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Neuroimage Clin. 2019 Jul 30;24:101965. doi: 10.1016/j.nicl.2019.101965. [Epub ahead of print]

White matter cortico-striatal tracts predict apathy subtypes in Huntington's disease.

Author information

1
Department of Neuroscience, Pomona College, Claremont, CA, United States; Cognition and Brain Plasticity Unit, Bellvitge Biomedical Research Institute - IDIBELL, 08097 L'Hospitalet de Llobregat, Barcelona, Spain.
2
Cognition and Brain Plasticity Unit, Bellvitge Biomedical Research Institute - IDIBELL, 08097 L'Hospitalet de Llobregat, Barcelona, Spain; Department of Cognition, Development and Education Psychology, Universitat de Barcelona, Barcelona, Spain; Radboud University, Donders Institute for Brain, Cognition and Behaviour, Nijmegen, The Netherlands; Radboud University Medical Center, Donders Institute for Brain Cognition and Behaviour, Department of Medical Psychology, Nijmegen, The Netherlands.
3
Cognition and Brain Plasticity Unit, Bellvitge Biomedical Research Institute - IDIBELL, 08097 L'Hospitalet de Llobregat, Barcelona, Spain; Department of Cognition, Development and Education Psychology, Universitat de Barcelona, Barcelona, Spain.
4
European Huntington's Disease Network, Germany; Movement Disorders Unit, Department of Neurology, Biomedical Research Institute Sant Pau (IIB-Sant Pau), Hospital de la Santa Creu i Sant Pau, Barcelona, Spain.
5
European Huntington's Disease Network, Germany; Movement Disorders Unit, Department of Neurology, Biomedical Research Institute Sant Pau (IIB-Sant Pau), Hospital de la Santa Creu i Sant Pau, Barcelona, Spain; CIBERNED (Center for Networked Biomedical Research on Neurodegenerative Diseases), Carlos III Institute, Madrid, Spain.
6
Hestia Duran i Reynals. Hospital Duran i Reynals, Hospitalet de Llobregat, Barcelona, Spain.
7
Hestia Duran i Reynals. Hospital Duran i Reynals, Hospitalet de Llobregat, Barcelona, Spain; Department of Clinical and Health Psychology, Universitat Autònoma de Barcelona, Barcelona, Spain.
8
Movement Disorders Unit, Neurology Service, Hospital Universitari de Bellvitge, Barcelona, Spain.
9
Movement Disorders Unit, Neurology Service, Hospital Clínic, Barcelona, Spain; IDIBAPS (Institut d'Investigacions Biomèdiques August Pi i Sunyer), Barcelona, Spain; Facultat de Medicina, University of Barcelona, Barcelona, Spain.
10
Movement Disorders Unit, Neurology Service, Hospital Clínic, Barcelona, Spain.
11
Department of Psychiatry and Forensic Medicine, Universitat Autònoma de Barcelona, Spain; Hospital Mare de Deu de la Mercè, Barcelona, Spain.
12
Hospital Mare de Deu de la Mercè, Barcelona, Spain.
13
Cognition and Brain Plasticity Unit, Bellvitge Biomedical Research Institute - IDIBELL, 08097 L'Hospitalet de Llobregat, Barcelona, Spain; Department of Cognition, Development and Education Psychology, Universitat de Barcelona, Barcelona, Spain; Institute of Neurosciences, Universitat de Barcelona, Barcelona, Spain; ICREA (Catalan Institute for Research and Advanced Studies), Barcelona, Spain.
14
Cognition and Brain Plasticity Unit, Bellvitge Biomedical Research Institute - IDIBELL, 08097 L'Hospitalet de Llobregat, Barcelona, Spain. Electronic address: ecamara@ub.edu.

Abstract

BACKGROUND:

Apathy is the neuropsychiatric syndrome that correlates most highly with Huntington's disease progression, and, like early patterns of neurodegeneration, is associated with lesions to cortico-striatal connections. However, due to its multidimensional nature and elusive etiology, treatment options are limited.

OBJECTIVES:

To disentangle underlying white matter microstructural correlates across the apathy spectrum in Huntington's disease.

METHODS:

Forty-six Huntington's disease individuals (premanifest (N = 22) and manifest (N = 24)) and 35 healthy controls were scanned at 3-tesla and underwent apathy evaluation using the short-Problem Behavior Assessment and short-Lille Apathy Rating Scale, with the latter being characterized into three apathy domains, namely emotional, cognitive, and auto-activation deficit. Diffusion tensor imaging was used to study whether individual differences in specific cortico-striatal tracts predicted global apathy and its subdomains.

RESULTS:

We elucidate that apathy profiles may develop along differential timelines, with the auto-activation deficit domain manifesting prior to motor onset. Furthermore, diffusion tensor imaging revealed that inter-individual variability in the disruption of discrete cortico-striatal tracts might explain the heterogeneous severity of apathy profiles. Specifically, higher levels of auto-activation deficit symptoms significantly correlated with increased mean diffusivity in the right uncinate fasciculus. Conversely, those with severe cognitive apathy demonstrated increased mean diffusivity in the right frontostriatal tract and left dorsolateral prefrontal cortex to caudate nucleus tract.

CONCLUSIONS:

The current study provides evidence that white matter correlates associated with emotional, cognitive, and auto-activation subtypes may elucidate the heterogeneous nature of apathy in Huntington's disease, as such opening a door for individualized pharmacological management of apathy as a multidimensional syndrome in other neurodegenerative disorders.

KEYWORDS:

Apathy; Diffusion MRI; Huntington's disease; Individual differences; Neurodegeneration; White matter microstructure

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