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dc.contributor.authorKosel, Filip
dc.date.accessioned2019-11-28T16:32:38Z
dc.date.available2019-11-28T16:32:38Z
dc.date.issued2019-11-28T16:32:38Z
dc.identifier.urihttp://hdl.handle.net/10222/76703
dc.description.abstractThe 5xFAD mouse strain is a double-transgenic Alzheimer’s disease (AD) model containing mutant APP (K670N/M671L, I716V, and V717I) and PS1 (M146L and L286V) genes. Mice expressing these mutations have rapid accumulation of beta-amyloid in the central nervous system, subsequent neurodegeneration, and impaired synaptic signaling. While previous work with the strain has focused on cognitive, sensory, and motor function, few studies have investigated if this strain models the social deficits commonly present in AD patients. This work examined responses to social odour cues, social approach, social novelty preference, social recognition memory, and reciprocal social interactions in 3- to 9-month old females, and aggression and dominance in 6- month-old males. Results indicate that 5xFAD transgenic male and female mice engage in reduced social interaction and 5xFAD transgenic male mice exhibit increased aggression leading to injury. This study has implications for future research on neurological underpinnings of social deficits in human AD patients.en_US
dc.language.isoenen_US
dc.subjectAlzheimer's diseaseen_US
dc.subject5xFADen_US
dc.subjecttransgenicen_US
dc.subjectmouse modelen_US
dc.subjectsocial behaviouren_US
dc.titleCHARACTERIZATION OF SOCIAL DEFICITS IN THE 5XFAD MOUSE MODEL OF ALZHEIMER'S DISEASEen_US
dc.date.defence2018-08-07
dc.contributor.departmentDepartment of Psychology and Neuroscienceen_US
dc.contributor.degreeMaster of Scienceen_US
dc.contributor.external-examinern/aen_US
dc.contributor.graduate-coordinatorDr. Gail Eskesen_US
dc.contributor.thesis-readerDr. Tamara B. Franklinen_US
dc.contributor.thesis-readerDr. Richard E. Brownen_US
dc.contributor.thesis-readerDr. Sultan Darveshen_US
dc.contributor.thesis-supervisorDr. Tamara B. Franklinen_US
dc.contributor.ethics-approvalReceiveden_US
dc.contributor.manuscriptsNoen_US
dc.contributor.copyright-releaseNot Applicableen_US
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