• Skip to main content
  • Skip to after header navigation
  • Skip to site footer
ERN: Emerging Researchers National Conference in STEM

ERN: Emerging Researchers National Conference in STEM

  • About
    • About AAAS
    • About the NSF
    • About the Conference
    • Partners/Supporters
    • Project Team
  • Conference
  • Abstracts
    • Undergraduate Abstract Locator
    • Graduate Abstract Locator
    • Abstract Submission Process
    • Presentation Schedules
    • Abstract Submission Guidelines
    • Presentation Guidelines
  • Travel Awards
  • Resources
    • Award Winners
    • Code of Conduct-AAAS Meetings
    • Code of Conduct-ERN Conference
    • Conference Agenda
    • Conference Materials
    • Conference Program Books
    • ERN Photo Galleries
    • Events | Opportunities
    • Exhibitor Info
    • HBCU-UP/CREST PI/PD Meeting
    • In the News
    • NSF Harassment Policy
    • Plenary Session Videos
    • Professional Development
    • Science Careers Handbook
    • Additional Resources
    • Archives
  • Engage
    • Webinars
    • ERN 10-Year Anniversary Videos
    • Plenary Session Videos
  • Contact Us
  • Login

Methamphetamine Mediated Mitochondrial Dysfunction and Microglial Apoptosis

Undergraduate #11
Discipline: Biological Sciences
Subcategory: Cell and Molecular Biology

Elizabeth Quaye - University at Buffalo
Co-Author(s): Donald Sykes, Stanley A. Schwartz, and Supriya D. Mahajan, University at Buffalo, Buffalo, NY



Meth induced damage of the nerve terminals of dopamine-producing neuronal cells triggers activation of apoptotic mechanisms resulting in the complete disintegration and death of neurons, astroglia and microglia. This results in neurotoxicity and neurodegeneration causing significant neuropsychological complications. The exact molecular mechanisms of Meth-induced neurotoxicity remain unclear. Meth mediated apoptosis is accompanied by nuclear damage and differential expression of pro- and antiapoptotic proteins. In the current study, we will examine an array of pro- and antiapoptotic biomarkers that are activated as a consequence of Meth treatment. This will help us identify the specific mechanisms that underlies Meth induced apoptosis. We hypothesized that increasing concentrations of Meth will cause microglial apoptosis which induces mitochondrial dysfunction leading to neurodegeneration. Our goal was to evaluate if Meth treatment induced the activation of the mitochondrion-dependent intrinsic pathway. Gene expression of pro- and antiapoptotic genes were quantitated with QPCR using RNA extracted from cultured microglial cell line (HTHU). Our results indicated that Meth treatment resulted in a significant increase in the gene expression levels of apoptotic proteins like APAF-1, BAX and BCL-2. Analysis of Western Blot data showed a significant modulation of the expression level of the antiapoptotic protein BCL-2 with varying Meth concentrations. Using immunofluorescence analysis we examined the expression of mitochondrial proteins, Cytochrome C, COX 4 and MCL-1, all of which were significantly activated on Meth treatment indicating the activation of the mitochondrion-dependent (intrinsic) apoptotic pathway. We conclude that Meth causes microglial apoptosis via the intrinsic pathway contributing to neurotoxicity and subsequent neurodegeneration.

Funder Acknowledgement(s): The CLIMB UP Summer Research Program, specifically the Institute for the Strategic Enhancement of Educational Diversity.

Faculty Advisor: Supriya Mahajan, smahajan@buffalo.edu

Role: The focus of my mentor and her lab members’ research is on the regulation of apoptosis and the various ways in which it is mediated. Some projects look at the role of Galectin-3 in apoptosis as a novel therapeutic target. My project, which was a subset of a larger initiative, looks at the way in which Meth mediates mitochondrial dysfunction or toxicity ultimately leading to the death of the brain’s support cells, the microglia. I was responsible for plating and splitting the cultured HTHU cells as well as Western Blot anaylsis, qPCR, TUNEL staining and an array of other biological assays.

Sidebar

Abstract Locators

  • Undergraduate Abstract Locator
  • Graduate Abstract Locator

This material is based upon work supported by the National Science Foundation (NSF) under Grant No. DUE-1930047. Any opinions, findings, interpretations, conclusions or recommendations expressed in this material are those of its authors and do not represent the views of the AAAS Board of Directors, the Council of AAAS, AAAS’ membership or the National Science Foundation.

AAAS

1200 New York Ave, NW
Washington,DC 20005
202-326-6400
Contact Us
About Us

  • LinkedIn
  • Facebook
  • Instagram
  • Twitter
  • YouTube

The World’s Largest General Scientific Society

Useful Links

  • Membership
  • Careers at AAAS
  • Privacy Policy
  • Terms of Use

Focus Areas

  • Science Education
  • Science Diplomacy
  • Public Engagement
  • Careers in STEM

Focus Areas

  • Shaping Science Policy
  • Advocacy for Evidence
  • R&D Budget Analysis
  • Human Rights, Ethics & Law

© 2023 American Association for the Advancement of Science