LaDu Lab

Mary Jo LaDu, PhD

1958-2023
In Memorium

Dr Mary Jo La Du passed away unexpectedly this week. This is a terrible loss for the Department, the College of Medicine and the University, bringing with it profound grief. MJ was a dynamic force and a change agent. She worked tirelessly to help students, postdocs and fellow faculty members on both the east and west campuses. It is hard to think of a role that she has not played in her time as a student and valued colleague in the academic success of UIC and particularly of the College of Medicine. This message reflects the memories of myself and others in the Department and the College.

After obtaining a BA from Grinnell College, MJ went on to earn her PhD at UIC in Physiology and Biophysics and Exercise Physiology in 1991 under the mentorship of Warren Palmer. Current members of the Physiology & Biophysics Department who remember her have expressed their feeling of loss. From there she went on to do research as a Post-Doctoral Fellow at the University of Chicago and industry before launching her own research program and becoming a Principal Investigator at Northwestern University in the Department of Medicine at Evanston and Northwestern Hospitals. MJ was a significant contributor to the Alzheimer's Disease Center at Northwestern University. She was a physiologist and biochemist who was early to realize the importance of developing animal models of Alzheimer's disease. An insight which catapulted her into the center of understanding of the disease.

Dr. Scott Brady, then Department Head of Anatomy & Cell Biology, recruited Dr. La Du back to UIC in 2005 as an Associate Professor. She brought with her the energy, enthusiasm and drive we all will remember her fondly for. MJ became a Full Professor in 2014, winning many accolades along the way. These bare facts do not, however, give an adequate description of the role she played at UIC. She was a proud UIC alumna and worked very hard to defend, advocate, and promote UIC. This was reflected in her roles and contributions at the University of Illinois system level, UIC Faculty Senate and College of Medicine. She was a life member of the University of Illinois President's Council, a University Scholar, a member of the Faculty-Administrator Leadership Program, an Innovator of Today winner, a Honors College Fellow of the Year, and a life member of the College of Medicine William W Root Society.

Dr. La Du was deeply involved in the governance of UIC and the College of Medicine through her service to the College and University. She was recognized as a leader and articulate spokesperson for the faculty by her peers. As a result, she was elected a member of the Executive Committee for the UI College of Medicine for 10 of the last 11 years. Similarly, she was a member of UIC Faculty Senate for 10 years, serving on the Executive Committee of the Senate for 8 of those years. She will be remembered for her invaluable and numerous service contributions ranging from standing committees to search committees for leadership positions to advisory committees for the leadership, including the UIC Senate and the University Senates Conference that have impacted the function of the Department absolutely, the college, UIC and the University as a whole. Outside of UIC MJ contributed to editorial and manuscript peer reviewing, grant reviewing at NIH, specifically two decades of service to the National Institute of Aging, and Foundations too numerous to count.

MJ ran a large NIH- and pharma-funded lab focusing on treatments and biomarkers for Alzheimer's disease, and her research has generated more than 100 publications, numerous research grants as primary investigator with continuous NIH funding since 1995, more than 80 grants, an NIH program project grant, the Alzheimer’s Association Zenith Award in 2008, the College of Medicine Innovator of the Year in 2016, the Mentor of the Year from the UIC Honors College in 2019 and numerous awards for her students and postdocs. She also received the Chancellor’s Innovation Fund and the new DPI Phase-2 Innovation Award. She was passionate about her research and continuously worked toward her goal of finding a cure for Alzheimer's disease.

MJ's contributions were profound. Over the last 30 years she pioneered research on identifying mechanisms of how APOE4 genotype, the greatest genetic risk for Alzheimer's disease impacts brain biology. Her science was truly impactful, and she found mechanistic pathways of how APOE4 and female sex interact to modulate Ab levels, inflammation, and other key aspects of Alzheimer's disease progression. She also conducted many preclinical compound screening studies in the hope of one day finding a therapy for Alzheimer's disease for APOE4 patients. Always the innovator, she developed antibodies, novel ELISAs and mouse models to address key questions of APOE biology. These key resources are used worldwide by faculty and industry researchers, to help understand Alzheimer's disease. One of her collaborators noted that “I can't imagine the last thirty years of APOE research without her.”

Among MJ's many legacies are that of an educator and mentor par excellence, an individual who lit the spark of discovery and creativity in her trainees. She had a special talent for recruiting bright undergraduate (Honors College and GPPA) students, novices of science, and instilling in them the importance of critical thinking, rigorous methodology and commitment while triggering their intellectual curiosity. An indelible memory we will all share is that of MJ with her bevy of postdoctoral, graduate and undergraduate trainees, holding “court” (i.e. lab discussions) replete with iPads and posters on the grassy green of the courtyard behind COMRB with its electric blue chairs.

The loss of MJ is incalculable. Her presence will be missed by the Department as well as numerous other colleagues and friends in the College, the University and far beyond. I struggle to come to terms with her passing and know from conversations and messages with you that I am far from alone in this. May she rest in peace and her memories be a blessing.

Simon Alford
Sweeney Professor of Basic Sciences and Head
Department of Anatomy and Cell Biology
University of Illinois at Chicago College of Medicine


Lab Focus

With a new case developing every 66 seconds in the US, Alzheimer's disease (AD) is a fatal neurodegenerative disease diagnosed post-mortem by the presence of amyloid plaques composed of amyloid-β peptide (Aβ) and neurofibrillary tangles composed of tau. 

While age is the greatest overall risk factor for AD, the APOE4 gene, encoding the apolipoprotein E4 (apoE4) isoform, is the greatest genetic risk factor for AD, increasing risk up to 15 fold compared to the common APOE3 genotype. APOE4 is associated with increased levels of Aβ, resulting in increased levels of both amyloid plaques and soluble neurotoxic oligomeric Aβ. Importantly, female APOE4 carriers have a greater lifetime risk for developing AD, and an accelerated accumulation of Aβ compared to male APOE4 carriers. Therefore, age, APOE genotype, and sex, are classified as universal biological variables (UBVs) for AD risk. 

Our lab focuses on the properties and interactions between the two proteins that are linked to AD: Aβ and apoE, in the context of the UBVs. Our research on AD is conducted using the novel EFAD transgenic mouse model that expresses human APOE and develops AD-like pathology, which allows for stratification by APOE genotype and sex. Thus, the EFAD mice allow us to assess the interaction between APOE and Aβ as influenced by the  UBVs.

Recent Publications

Taixer.NeuroAging.2022.pdf

Taxier LR, Philippi SM, Fleischer AW, York JM, LaDu MJ, Frick KM.

APOE4 homozygote females are resistant to the beneficial effects of 17β-estradiol on memory and CA1 dendritic spine density in the EFAD mouse model of Alzheimer's disease.

Neurobiology of aging. 2022 doi: 10.1016/j.celrep.2022.111417.


Taxier.NeuroAging.2022.pdf

Taxier, L.R., Philippi, S.M., York, J.M., LaDu, M.J., and K.M. Frick.

The detrimental effects of APOE4 on risk for Alzheimer’s disease may result from altered dendritic spine density, synaptic proteins, and estrogen receptor alpha. 

Neurobiology of Aging. 2022 doi: 10.1016/j.neurobiolaging.2021.12.006


The LaDu lab is funded by NIH (NIA) R01 AG056472, R01 AG057008, UH2/3 NS10012, R56 AG058655, 1R44 AG060826, AD Assoc. SAGA, UIC-DPI Phase 2 POC Award, pharmaceutical company contracts and philanthropic support from Lou and Christine Friedrich.