• Login
    View Item 
    •   SMARTech Home
    • Undergraduate Research Opportunities Program (UROP)
    • Undergraduate Research Option Theses
    • View Item
    •   SMARTech Home
    • Undergraduate Research Opportunities Program (UROP)
    • Undergraduate Research Option Theses
    • View Item
    JavaScript is disabled for your browser. Some features of this site may not work without it.

    A Meta-Analysis Assessing the Role of Phosphorylated Tau and Amyloid-Beta on Cognitive Decline in a Preclinical Model Of Alzheimer's Disease

    Thumbnail
    View/Open
    HUBER-UNDERGRADUATERESEARCHOPTIONTHESIS-2017.pdf (1.242Mb)
    Author
    Huber, Colin Michael
    Metadata
    Show full item record
    Abstract
    Alzheimer’s Disease (AD) pathology is characterized by the accumulation of extracellular amyloid-β (Aβ) plaques in the brain followed by growth of phosphorylated tau (pTau) proteins into neurofibrillary tangles (NFTs). Both Aβ plaques and NFTs interfere with normal neuronal cell function by disrupting proper synaptic signaling and inflicting damage to neurons, eliciting cognitive decline. The presence of Aβ coincides with a decrease in cognitive performance; however, quantified Aβ accumulation does not correlate with cognitive decline. There have been no FDA-approved drugs capable of curing AD or delaying disease progression with research efforts heavily focused on amyloid-β as the primary causative agent in AD pathology. We performed a meta-analysis examining research studies matching inclusion criteria extracted from a database of more than 3,000 Alzheimer’s mouse model peer-reviewed articles. Phosphorylated tau, total tau, and amyloid-β levels were compared to measure the largest impact on cognitive performance by correlative assessment with Morris water maze escape latency and Novel Object Recognition. Phosphorylated tau accumulation into NFTs more strongly correlates with cognitive decline than Aβ despite a smaller total concentration, and therefore, pTau may contribute more to Alzheimer’s Disease progression. The two proteins interact through GSK3β and other phosphorylation pathways causing more rapid cognitive decline, and the onset of Aβ leads to the development of NFTs. Aβ and tau pathologies are interwoven in a complex manner that prevents separation. Alzheimer’s disease treatment will require the removal of both protein accumulation, and research should focus on combination drugs and defining the connection between Aβ and pTau.
    URI
    http://hdl.handle.net/1853/60328
    Collections
    • Department of Biomedical Engineering Undergraduate Research Option Theses [169]
    • Undergraduate Research Option Theses [631]

    Browse

    All of SMARTechCommunities & CollectionsDatesAuthorsTitlesSubjectsTypesThis CollectionDatesAuthorsTitlesSubjectsTypes

    My SMARTech

    Login

    Statistics

    View Usage StatisticsView Google Analytics Statistics
    • About
    • Terms of Use
    • Contact Us
    • Emergency Information
    • Legal & Privacy Information
    • Accessibility
    • Accountability
    • Accreditation
    • Employment
    • Login
    Georgia Tech

    © Georgia Institute of Technology

    • About
    • Terms of Use
    • Contact Us
    • Emergency Information
    • Legal & Privacy Information
    • Accessibility
    • Accountability
    • Accreditation
    • Employment
    • Login
    Georgia Tech

    © Georgia Institute of Technology