Abstract Details

Title Quantitative Susceptibility Mapping MRI to Assess the Relationship Between Iron Accumulation and Hippocampal Atrophy as a Measure of the N Aspect of the A/T/N Alzheimer’s Disease Definition

Topic Aging, Dementia, and Behavioral Neurology

Presentation(s) P2 - Poster Session 2 (8:00 AM-9:00 AM)

Poster/Presentation
Number 10-009

Objective The objective of this study was to determine if there is a relationship between iron accumulation in the brain as assessed by susceptibility changes measured with Quantitative Susceptibility MRI (QSM-MRI) and hippocampal volume in participants across the spectrum from intact cognition to the early stages of Alzheimer’s disease.

Background Iron is an essential element for normal neuronal functioning. It is required for metabolic processes and it is required for the production of myelin. The accumulation of brain iron may signal a reduction in neuronal metabolism and/or trigger a neuroinflammatory microglial response. This has led to the hypothesis that disruption of brain iron homeostasis contributes to Alzheimer’s disease.

Design/Methods This study used a cross-sectional design. MRI scans (T1 MPRAGE, QSM-MRI with multi-echo acquisition) were acquired at the Center for Biomedical Imaging on 57 participants from the Boston University Alzheimer’s Disease Center. Freesurfer 6.0 was used to generate regional brain volumes. The T1 maps from Freesurfer were co-registered with the QSM scans to get regional brain QSM intensity values using PETSurfer. In order to reduce the number of variables, values from the two hemispheres were combined (volumes added, intensity values averaged). Stepwise multiple regression was conducted in JMP 14 with measures of brain size, atrophy and total cerebral white matter volume forced into the analyses as control variables.

Results The multiple regression produced a significant model (Adjusted R Squared = 0.728). Following FDR correction, susceptibility values from regions known for Tau accumulation (Entorhinal Cortex, Hippocampus) and Amyloid accumulation (Superior Parietal, Precuneous, Banks STS, Superior Frontal, Superior Temporal) remained as significant contributors to the model of hippocampal volume.

Conclusions These findings lend credence to the notion that a disruption of brain iron homeostasis is a credible component of the neuropathological events that produce the biological definition of Alzheimer’s disease.

Authors/Disclosures
Ronald J. Killiany, PhD (Boston University School of Medicine) PRESENTER	Dr. Killiany has nothing to disclose.
	No disclosure on file
	No disclosure on file
	No disclosure on file
Michael Alosco, PhD (Boston University)	The institution of Michael Alosco, PhD has received research support from NIH. The institution of Michael Alosco, PhD has received research support from Life Molecular Imaging Inc.
Jesse B. Mez, MD (Boston University School of Medicine)	The institution of Dr. Mez has received research support from NIH, DOD.
Robert Stern, PhD (Boston University School of Medicine)	Robert Stern, PhD has received personal compensation in the range of $10,000-$49,999 for serving as a Consultant for Biogen. The institution of Robert Stern, PhD has received research support from Eisai. The institution of Robert Stern, PhD has received research support from Lilly. The institution of Robert Stern, PhD has received research support from ATRI/NIA. Robert Stern, PhD has received publishing royalties from a publication relating to health care. Robert Stern, PhD has a non-compensated relationship as a Member with NFLPA Mackey-White Committee that is relevant to �鶹��ýӳ�� interests or activities.

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