Currently seeking post doctoral fellows: information here
Congratulations to Dr. Mary Jo LaDu, named the Dept of Anatomy 2013 Faculty of the Year (Mar '13)!
UIC News Release (Feb '13) New Alzheimer's test may identify those at risk
Recent publication (Feb '13) selected JBC Paper of the Week (Author Profile):
"Levels of soluble apolipoprotein E/amyloid-β complex are reduced and oligomeric Aβ increased with APOE4 and Alzheimer disease in a transgenic mouse model and human samples" (Tai, Leon M., et. al, LaDu, MJ)
Recent publication (Dec '12) selected :
"APOE4-specific changes in Aβ accumulation in a new transgenic mouse model of Alzheimer's disease" (Youmans, KL., Tai, Leon M., et. al, LaDu, MJ)
Congratulations to Dr. Leon Tai for winning the ADDF Young Investigator Scholarship (Dec '12)
Congratulations to Dr. Leon Tai for winning the Gold First prize in the post-doctoral category of the COM Research Forum 2012 poster competition! (Nov '12)
UIC News Release (Nov '12):
New, Improved Mouse Model of Human Alzheimer's May Enable Drug Discovery
Welcome to the LaDu Neurodegeneration Research lab
Alzheimer disease (AD) has reached epidemic proportions, representing a serious economic and social burden worldwide.
- Over the last decade, AD mortality has increased 66% to become the sixth leading cause of death.
- AD occurs in 1 of 8 Americans aged 65 and 50% over age 85.
- The current annual cost to America is ~$183 billion, increasing to 1.1 trillion by 2050.
- Currently there is no cure and only temporary symptomatic management is available.
Mary Jo LaDu, PhD
Department of Anatomy and Cell Biology
University of Illinois at Chicago
Dr LaDu's lab studies the pathology of Alzheimer disease (AD) by focusing on the structure/function
interactions between the human isoforms of apolipoprotein E (apoE) and
amyloid-β peptide (Aβ). A naturally occurring isoform of the
APOE gene, apoE4, increases lifetime risk for AD 60-fold compared to the
more common apoE3. Aβ, particularly oligomeric aggregates (oAβ),
is considered a major cause of AD. Our overall hypothesis is that apoE4
and oAβ act synergistically to compromise neuronal viability. We
utilize an integrated approach to address the complexity of apoE/Aβ
interactions, including biochemical, molecular biology, and cell biology
methods using in vitro, ex vivo, and in vivo models. Our goal is to
develop oAβ and apoE/Aβ complex as "mechanistic biomarkers" and
therapeutic targets as both are significant prior to neuronal damage.
Neuron stained via novel method to identify earliest possible markers for
neuronal distress. Heath, JNS, 2012
Current research interests include:
- Effect of APOE genotype on Aβ accumulation and speciation
- Role of apoE/Aβ complex in Aβ clearance with a focus on ApoE isoform, apoE levels and apoE lipidation.
- oAβ and apoE/Aβ ELISAs as mechanistic biomarkers for AD
- Effect of apoE isoform on inflammation and synapse viability.
- Development and testing of AD therapeutics including:
- ApoE-dependent therapeutics targeting apoE/Aβ complex and
- ApoE-independent therapeutics whose efficacy may be affected by apoE