Mackenzie Beam

330 North Orchard Street, Room 4170T-1
Madison WI 53715
Preferred pronouns: she/her/hers
Joined WID: 2021

Mechanism that links neurodegenerative diseases to lysosomal and endosomal dysfunction.


Mackenzie was born in Columbus, Ohio and moved to Madison to pursue a bachelors in Biomedical Engineering and a certificate in Gender and Women's Studies. She is anticipated to graduate in May of 2023.


  • BS, Biomedical Engineering, UW–Madison (in progress)
  • Certificate in Gender and Women's Studies, UW–Madison (in progress)

Research Description

Individuals with Down Syndrome (DS) exhibit a significantly higher risk of developing Alzheimer’s disease (AD) compared to the general population due to a triplication of the APP gene. Recent studies have shown that that APP-Beta-C terminal fragments (APP-BetaCTFs), formed through cleavage of APP by Beta-secretase, play a key role in the development of endosomal/lysosomal pathway dysfunction in DS and AD. This dysfunction occurs early in the course of both AD and DS and contributes to the mechanisms of neurodegeneration. Our lab has previously shown that CRISPR/Cas9 mediated knockout of the APP C-terminal region reduces Beta-secretase cleavage and down regulates APP-BetaCTF production. Therefore, we hypothesize that this editing strategy can be used to ameliorate endosomal/lysosomal pathway dysfunction in DS fibroblasts.To test this hypothesis, Haley Feinzig and I will evaluate the size and number of early endosomes, lysosomal acidification, and cathepsin activity in edited DS fibroblasts compared to both untreated DS fibroblasts and age-matched control fibroblasts. Results of this study will help to elucidate early pathological mechanisms in DS and AD that will further aid the research for potential therapeutics. Haley and I are conducting this research under the guidance and mentorship of Kirstan Gimse.


  • ACLU - Undergraduate organization
  • Biomedical Engineering Society


Dean's Honor List (Fall 2019, Spring 2020, Fall 2020, Spring 2021)