Brain-immune Interactions in Neurodegenerative Disease (2016-2017)


Alzheimer’s disease is a complex chronic disease of the brain that significantly decreases memory and learning, and is ultimately fatal. The mechanism behind the onset or progression of Alzheimer’s remains unknown. Although the common view is that A-beta peptide is the principal causative factor, multiple unsuccessful clinical trials have lessened the enthusiasm for this concept and have stimulated the search for alternative pathways. Understanding these pathways may increase our ability to offset this devastating disease process.

Project Description

This project team focuses on the study of neurodegeneration and, in particular, Alzheimer’s disease (AD). Our experiments are designed to understand basic pathophysiological mechanisms of brain disease. We have found that an integrated research team best carries out this approach and will incorporate the Colton, Gottshalk and Chiba-Falek Labs in the Department of Neurology. Team interactions include a monthly joint lab meeting and interaction with the other research labs located on the same floor of the Bryan Research Building.

In 2016-17 we will emphasize two major areas: clinical research (overview of the planning and execution of successful human studies, including the scientific, legal and ethical aspects of study design, and subject recruitment and retention for the length of the study; and caregivers of AD patients (social work and educational aspects of the AD caregiver community). We also continue our groundbreaking studies on the causes of AD. This year we will accelerate our use of large data sets and bioinformatics to understand mechanisms and how biological systems are changed in AD.

Students will complete all required safety courses for work in research labs at Duke and will also complete modules on the humane treatment of animals in research. Although the projects throughout the team are interconnected, students are expected to focus on one ongoing research project in one of the three faculty labs.

In the Colton lab, we are particularly interested in the role that the immune system plays in chronic brain disease such as AD. In the Gottshalk lab, we are interested in mitochondrial effects of a recently discovered risk polymorphism for late-onset AD that is located in the TOMM40 gene. In the Chiba-Falek lab, we are interested in the genetic factors and molecular mechanisms underlying neurodegenerative diseases of the aging brain in particular Alzheimer’s diseases and related dementia conditions.

Student projects will address aspects of research on Alzheimer’s disease and will include the design, execution and analysis of a specific research plan. Students are asked to read appropriate scientific literature to understand the basis for their project and be able to discuss these topics and their experiments in the lab, at lab/team meetings and at other scientific meetings. If the opportunity is available, students are encouraged to participate or present data in meetings outside of Duke.

Anticipated Outcomes

This team will generate basic research data and present findings at scientific meetings and in publication format. Students are encouraged to participate fully as team members and as such, will represent the labs in many different formats including publications, abstracts and website information.  


Summer 2016 (May 31 – August 5) – Spring 2017

Team Outcomes to Date

Genomic Instability in Alzheimer’s Disease: TOMM40 Poly-T Variations (Kathy Z. Dai, Omolara-Chinue Glenn, Julio A. Barrera, Ornit Chiba-Falek)

See earlier related team, Brain-immune Interactions in Neurodegenerative Disease (2015-2016).

Faculty/Staff Team Members

Ornit Chiba-Falek, School of Medicine - Neurology*
Carol Colton, School of Medicine - Neurology
William Gottschalk, School of Medicine - Neurology*

Undergraduate Team Members

Kathy Dai, Chemistry (AB), Neuroscience (AB2)
Ryan Kramer, Evolutionary Anthropology (BS)
Christine O'Connell, Neuroscience (AB)
Rema Shah, Neuroscience (AB)

* denotes team leader