Network connectivity determines cortical thinning in early Parkinson's disease progression

Y Yau; Y Zeighami; T E Baker; K Larcher; U Vainik; M Dadar; V S Fonov; P Hagmann; A Griffa; B Mišić; D L Collins; A Dagher

doi:10.1038/s41467-017-02416-0

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Network connectivity determines cortical thinning in early Parkinson's disease progression

Journal article

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Peer reviewed

Network connectivity determines cortical thinning in early Parkinson's disease progression

Y Yau, Y Zeighami, T E Baker, K Larcher, U Vainik, M Dadar, V S Fonov, P Hagmann, A Griffa, B Mišić, …

Nature communications, Vol.9(1), pp.12-12

01/02/2018

DOI: https://doi.org/10.1038/s41467-017-02416-0

PMCID: PMC5750227

PMID: 29295991

Abstract

Aged

Case-Control Studies

Cerebral Cortex - pathology

Cognition

Connectome

Disease Progression

Female

Humans

Longitudinal Studies

Male

Middle Aged

Parkinson Disease - cerebrospinal fluid

Parkinson Disease - etiology

Parkinson Disease - pathology

Parkinson Disease - psychology

Here we test the hypothesis that the neurodegenerative process in Parkinson's disease (PD) moves stereotypically along neural networks, possibly reflecting the spread of toxic alpha-synuclein molecules. PD patients (n = 105) and matched controls (n = 57) underwent T1-MRI at entry and 1 year later as part of the Parkinson's Progression Markers Initiative. Over this period, PD patients demonstrate significantly greater cortical thinning than controls in parts of the left occipital and bilateral frontal lobes and right somatomotor-sensory cortex. Cortical thinning is correlated to connectivity (measured functionally or structurally) to a "disease reservoir" evaluated by MRI at baseline. The atrophy pattern in the ventral frontal lobes resembles one described in certain cases of Alzheimer's disease. Our findings suggest that disease propagation to the cortex in PD follows neuronal connectivity and that disease spread to the cortex may herald the onset of cognitive impairment.

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Title: Network connectivity determines cortical thinning in early Parkinson's disease progression
Creators: Y Yau - Montreal Neurological Institute, McGill University, 3801 University Street, Montreal, QC, H3A 2B4, Canada
Y Zeighami - Montreal Neurological Institute, McGill University, 3801 University Street, Montreal, QC, H3A 2B4, Canada
T E Baker - Center for Molecular and Behavioral Neuroscience, Rutgers University, 197 University Avenue, Newark, NJ, 07102, USA
K Larcher - Montreal Neurological Institute, McGill University, 3801 University Street, Montreal, QC, H3A 2B4, Canada
U Vainik - Institute of Psychology, Faculty of Social Sciences, University of Tartu, Näituse 2, 50409, Tartu, Estonia
M Dadar - Montreal Neurological Institute, McGill University, 3801 University Street, Montreal, QC, H3A 2B4, Canada
V S Fonov - Montreal Neurological Institute, McGill University, 3801 University Street, Montreal, QC, H3A 2B4, Canada
P Hagmann - Department of Radiology, Lausanne University Hospital and University of Lausanne, Rue du Bugnon 21, 1011, Lausanne, Switzerland
A Griffa - Brain Center Rudolf Magnus, UMC Utrecht, Heidelberglaan 100, A01.126, 3508 GA, Utrecht, The Netherlands
B Mišić - Montreal Neurological Institute, McGill University, 3801 University Street, Montreal, QC, H3A 2B4, Canada
D L Collins - Montreal Neurological Institute, McGill University, 3801 University Street, Montreal, QC, H3A 2B4, Canada
A Dagher - Montreal Neurological Institute, McGill University, 3801 University Street, Montreal, QC, H3A 2B4, Canada. alain.dagher@mcgill.ca
Publication Details: Nature communications, Vol.9(1), pp.12-12
Date published: 01/02/2018
Academic Unit: Center for Molecular and Behavioral Neuroscience
Language: English
Resource Type: Journal article
Identifiers: 991031665811504646