Dataset Information

Sensorimotor Inhibition and Mobility in Genetic Subgroups of Parkinson's Disease.

ABSTRACT: Background: Mobility and sensorimotor inhibition impairments are heterogeneous in Parkinson's disease (PD). Genetics may contribute to this heterogeneity since the apolipoprotein (APOE) ?4 allele and glucocerebrosidase (GBA) gene variants have been related to mobility impairments in otherwise healthy older adult (OA) and PD cohorts. The purpose of this study is to determine if APOE or GBA genetic status affects sensorimotor inhibition and whether the relationship between sensorimotor inhibition and mobility differs in genetic sub-groups of PD. Methods: Ninety-three participants with idiopathic PD (53 non-carriers; 23 ?4 carriers; 17 GBA variants) and 72 OA (45 non-carriers; 27 ?4 carriers) had sensorimotor inhibition characterized by short-latency afferent inhibition. Mobility was assessed in four gait domains (pace/turning, rhythm, trunk, variability) and two postural sway domains (area/jerkiness and velocity) using inertial sensors. Results: Sensorimotor inhibition was worse in the PD than OA group, with no effect of genetic status. Gait pace/turning was slower and variability was higher (p < 0.01) in PD compared to OA. Postural sway area/jerkiness (p < 0.01) and velocity (p < 0.01) were also worse in the PD than OA group. Genetic status was not significantly related to any gait or postural sway domain. Sensorimotor inhibition was significantly correlated with gait variability (r = 0.27; p = 0.02) and trunk movement (r = 0.23; p = 0.045) in the PD group. In PD non-carriers, sensorimotor inhibition related to variability (r = 0.35; p = 0.010) and trunk movement (r = 0.31; p = 0.025). In the PD ?4 group, sensorimotor inhibition only related to rhythm (r = 0.47; p = 0.024), while sensorimotor inhibition related to pace/turning (r = -0.49; p = 0.046) and rhythm (r = 0.59; p = 0.013) in the PD GBA group. Sensorimotor inhibition was significantly correlated with gait pace/turning (r = -0.27; p = 0.04) in the OA group. There was no relationship between sensorimotor inhibition and postural sway. Conclusion: ?4 and GBA genetic status did not affect sensorimotor inhibition or mobility impairments in this PD cohort. However, worse sensorimotor inhibition was associated with gait variability in PD non-carriers, but with gait rhythm in PD ?4 carriers and with gait rhythm and pace in PD with GBA variants. Impaired sensorimotor inhibition had a larger effect on mobility in people with PD than OA and affected different domains of mobility depending on genetic status.

SUBMITTER: Martini DN

PROVIDER: S-EPMC7498564 | biostudies-literature | 2020

REPOSITORIES: biostudies-literature

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Publications

Sensorimotor Inhibition and Mobility in Genetic Subgroups of Parkinson's Disease.

Martini Douglas N DN Morris Rosie R Kelly Valerie E VE Hiller Amie A Chung Kathryn A KA Hu Shu-Ching SC Zabetian Cyrus P CP Oakley John J Poston Kathleen K Mata Ignacio F IF Edwards Karen L KL Lapidus Jodi A JA Grabowski Thomas J TJ Montine Thomas J TJ Quinn Joseph F JF Horak Fay F

Frontiers in neurology 20200904

Background: Mobility and sensorimotor inhibition impairments are heterogeneous in Parkinson's disease (PD). Genetics may contribute to this heterogeneity since the apolipoprotein (APOE) ε4 allele and glucocerebrosidase (GBA) gene variants have been related to mobility impairments in otherwise healthy older adult (OA) and PD cohorts. The purpose of this study is to determine if APOE or GBA genetic status affects sensorimotor inhibition and whether the relationsh ...[more]

PMID: 33013627

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Project description:Embodied cognition theories propose that the semantic representations engaged in during language comprehension are partly supported by perceptual and motor systems, via simulation. Activation in modality-specific regions of cortex is associated with the comprehension of literal language that describes the analogous modalities, but studies addressing the grounding of non-literal or figurative language, such as metaphors, have yielded mixed results. Differences in the psycholinguistic characteristics of sentence stimuli across studies have likely contributed to this lack of consensus. Furthermore, previous studies have been largely correlational, whilst patient studies are a critical way of determining if intact sensorimotor function is necessary to understand language drawing on sensorimotor information. We designed a battery of metaphorical and literal sentence stimuli using action and sound words, with an unprecedented level of control over critical psycholinguistic variables, to test hypotheses about the grounding of metaphorical language. In this Registered Report, we assessed the comprehension of these sentences in 41 patients with Parkinson's disease, who were predicted to be disproportionately affected by the action sentences relative to the sound sentences, and compared their performance to that of 39 healthy age-matched controls who were predicted to show no difference in performance due to sensory modality. Using preregistered Bayesian model comparison methods, we found that PD patients' comprehension of literal action sentences was not impaired, while there was some evidence for a slowing of responses to action metaphors. Follow up exploratory analyses suggest that this response time modality effect was driven by one type of metaphor (predicate) and was absent in another (nominal), despite the fact that the action semantics were similar in both syntactic forms. These results suggest that the conditions under which PD patients demonstrate hypothesized embodiment effects are limited. We offer a critical assessment of the PD action language literature and discuss implications for the embodiment debate. In addition, we suggest how future studies could leverage Bayesian statistical methods to provide more convincing evidence for or against embodied cognition effects.

Dataset Information

Sensorimotor Inhibition and Mobility in Genetic Subgroups of Parkinson's Disease.

Publications

Sensorimotor Inhibition and Mobility in Genetic Subgroups of Parkinson's Disease.

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