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Alzheimers Dement (Amst). 2015 Dec 28;2:58-67. doi: 10.1016/j.dadm.2015.11.008. eCollection 2016.

Prediction of Alzheimer's disease pathophysiology based on cortical thickness patterns.

Author information

1
Department of Neurology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea.
2
Department of Neurology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea; Department of Medical Engineering, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea.
3
Department of Biomedical Engineering, Hanyang University, Seoul, Korea.
4
Department of Neurology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea; Department of Anatomy and Cell Biology, Cell Dysfunction Research Center (CDRC), University of Ulsan College of Medicine, Seoul, Korea.
5
Department of Neurology, Samsung Medical Center, School of Medicine, Sungkyunkwan University, Seoul, Korea; Neuroscience Center, Samsung Medical Center, Seoul, Korea; Department of Health Sciences and Technology, SAIHST, Sungkyunkwan University, Seoul, Korea.

Abstract

INTRODUCTION:

Recent studies have shown that pathologically defined subtypes of Alzheimer's disease (AD) represent distinctive atrophy patterns and clinical characteristics. We investigated whether a cortical thickness-based clustering method can reflect such findings.

METHODS:

A total of 77 AD subjects from the Alzheimer's Disease Neuroimaging Initiative 2 data set who underwent 3-T magnetic resonance imaging, [(18)F]-fluorodeoxyglucose-positron emission tomography (PET), [(18)F]-Florbetapir PET, and cerebrospinal fluid (CSF) tests were enrolled. After clustering based on cortical thickness, diverse imaging and biofluid biomarkers were compared between these groups.

RESULTS:

Three cortical thinning patterns were noted: medial temporal (MT; 19.5%), diffuse (55.8%), and parietal dominant (P; 24.7%) atrophy subtypes. The P subtype was the youngest and represented more glucose hypometabolism in the parietal and occipital cortices and marked amyloid-beta accumulation in most brain regions. The MT subtype revealed more glucose hypometabolism in the left hippocampus and bilateral frontal cortices and less performance in memory tests. CSF test results did not differ between the groups.

DISCUSSION:

Cortical thickness patterns can reflect pathophysiological and clinical changes in AD.

KEYWORDS:

Alzheimer's Disease Neuroimaging Initiative; Alzheimer's disease; Cortical thickness; Magnetic resonance imaging; Positron emission tomography

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