Neuroinflammation Imaging in Alzheimer’s Disease

Quantification of Neuroinflammation in Alzheimer’s Disease Using Diffusion Basis Spectrum Imaging

Our team has previously established the validity of diffusion basis spectrum imaging magnetic resonance imaging (DBSI MRI) for neuroinflammation in multiple sclerosis. We have used this in both in vivo and ex vivo mouse and human studies. We are now able to extend this novel biomarker of neuroinflammation to Alzheimer’s disease (AD).

Our hypothesis is that this relationship will be present in the earliest preclinical stages of AD, when cerebrospinal fluid (CSF) has abnormally low levels of Aβ but before abnormal levels of tau are observed.

We will validate this marker in vivo with positron emission tomography (PET) imaging of regional neuroinflammation. After validation, we will confirm with ex vivo autopsy of human microglial infiltration using immunohistochemistry and autoradiography. DBSI MRI sequences are FDA approved which makes this method ready for clinical trials.

PET-MRI Imaging of White Matter Damages and Inflammation in AD 

In this project will develop and validate a novel PET-MR imaging method by integrating amyloid PET and diffusion basis spectrum imaging (DBSI) to simultaneously measure white matter (WM) demyelination and inflammation in vivo.

Antecedent Biomarkers for AD: the Adult Children Study. Project 4: Structural Magnetic Resonance Imaging (MRI) to Assess Volume, Shape, and Thickness of Selected Brain Regions

This project uses structural MRI, diffusion tensor imaging, resting state functional MRI (fs-fcMRI), and arterial spin labeling (ASL) to identify the earliest possible imaging correlates of AD prior to symptoms onset. The focus of the ACS and this project is the discovery of predictive and diagnostic biomarkers of AD. A more complete view of brain metabolism, specifically as it relates to synaptic function, and AD pathology would be extremely helpful in achieving a better understanding of AD pathophysiology and assisting in the design and control of appropriate preventive treatments which may seek to modify synaptic function.