2021 Alzheimer's Association Research Fellowship (AARF)

Amyloid-beta and Tau Propagation Along Gradients of Connectivity in AD

What is the biology by which abnormal proteins are transported in the brain in Alzheimer’s?

Julie Ottoy, Ph.D.
Sunnybrook Research Institute
Toronto, Canada

Background

The proteins beta-amyloid and tau accumulate to form plaques and tangles respectively, the two main hallmark brain changes observed in Alzheimer’s. Studies show that abnormal levels of beta-amyloid and tau proteins may be associated with nerve cell damage and death and this could impact memory and cognition. However, the biological mechanisms by which these abnormal proteins move throughout the brain is not yet well understood.

Research Plan

Dr. Julie Ottoy and colleagues will study how brain’s structure and function may be impacted in individuals with Alzheimer’s. The researchers will leverage brain scan datasets (including PET, Positron Emission Tomography and MRI, Magnetic Resonance Imaging) of more than 700 individuals from two large ongoing studies of aging - the Alzheimer’s Disease Neuroimaging Initiative (ADNI) and Montreal Translational Biomarkers of Aging and Dementia (TRIAD). These individuals include those who are cognitively unimpaired and other individuals in different stages of Alzheimer’s. 

Dr. Ottoy and colleagues will use advanced statistical and computational techniques to study the biological pathways associated with the movement of abnormal proteins across brain areas. Further, the researchers will study whether the movement of these proteins in the brain may be associated with changes in cognition in the participants. Dr. Ottoy believes that using these sophisticated techniques to analyze large datasets, may help them understand differences in the biology of movement of abnormal proteins in the brain and their potential impact on cognition among individual participants.

Impact

This project may contribute to the understanding the biology of how abnormal proteins could be transported in the brains of individuals with Alzheimer’s. The results could lead to the development of potentially personalized treatment strategies that may tackle the movement of abnormal proteins in the brain in Alzheimer’s.