BACKGROUND: Brain-derived neurotrophic factor (BDNF) has a very important role in repairing intact and injured brain, also known as neuroplasticity. Risk factors may affect neuroplasticity. OBJECTIVES: In this study, our aim was to delineate the levels of BDNF in acute stroke with different etiology and impact of risk factors on its levels. METHODS: In this prospective study, 208 patients with first-ever stroke, between 18 and 75 years, were included. All individuals were assessed for severity and type of stroke, risk factors, levels of BDNF in the acute stroke, and its association with outcome of stroke. RESULTS: The mean age of the patients in our study was 55.29 ± 11.6 years. Compared to healthy controls, a significant decline in the levels of BDNF was observed after stroke ( P < 0.01). Patients with National Institutes of Health Stroke Scale (NIHSS) <6 on the 1 st day of stroke had significantly higher levels of BDNF than those with NIHSS >6 (9.8 ng/ml ± 3.8; P < 0.01). A significant difference in the levels of BDNF was observed on comparing the stroke patients and healthy individuals of age <55 and >55 years (<55 years: 10.4 ng/ml ± 3.2; >55 years: 9.8 ng/ml ± 4.5 and in healthy individuals <55 years: 22.97 ± 3.8, >55 years: 15.4 ± 4.9; P < 0.01). Risk factors have negative impact on levels of BDNF (diabetics, P = 0.001; alcoholics, P = 0.003; both diabetes mellitus + hypertension, P = 0.002; smokers, P = 0.001). The difference was not significant between hypertensives and nonhypertensives ( P = 0.06). CONCLUSION: BDNF level is significantly reduced in acute stroke. The presence of risk factors further affects its level.
Background: Brain-derived neurotrophic factor (BDNF) plays an important role in repairing normal as well as in the injured brain. Physical exercise may have a positive impact on the release of BDNF. Objective: PNF is a neurophysiological approach that facilitates the stimulation of central and peripheral nervous systems. In this study, our aim was to assess the levels of BDNF as well as functional recovery before and after the intervention of PNF in patients with acute stroke. Methods: A total of 208 patients with first time confirmed stroke were recruited and assessed for stroke severity, type, mini-mental state exam (MMSE), functional independence measure scale, and BDNF levels before and after PNF intervention. BDNF levels were also assessed in healthy individuals for control values. Results: A significant decline in levels of BDNF was observed after in stroke. BDNF levels in patients (with different risk factors) with diabetes, hypertension and DM+ HTN, alcohol, and smoking history were 8.8 ± 4.04 ng/mL, 8.86 ± 4.68 ng/mL, 8.65 ± 3.26 ng/mL, 8.51 ± 4.26 ng/mL, and 8.9 ± 3.4 ng/mL, respectively. A decline in BDNF levels was observed in accordance with the severity of stroke in both ischemic and hemorrhagic stroke with the least level being in severe stroke (NIHSS >15 and ICH >3). Despite the type of stroke and the presence of risk factors, a significant improvement in BDNF levels and FIM scale scores was seen in all subjects who received PNF exercises. Conclusion: Thus, PNF is efficient in improving functional level in acute stroke irrespective of the type of stroke and risk factors.
Memory-epigenetics which is the loss of memory due to epigenetic modifications can be due to the silencing of genes involved in cognitive functions and this is the basis of the current study. We hypothesize that a diet containing high methionine and low vitamins can lead to memory impairment by increasing global DNA methylation and therefore, silencing the netrin-1 gene, which encodes the glycoprotein involved in neurogenesis, axonal guidance and maintenance of the synaptic plasticity. Wild type (C57BL/6J) mice were fed with a diet containing excess methionine (1.2%), low-folate (0.08 mg/kg), vitamin B 6 (0.01 mg/kg), and B 12 (10.4 mg/kg) for 6 weeks. Mice were examined weekly for the long-term memory function, using a passive avoidance test, which determined loss of fear-motivated long-term memory starting from the fourth week of diet. Similarly, an increase in brain %5-methyl cytosine was observed starting from the 4 th week of diet in mice. Mice fed with a high methionine, low folate and vitamins containing diet showed a decrease in netrin-1 protein expression and an increase in netrin-1 gene promotor methylation, as determined by methylation-sensitive restriction enzyme-polymerase chain reaction analysis. The increase in methylation of netrin-1 gene was validated by high-resolution melting and sequencing analysis. Furthermore, the association of netrin-1 with memory was established by administering netrin that considerably restored long-term fear motivated memory. Taken together, these results suggest that a diet rich in methionine and lacking in folate and vitamin B 6 /B 12 can induce defects in learning and memory. Furthermore, the data indicates that decrease in netrin-1 expression due to hyper-methylation of its gene can be associated with memory loss. The animal procedures were approved by the Institutional Animal Care and Use Committee, University of Louisville, USA (No. A3586-01) on February 2, 2018.
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