Abstract Details

Title Subfields of Medial Temporal Lobe Involvement in Prodromal Alzheimer's Disease and Semantic Dementia

Topic Aging and Dementia

Presentation(s) P06 - (-)

Poster/Presentation
Number 027

Objective

Background BACKGROUND: Both AD and SD have gross MTL atrophy. However, it is unclear whether MTL structures affected in AD are equally compromised in SD. Different forms of memory are relatively impaired: episodic memory loss is observed in AD, while semantic memory is impaired in SD. Differences in the distribution of atrophy in the MTL may explain distinct memory deficits. Therefore, we characterized patterns of MTL involvement in SD and prodromal AD, aMCI.

Design/Methods DESIGN/METHODS: Twelve SD patients (age range: 52-73), nineteen aMCI patients (age range: 58-80), and thirty control subjects (age range: 54-85) underwent a high in-plane resolution (0.4x0.4mm) T2 MRI imaging with contrast that allows visualization of the dark band that separates the cornu ammonis (CA) from dentate gyrus (DG). A semi-automated process based on a multi-atlas template of in vivo 4T MRI scans informed by hippocampal histology was applied to these images, with subsequent manual correction. In this analysis, we focus on subfields of the hippocampus (CA1, CA2, CA3 and DG). Shapiro-Wilks tests, ANCOVA and Turkey's HSD post-hoc test were employed.

Results RESULTS: We observed different patterns of MTL atrophy in aMCI and SD relative to to controls (CA1: pControl-aMCI=0.004, pControl-SD<0.001, pSD-aMCI<0.001; DG: pControl-aMCI>0.05, pControl-SD<0.001, pSD-aMCI<0.001). In aMCI, MTL atrophy involves hippocampal CA subfields, while DG is spared. However, all subfields in SD showed highly significant atrophy relative to aMCI and controls.

Conclusions CONCLUSIONS: Our findings demonstrate distinct patterns of MTL atrophy in aMCI and SD, and this may contribute to different memory system disorders in these conditions. Future work will examine this hypothesis with direct correlations between hippocampal subfields and memory performance.

Authors/Disclosures
PRESENTER	No disclosure on file
	No disclosure on file
Stephen Wanaski, PhD (Paragon Biosciences)	Dr. Wanaski has received personal compensation for serving as an employee of Paragon Biosciences. Dr. Wanaski has or had stock in Paragon Biosciences.Dr. Wanaski has or had stock in Emalex Biosciences.
	No disclosure on file
David A. Wolk, MD, FAAN (University of Pennsylvania)	Dr. Wolk has received personal compensation in the range of $500-$4,999 for serving as a Consultant for Eli Lilly. Dr. Wolk has received personal compensation in the range of $500-$4,999 for serving on a Scientific Advisory or Data Safety Monitoring board for Functional Neuromodulation. Dr. Wolk has received personal compensation in the range of $500-$4,999 for serving on a Scientific Advisory or Data Safety Monitoring board for GSK. The institution of Dr. Wolk has received research support from Biogen. Dr. Wolk has received publishing royalties from a publication relating to health care. Dr. Wolk has received personal compensation in the range of $5,000-$9,999 for serving as a CME speaker with Eli Lilly.
Murray Grossman, MD, FAAN (University of Pennsylvania)	Dr. Grossman has received personal compensation in the range of $5,000-$9,999 for serving as an Editor, Associate Editor, or Editorial Advisory Board Member for Neurology. The institution of Dr. Grossman has received research support from NIH.

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