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Full-Text Articles in Genetic Phenomena
Discovery Of Distinct Mechanisms Underlying The Relationship Between Drug Taking And Predisposing Behaviors, Tyler A. Roy
Discovery Of Distinct Mechanisms Underlying The Relationship Between Drug Taking And Predisposing Behaviors, Tyler A. Roy
Electronic Theses and Dissertations
Drug addiction is a heritable disease characterized by compulsive drug use. The biological mechanisms driving addiction remain largely unknown.1 Previous studies show shared genetic mechanisms underlying addiction risk phenotypes such as anxiety, depression, and novelty/sensation seeking.2,3 Therefore, high-throughput behavioral screening of these traits in single gene knockout mice can allow for the rapid detection of addiction risk candidate genes and mechanisms. Many of these traits are represented in the Knock-Out Mouse Program (KOMP) phenotyping pipeline. Of the initial two hundred twenty-one strains screened in this program, we tested nineteen phenodeviant knock-out mouse strains with C57BL/6NJ controls (N = …
Mitochondrial Mislocalization Underlies Abeta42-Induced Neuronal Dysfunction In A Drosophila Model Of Alzheimer's Disease., Kanae Iijima-Ando, Stephen A Hearn, Christopher Shenton, Anthony Gatt, Lijuan Zhao, Koichi Iijima
Mitochondrial Mislocalization Underlies Abeta42-Induced Neuronal Dysfunction In A Drosophila Model Of Alzheimer's Disease., Kanae Iijima-Ando, Stephen A Hearn, Christopher Shenton, Anthony Gatt, Lijuan Zhao, Koichi Iijima
Department of Biochemistry and Molecular Biology Faculty Papers
The amyloid-beta 42 (Abeta42) is thought to play a central role in the pathogenesis of Alzheimer's disease (AD). However, the molecular mechanisms by which Abeta42 induces neuronal dysfunction and degeneration remain elusive. Mitochondrial dysfunctions are implicated in AD brains. Whether mitochondrial dysfunctions are merely a consequence of AD pathology, or are early seminal events in AD pathogenesis remains to be determined. Here, we show that Abeta42 induces mitochondrial mislocalization, which contributes to Abeta42-induced neuronal dysfunction in a transgenic Drosophila model. In the Abeta42 fly brain, mitochondria were reduced in axons and dendrites, and accumulated in the somata without severe mitochondrial …