Stroke
Conditions
Keywords
Stroke, FKBP5, Motor, Transcranial direct current stimulation, Plasticity, Stress
Brief summary
With contemporary lifestyle changes and global aging, it is important yet unknown how stress interacts to post-stroke outcomes. This proposal aims to study the link between the stress-responsive FKBP51-related pathways and neural plasticity after stroke, elucidating FKBP5 gene polymorphisms and blood FKBP51 regulation in relation to brain excitability and functions, understanding the effects of transcranial direct current stimulation, and characterizing brain mechanisms for individualized early rehabilitation after stroke.
Detailed description
Stress is an underestimated risk factor and also a consequence of cardiovascular diseases and stroke. FK506-binding protein 51 (FKBP51) modulates stress responses by acting as a co-chaperone that negatively regulates glucocorticoid receptor (GR) to cortisol binding and nuclear signaling. In an oxygen-glucose deprivation (OGD) model of acute mouse hippocampal slices, FKBP5 deletion reduced ischemic neuronal hyperexcitation, and cathodal electrical stimulation of OGD-injured wild-type decreased FKBP51 levels. However, clinical implications of FKBP5 polymorphisms and FKBP51 regulation in post-stroke outcomes and neuromodulation-induced plasticity are unknown. We aim to assess the link between FKBP5 polymorphisms and blood FKBP51 regulation after stroke, and their relationship with stroke phenotypes, brain connectivity and functional outcomes.
Interventions
DEVICEBihemispheric tDCS
The anode and cathode are placed over the ipsilesional and contralesional primary motor cortex (C3 or C4 based on 10-20 system), respectively. The size of the electrode is 5x5 cm.
Sponsors
Taipei Veterans General Hospital, Taiwan
Study design
Allocation
RANDOMIZED
Intervention model
PARALLEL
Primary purpose
OTHER
Masking
DOUBLE (Subject, Outcomes Assessor)
Intervention model description
Anticipated 100 participants are assigned to the experimental or sham-controlled groups with an allocation rate of 1:1, for the clinical trial. In addition, another group of patients participates in the observational study (no intervention).
Eligibility
Sex/Gender
ALL
Age
20 Years to 80 Years
Healthy volunteers
No
Inclusion criteria
* Unilateral ischemic or hemorrhagic stroke * Aged 20-80 years old
Exclusion criteria
* FMA-UE is over 49 points * Major psychiatric diseases * Major neurologic diseases * Global aphasia
Design outcomes
Primary
| Measure | Time frame | Description |
|---|---|---|
| Fugl-Meyer Assessment of Upper Extremity, FMA-UE | Change score from baseline (~10 days poststroke) to 90 days poststroke | Motor recovery of upper extremity poststroke |
Secondary
| Measure | Time frame | Description |
|---|---|---|
| Action Research Arm Test, ARAT | Change score from baseline (~10 days poststroke) to 90 days poststroke | Motor function of upper extremity poststroke |
| Fugl-Meyer Assessment of Lower Extremity, FMA-LE | Change score from baseline (~10 days poststroke) to 90 days poststroke | Motor recovery of lower extremity poststroke |
| Perceived Stress Scale-10 | Change score from baseline (~10 days poststroke) to 90 days poststroke | Stress level poststroke |
| Protein and gene test | Change score from baseline (~10 days poststroke) to 90 days poststroke | Protein expression poststroke and identifying genotypes of participants |
Other
| Measure | Time frame | Description |
|---|---|---|
| Resting-state structural and functional connectivity by magnetic resonance imaging | Change score from baseline (~10 days poststroke) to 90 days poststroke | Connectivity-level plasticity post-intervention/poststroke |
Countries
Taiwan
Contacts
Primary ContactI-Hui Lee, MD, PhD
Outcome results
None listed