Static and dynamic postural control deficits in aging fragile X mental retardation 1 (FMR1) gene premutation carriers.


Journal

Journal of neurodevelopmental disorders
ISSN: 1866-1955
Titre abrégé: J Neurodev Disord
Pays: England
ID NLM: 101483832

Informations de publication

Date de publication:
21 01 2019
Historique:
received: 05 09 2018
accepted: 26 12 2018
entrez: 23 1 2019
pubmed: 23 1 2019
medline: 4 8 2020
Statut: epublish

Résumé

Individuals with premutation alleles of the fragile X mental retardation 1 (FMR1) gene are at risk of developing fragile X-associated tremor/ataxia syndrome (FXTAS) during aging. Characterization of motor issues associated with aging in FMR1 premutation carriers is needed to determine neurodegenerative processes and establish new biobehavioral indicators to help identify individuals at greatest risk of developing FXTAS. We examined postural stability in 18 premutation carriers ages 46-77 years and 14 age-matched healthy controls. Participants completed a test of static stance and two tests of dynamic postural sway on a force platform to quantify postural variability and complexity. CGG repeat length was measured for each premutation carrier, and MRI and neurological evaluations were conducted to identify carriers who currently met criteria for FXTAS. Of the 18 premutation carriers, seven met criteria for definite/probable FXTAS (FXTAS+), seven showed no MRI or neurological signs of FXTAS (FXTAS-), and four were inconclusive due to insufficient data. Compared to controls, premutation carriers showed increased center of pressure (COP) variability in the mediolateral (COP Our findings indicate that aging FMR1 premutation carriers show static and dynamic postural control deficits relative to healthy controls implicating degenerative processes of spinocerebellar and cerebellar-brainstem circuits that may be independent of or precede the onset of FXTAS. Our finding that FXTAS+ and FXTAS- premutation carriers differed on their level of intentional AP sway suggests that neural mechanisms of dynamic postural control may be differentially impacted in patients with FXTAS, and its measurement may be useful for rapidly and precisely identifying disease presence and onset.

Sections du résumé

BACKGROUND
Individuals with premutation alleles of the fragile X mental retardation 1 (FMR1) gene are at risk of developing fragile X-associated tremor/ataxia syndrome (FXTAS) during aging. Characterization of motor issues associated with aging in FMR1 premutation carriers is needed to determine neurodegenerative processes and establish new biobehavioral indicators to help identify individuals at greatest risk of developing FXTAS.
METHODS
We examined postural stability in 18 premutation carriers ages 46-77 years and 14 age-matched healthy controls. Participants completed a test of static stance and two tests of dynamic postural sway on a force platform to quantify postural variability and complexity. CGG repeat length was measured for each premutation carrier, and MRI and neurological evaluations were conducted to identify carriers who currently met criteria for FXTAS. Of the 18 premutation carriers, seven met criteria for definite/probable FXTAS (FXTAS+), seven showed no MRI or neurological signs of FXTAS (FXTAS-), and four were inconclusive due to insufficient data.
RESULTS
Compared to controls, premutation carriers showed increased center of pressure (COP) variability in the mediolateral (COP
CONCLUSION
Our findings indicate that aging FMR1 premutation carriers show static and dynamic postural control deficits relative to healthy controls implicating degenerative processes of spinocerebellar and cerebellar-brainstem circuits that may be independent of or precede the onset of FXTAS. Our finding that FXTAS+ and FXTAS- premutation carriers differed on their level of intentional AP sway suggests that neural mechanisms of dynamic postural control may be differentially impacted in patients with FXTAS, and its measurement may be useful for rapidly and precisely identifying disease presence and onset.

Identifiants

pubmed: 30665341
doi: 10.1186/s11689-018-9261-x
pii: 10.1186/s11689-018-9261-x
pmc: PMC6341725
doi:

Substances chimiques

FMR1 protein, human 0
Fragile X Mental Retardation Protein 139135-51-6

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

2

Subventions

Organisme : National Institute of Child Health and Human Development
ID : U54HD090216
Pays : International

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Auteurs

Zheng Wang (Z)

Department of Occupational Therapy, University of Florida, Gainesville, FL, 32611, USA. zheng.wang@phhp.ufl.edu.
University of Florida, 1225 Center Drive, PO Box 100164, Gainesville, FL, 326100164, USA. zheng.wang@phhp.ufl.edu.

Pravin Khemani (P)

Department of Neurology, Swedish Neuroscience Institute, Seattle, WA, 98121, USA.

Lauren M Schmitt (LM)

Division of Developmental and Behavioral Pediatrics, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, 45229, USA.

Su Lui (S)

Huaxi Magnetic Resonance Research Center (HMRRC), Department of Radiology, West China Hospital of Sichuan University, Chengdu, 610041, Sichuan, China.

Matthew W Mosconi (MW)

Schiefelbusch Institute for Life Span Studies, University of Kansas, Lawrence, KS, 66045, USA.
Clinical Child Psychology Program, University of Kansas, Lawrence, KS, 66045, USA.
Kansas Center for Autism Research and Training (K-CART), University of Kansas, Lawrence, KS, 66045, USA.

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Classifications MeSH