PMID- 30338813 OWN - NLM STAT- MEDLINE DCOM- 20191212 LR - 20191217 IS - 2284-0729 (Electronic) IS - 1128-3602 (Linking) VI - 22 IP - 19 DP - 2018 Oct TI - Research on changes in cognitive function, beta-amyloid peptide and neurotrophic factor in stroke patients. PG - 6448-6455 LID - 16057 [pii] LID - 10.26355/eurrev_201810_16057 [doi] AB - OBJECTIVE: To investigate the changes as well as the related mechanism in cognitive function and levels of serum beta-amyloid peptide (Abeta) and brain-derived neurotrophic factor (BDNF) in stroke patients. PATIENTS AND METHODS: A total of 30 patients with acute stroke treated in our hospital from June 2015 to September 2016 were selected as stroke group, while 30 volunteers during the same period were enrolled as control group. Changes in cognitive function of patients were evaluated using the Montreal Cognitive Assessment (MoCA) and mini-mental state examination (MMSE) before and after the treatment. At the same time, the concentrations of serum Abeta1-40 and BDNF were detected, and their correlations with the MMSE score were analyzed. Finally, levels of serum cyclic adenosine monophosphate (cAMP) and phosphorylated-cAMP-response element binding protein (p-CREB), and the phosphorylation level of Tau protein were detected by Western blotting. RESULTS: MoCA and MMSE scores of patients in stroke group were significantly lower than those in control group (p < 0.01), and the scores were significantly higher in stroke patients after treatment than those before treatment (p < 0.01). Compared with those in control group, the serum Abeta1-40 concentration in patients in stroke group was significantly increased (p < 0.01), but the BDNF level was significantly decreased (p < 0.01). Compared with those before treatment, the serum Abeta1-40 concentration in patients was significantly decreased after treatment (p < 0.01), but the BDNF concentration was significantly increased (p < 0.01). Correlation analysis showed that the MMSE score was negatively correlated with the concentration of Abeta1-40 (r2 = 0.764, p < 0.01), but positively related to the level of BDNF (r2 = 0.827, p < 0.01). Compared with those in control group, the content of serum cAMP and p-CREB in stroke patients was significantly decreased (p < 0.01), but the expression of p-Tau was statistically increased (p < 0.01). CONCLUSIONS: The cognitive function in stroke patients is impaired, with the rising content of serum Abeta1-40 and reduction of BDNF, the mechanism of which is related to the decrease of cAMP and p-CREB and the increase of p-Tau. This provides a theoretical basis for searching the new therapeutic targets and new drugs for stroke. FAU - Chen, H-G AU - Chen HG AD - Department of Neurosurgery, Yantai Yuhuangding Hospital, Yantai, Shandong Province, China. guangqiangcui@163.com. FAU - Wang, M AU - Wang M FAU - Jiao, A-H AU - Jiao AH FAU - Tang, G-T AU - Tang GT FAU - Zhu, W AU - Zhu W FAU - Zou, P AU - Zou P FAU - Li, T AU - Li T FAU - Cui, G-Q AU - Cui GQ FAU - Gong, P-Y AU - Gong PY LA - eng PT - Journal Article PL - Italy TA - Eur Rev Med Pharmacol Sci JT - European review for medical and pharmacological sciences JID - 9717360 RN - 0 (Amyloid beta-Peptides) RN - 0 (Biomarkers) RN - 0 (Brain-Derived Neurotrophic Factor) RN - 0 (CREB1 protein, human) RN - 0 (Cyclic AMP Response Element-Binding Protein) RN - 0 (MAPT protein, human) RN - 0 (Peptide Fragments) RN - 0 (amyloid beta-protein (1-40)) RN - 0 (tau Proteins) RN - 7171WSG8A2 (BDNF protein, human) RN - E0399OZS9N (Cyclic AMP) SB - IM MH - Aged MH - Amyloid beta-Peptides/*blood MH - Biomarkers/blood MH - Brain-Derived Neurotrophic Factor/*blood MH - Case-Control Studies MH - *Cognition MH - Cyclic AMP/blood MH - Cyclic AMP Response Element-Binding Protein/blood MH - Female MH - Humans MH - Male MH - Middle Aged MH - Peptide Fragments/*blood MH - Phosphorylation MH - Prognosis MH - Stroke/*blood/diagnosis/psychology/therapy MH - Time Factors MH - tau Proteins/blood EDAT- 2018/10/20 06:00 MHDA- 2019/12/18 06:00 CRDT- 2018/10/20 06:00 PHST- 2018/10/20 06:00 [entrez] PHST- 2018/10/20 06:00 [pubmed] PHST- 2019/12/18 06:00 [medline] AID - 16057 [pii] AID - 10.26355/eurrev_201810_16057 [doi] PST - ppublish SO - Eur Rev Med Pharmacol Sci. 2018 Oct;22(19):6448-6455. doi: 10.26355/eurrev_201810_16057.