicating that oxidative stress can promote the pathogenesis of AD and support the feasibility of antioxidant approaches for AD therapy.
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Impaired PGC-1α function in muscle in Huntington's disease

TL;DR: Findings show that impaired function of PGC-1alpha plays a critical role in muscle dysfunction in Huntington's disease, and that treatment with agents to enhance P GC-1 alpha function could exert therapeutic benefits, and muscle may provide a readily accessible tissue in which to monitor therapeutic interventions.