Loading…

Excessive tau accumulation in the parieto-occipital cortex characterizes early-onset Alzheimer’s disease

Abstract Early-onset Alzheimer’s disease (EOAD) is characterized by greater non-memory dysfunctions, more rapid progression, and greater hypometabolism and atrophy than late-onset AD (LOAD). We sought to investigate the differences in tau accumulation patterns between early- and late-onset patients...

Full description

Saved in:
Bibliographic Details
Published in:Neurobiology of aging 2017-05, Vol.53, p.103-111
Main Authors: Cho, Hanna, Choi, Jae Yong, Lee, Seung Ha, Lee, Jae Hoon, Choi, Young Chul, Ryu, Young Hoon, Lee, Myoung Sik, Lyoo, Chul Hyoung
Format: Article
Language:English
Subjects:
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Abstract Early-onset Alzheimer’s disease (EOAD) is characterized by greater non-memory dysfunctions, more rapid progression, and greater hypometabolism and atrophy than late-onset AD (LOAD). We sought to investigate the differences in tau accumulation patterns between early- and late-onset patients with AD and mild cognitive impairment (MCI). In 90 patients who completed18 F-AV-1451 and18 F-florbetaben positron emission tomography scans, only 59 amyloid-positive patients (11 EOAD, 10 EOMCI, 21 LOAD, and 17 LOMCI) were included in this study. We compared cortical18 F-AV-1451 binding between each patient group and corresponding amyloid-negative age-matched controls. In contrast to no difference in cortical binding between the EOMCI and LOMCI groups, EOAD showed greater binding in the parieto-occipital cortex than LOAD. The parieto-occipital binding correlated with visuospatial dysfunction in the EOAD spectrum, while binding in the temporal cortex correlated with verbal memory dysfunction in the LOAD spectrum. Our findings suggest that distinct topographic distribution of tau may influence the nature of cognitive impairment in EOAD patients.
ISSN:0197-4580
1558-1497
DOI:10.1016/j.neurobiolaging.2017.01.024