AI Article Synopsis
- There is significant variability in the severity of post-stroke aphasia, and traditional prediction methods often overlook neurophysiological and genetic factors that could influence recovery.
- The study aims to determine if a specific genetic variant (ValMet) in the BDNF gene affects aphasia severity and interacts with neuroplasticity indicators to enhance recovery predictions.
- Results showed that individuals with the ValVal genetic variant had less severe aphasia and exhibited expected age-related effects, while ValMet carriers displayed weaker correlations with neuroplasticity indicators, indicating the genetic variant’s role in recovery outcomes.
Article Abstract
Background: There is high variability in post-stroke aphasia severity and predicting recovery remains imprecise. Standard prognostics do not include neurophysiological indicators or genetic biomarkers of neuroplasticity, which may be critical sources of variability.
Objective: To evaluate whether a common polymorphism (ValMet) in the gene for brain-derived neurotrophic factor (BDNF) contributes to variability in post-stroke aphasia, and to assess whether BDNF polymorphism interacts with neurophysiological indicators of neuroplasticity (cortical excitability and stimulation-induced neuroplasticity) to improve estimates of aphasia severity.
Methods: Saliva samples and motor-evoked potentials (MEPs) were collected from participants with chronic aphasia subsequent to left-hemisphere stroke. MEPs were collected prior to continuous theta burst stimulation (cTBS; index for cortical excitability) and 10 minutes following cTBS (index for stimulation-induced neuroplasticity) to the right primary motor cortex. Analyses assessed the extent to which BDNF polymorphism interacted with cortical excitability and stimulation-induced neuroplasticity to predict aphasia severity beyond established predictors.
Results: ValVal carriers showed less aphasia severity than ValMet carriers, after controlling for lesion volume and time post-stroke. Furthermore, ValVal carriers showed expected effects of age on aphasia severity, and positive associations between severity and both cortical excitability and stimulation-induced neuroplasticity. In contrast, ValMet carriers showed weaker effects of age and negative associations between cortical excitability, stimulation-induced neuroplasticity and aphasia severity.
Conclusions: Neurophysiological indicators and genetic biomarkers of neuroplasticity improved aphasia severity predictions. Furthermore, BDNF polymorphism interacted with cortical excitability and stimulation-induced neuroplasticity to improve predictions. These findings provide novel insights into mechanisms of variability in stroke recovery and may improve aphasia prognostics.
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Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9133188 | PMC |
| http://dx.doi.org/10.1177/15459683221096391 | DOI Listing |
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