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Lookup NU author(s): Lina Patterson, Dr Michael FirbankORCiD, Dr Sean Colloby, Professor Johannes Attems, Professor Alan ThomasORCiD, Dr Christopher Morris
This work is licensed under a Creative Commons Attribution 4.0 International License (CC BY 4.0).
The cingulate island sign (CIS) refers to the relative sparing of metabolism in the posterior cingulate cortex (PCC) and represents an important biomarker in distinguishing dementia with Lewy bodies (DLB) from Alzheimer disease (AD). The underlying basis of the CIS is unknown; therefore, our aim was to investigate which neurodegenerative changes underpin the formation of CIS. Using quantitative neuropathology, α-synuclein, phosphorylated Tau, and amyloid-β pathology was assessed in 12 DLB, 9 AD and 6 age-matched control patients in the anterior cingulate (ACC), midcingulate, PCC, precuneus/cuneus and parahippocampal gyrus. All participants had undergone 99mTc-hexamethylpropyleneamine oxime (HMPAO) single-photon emission computed tomography imaging during life to define the presence or absence of CIS. In the DLB group, no significant correlations were observed between CIS ratios and neurodegenerative pathology in PCC. In DLB, however, the ACC showed lower HMPAO uptake, as well as significantly higher α-synuclein and amyloid-β burden compared with PCC, possibly underlying the relative preservation of perfusion in PCC when compared with ACC. Our findings suggest that neurodegenerative pathology does not directly correlate with the CIS in DLB, and other metabolic or pathological changes are therefore more likely to be relevant for the development of the CIS.
Author(s): Patterson L, Firbank MJ, Colloby SJ, Attems J, Thomas AJ, Morris CM
Publication type: Article
Publication status: Published
Journal: Journal of Neuropathology and Experimental Neurology
Year: 2019
Volume: 78
Issue: 8
Pages: 717–724
Print publication date: 01/08/2019
Online publication date: 24/05/2019
Acceptance date: 17/05/2019
Date deposited: 02/08/2019
ISSN (print): 0022-3069
ISSN (electronic): 1554-6578
Publisher: Oxford University Press
URL: https://doi.org/10.1093/jnen/nlz047
DOI: 10.1093/jnen/nlz047
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