Clinical and Dopamine Transporter Imaging Characteristics of Leucine Rich Repeat Kinase 2 (LRRK2) and Glucosylceramidase Beta (GBA) Parkinson's Disease Participants in the Parkinson's Progression Markers Initiative: A Cross-Sectional Study.


Journal

Movement disorders : official journal of the Movement Disorder Society
ISSN: 1531-8257
Titre abrégé: Mov Disord
Pays: United States
ID NLM: 8610688

Informations de publication

Date de publication:
05 2020
Historique:
received: 08 10 2019
revised: 13 01 2020
accepted: 14 01 2020
pubmed: 20 2 2020
medline: 28 4 2021
entrez: 20 2 2020
Statut: ppublish

Résumé

There are limited data on the phenotypic and dopamine transporter (DAT) imaging characterization of the Parkinson's disease (PD) patients with leucine rich kinase 2 (LRRK2) and glucosylceramidase beta (GBA) mutations. The objective of this study was to examine baseline clinical and DAT imaging characteristics in GBA and LRRK2 mutation carriers with early PD compared with sporadic PD. The Parkinson's Progression Markers Initiative is an ongoing observational longitudinal study that enrolled participants with sporadic PD, LRRK2 and GBA PD carriers from 33 sites worldwide. All participants are assessed annually with a battery of motor and nonmotor scales, 123-I Ioflupane DAT imaging, and biologic variables. We assessed 158 LRRK2 (89% G2019S), 80 GBA (89 %N370S), and 361 sporadic PD participants with the mean (standard deviation) disease duration of 2.9 (1.9), 3.1 (2.0), and 2.6 (0.6) years, respectively. When compared with sporadic PD, the GBA PD patients had no difference in any motor, cognitive, or autonomic features. The LRRK2 PD patients had less motor disability and lower rapid eye movement behavior disorder questionnaire scores, but no meaningful difference in cognitive or autonomic features. Both genetic cohorts had a higher score on the impulse control disorders scale when compared with sporadic PD, but no difference in other psychiatric features. Both genetic PD cohorts had less loss of dopamine transporter on DAT imaging when compared with sporadic PD. We confirm previous reports of milder phenotype associated with LRRK2-PD. A previously reported more aggressive phenotype in GBA-PD is not evident early in the disease in N370s carriers. This observation identifies a window for potential disease-modifying interventions. Longitudinal data will be essential to define the slope of progression for both genetic cohorts. ClinicalTrials.gov (NCT01141023). © 2020 The Authors. Movement Disorders published by Wiley Periodicals, Inc. on behalf of International Parkinson and Movement Disorder Society.

Sections du résumé

BACKGROUND
There are limited data on the phenotypic and dopamine transporter (DAT) imaging characterization of the Parkinson's disease (PD) patients with leucine rich kinase 2 (LRRK2) and glucosylceramidase beta (GBA) mutations.
OBJECTIVE
The objective of this study was to examine baseline clinical and DAT imaging characteristics in GBA and LRRK2 mutation carriers with early PD compared with sporadic PD.
METHODS
The Parkinson's Progression Markers Initiative is an ongoing observational longitudinal study that enrolled participants with sporadic PD, LRRK2 and GBA PD carriers from 33 sites worldwide. All participants are assessed annually with a battery of motor and nonmotor scales, 123-I Ioflupane DAT imaging, and biologic variables.
RESULTS
We assessed 158 LRRK2 (89% G2019S), 80 GBA (89 %N370S), and 361 sporadic PD participants with the mean (standard deviation) disease duration of 2.9 (1.9), 3.1 (2.0), and 2.6 (0.6) years, respectively. When compared with sporadic PD, the GBA PD patients had no difference in any motor, cognitive, or autonomic features. The LRRK2 PD patients had less motor disability and lower rapid eye movement behavior disorder questionnaire scores, but no meaningful difference in cognitive or autonomic features. Both genetic cohorts had a higher score on the impulse control disorders scale when compared with sporadic PD, but no difference in other psychiatric features. Both genetic PD cohorts had less loss of dopamine transporter on DAT imaging when compared with sporadic PD.
CONCLUSIONS
We confirm previous reports of milder phenotype associated with LRRK2-PD. A previously reported more aggressive phenotype in GBA-PD is not evident early in the disease in N370s carriers. This observation identifies a window for potential disease-modifying interventions. Longitudinal data will be essential to define the slope of progression for both genetic cohorts.
TRIAL REGISTRATION
ClinicalTrials.gov (NCT01141023). © 2020 The Authors. Movement Disorders published by Wiley Periodicals, Inc. on behalf of International Parkinson and Movement Disorder Society.

Identifiants

pubmed: 32073681
doi: 10.1002/mds.27989
pmc: PMC7231646
mid: NIHMS1567614
doi:

Substances chimiques

Dopamine Plasma Membrane Transport Proteins 0
LRRK2 protein, human EC 2.7.11.1
Leucine-Rich Repeat Serine-Threonine Protein Kinase-2 EC 2.7.11.1
Glucosylceramidase EC 3.2.1.45
Leucine GMW67QNF9C

Banques de données

ClinicalTrials.gov
['NCT01141023']

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

833-844

Subventions

Organisme : NIA NIH HHS
ID : U19 AG062418
Pays : United States

Informations de copyright

© 2020 The Authors. Movement Disorders published by Wiley Periodicals, Inc. on behalf of International Parkinson and Movement Disorder Society.

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Auteurs

Tanya Simuni (T)

Department of Neurology, Northwestern University Feinberg School of Medicine, Chicago, Illinois, USA.

Michael C Brumm (MC)

Department of Biostatistics, College of Public Health, University of Iowa, Iowa City, Iowa, USA.

Liz Uribe (L)

Department of Biostatistics, College of Public Health, University of Iowa, Iowa City, Iowa, USA.

Chelsea Caspell-Garcia (C)

Department of Biostatistics, College of Public Health, University of Iowa, Iowa City, Iowa, USA.

Christopher S Coffey (CS)

Department of Biostatistics, College of Public Health, University of Iowa, Iowa City, Iowa, USA.

Andrew Siderowf (A)

Departments of Neurology Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA.

Roy N Alcalay (RN)

Department of Neurology, The Taub Institite for Research on Alzheimer's Disease and the Aging Brain, Columbia University, New York, New York, USA.

John Q Trojanowski (JQ)

Departments of Pathology and Laboratory Medicine Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA.

Leslie M Shaw (LM)

Departments of Pathology and Laboratory Medicine Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA.

John Seibyl (J)

Institute for Neurodegenerative Disorders, New Haven, Connecticut, USA.

Andrew Singleton (A)

Laboratory of Neurogenetics, National Institute on Aging, NIH, Bethesda, Maryland, USA.

Arthur W Toga (AW)

Laboratory of Neuroimaging (LONI), University of Southern California, Los Angeles, California, USA.

Doug Galasko (D)

Department of Neurology, University of California, San Diego, California, USA.

Tatiana Foroud (T)

Department of Medical and Molecular Genetics, Indiana University, Indianapolis, Indiana, USA.

Kelly Nudelman (K)

Department of Medical and Molecular Genetics, Indiana University, Indianapolis, Indiana, USA.

Duygu Tosun-Turgut (D)

Department of Neurology, University of California San Francisco, San Francisco, California, USA.

Kathleen Poston (K)

Department of Neurology and Neurological Sciences, Stanford University, Stanford, California, USA.

Daniel Weintraub (D)

Departments of Psychiatry and Neurology Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA.

Brit Mollenhauer (B)

Department of Neurology, University Medical Center Goettingen, Goettingen, Germany and Paracelsus-Elena-Klinik, Kassel, Germany.

Caroline M Tanner (CM)

Department of Neurology, University of California San Francisco, San Francisco, California, USA.

Karl Kieburtz (K)

Department of Neurology, University of Rochester Medical Center, Rochester, New York, USA.

Lana M Chahine (LM)

Department of Neurology, University of Pittsburgh, Pittsburgh, Pennsylvania, USA.

Alyssa Reimer (A)

The Michael J. Fox Foundation for Parkinson's Research, New York, New York, USA.

Samantha Hutten (S)

The Michael J. Fox Foundation for Parkinson's Research, New York, New York, USA.

Susan Bressman (S)

Icahn School of Medicine, Mount Sinai, New York, New York, USA.

Kenneth Marek (K)

Institute for Neurodegenerative Disorders, New Haven, Connecticut, USA.

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