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Published on: November 19, 2012
Rehabilitation training improves cognitive disorder after cerebrovascular accident by improving BDNF Bcl-2 and Bax
1Department of Rehabilitation Medicine, The Second Affiliated Hospital of Qiqihar Medical University, Qiqihar, P.R. China. Cg20200618@163.com.
Insights
Rehabilitation training significantly improves cognitive function and motor skills after cerebrovascular accident by reducing harmful factors and increasing beneficial ones. This approach enhances brain health and may prevent cell death.
Area of Science:
- Neuroscience
- Rehabilitation Medicine
- Molecular Biology
Background:
- Cerebrovascular accident (stroke) frequently leads to cognitive impairment.
- Rehabilitation strategies are crucial for recovery but their underlying mechanisms require further elucidation.
Purpose of the Study:
- To investigate the efficacy of rehabilitation training on cognitive impairment post-cerebrovascular accident.
- To explore the molecular mechanisms, including inflammation, neurotrophic factors, and apoptosis, associated with rehabilitation training.
Main Methods:
- A study involving 100 cerebrovascular accident patients (50 in control, 50 in rehabilitation group) and a rat cerebral ischemia model.
- Assessment of cognitive function, motor skills, and serum/tissue molecular markers (e.g., BDNF, Bcl-2, Bax, CRP, glutamate) before and after 6 months of intervention.
- Analysis of hippocampal, amygdala, and prefrontal tissue in the animal model.
Main Results:
- Rehabilitation group showed significant improvements in cognitive (MoCA, MMSE) and motor (BI, FM) scores compared to the control group.
- Serum levels of brain-derived neurotrophic factor (BDNF), Bcl-2, and norepinephrine were elevated, while C-reactive protein (CRP), Bax, and glutamate were reduced in the rehabilitation group.
- Animal studies indicated increased BDNF and its activated receptors, with decreased JNK signaling in key brain regions following rehabilitation training.
Conclusions:
- Rehabilitation training effectively improves cognitive and motor functions after cerebrovascular accident.
- The mechanism involves modulating inflammatory and apoptotic pathways, potentially by upregulating BDNF signaling and inhibiting JNK.
- This suggests rehabilitation is a promising therapeutic strategy for mitigating post-stroke cognitive deficits.
Objective:
To explore the effect of rehabilitation training on cognitive impairment after cerebrovascular accident and its potential mechanism.
Patients And Methods:
100 patients of cerebrovascular accident treated in our hospital from August 2018 to August 2019 were selected as the subjects, and 50 patients with physical examination were selected as healthy control group. The patients with cerebrovascular accident were randomly divided into control group (50 patients) and research group (50 patients). The patients in the control group were given routine medication, the patients in research group were given rehabilitation training on the basis of routine drug therapy. The blood samples were collected on admission and 6 months after admission to detect the molecular markers related to inflammation, nerve cell nutrition and function and apoptosis in the serum. The cognitive function was evaluated by scales. We established a rat cerebral ischemia model, compared the differences in the evasive latency, serum CRP, BNDF, Bcl-2, BAX, Glu, NE levels and BNDF, TrkB, pTrkB, JNK levels in hippocampus, amygdala, and prefrontal tissue between model rats after rehabilitation training and model rats without rehabilitation training.
Results:
On admission, there were no significant differences in the scores of Barthel index (BI), Fugl-Meyer motor function scale (FM), Montreal cognitive assessment scale (MoCA) and mini-mental state examination (MMSE) (p>0.05). 6 months later, the above scores and BNDF, Bcl-2, and norepinephrine were significantly higher in the research group (p<0.05), while CRP, Bax, 5-HT and glutamate in the research group were significantly lower than those in the control group (p<0.05).
Conclusions:
Rehabilitation training can improve the motor function, mental state and cognitive level of patients, reduce the levels of neurotoxic factors, pro-inflammatory factors and pro-apoptotic factors, and improve the levels of inhibiting apoptotic factors, neurotrophic factors and neurotransmitters. In animal experiments, rehabilitation training can increase BDNF and its activated receptors in hippocampus, amygdala and prefrontal lobe of rats, and decrease JNK of apoptotic protein, suggesting that rehabilitation training may regulate the expression of apoptotic proteins Bcl-2 and Bax by upregulating BDNF and its receptors and acting on JNK pathway, thereby inhibiting cell apoptosis and improving cognitive impairment after cerebrovascular accident.
