Naps and cardiovascular disease risk in different age and sex groups: evidence from a large community cohort.

STUDY OBJECTIVES: This study examined the relationship between naps and cardiovascular disease (CVD) events or death in different age and sex groups. METHODS: A total of 3069 participants stratified by age (<65, 65-74, and ≥75 years old) and sex, underwent Cox regression analysis to assess nap's impact on CVD risk. Restricted cubic spline plots (RCS) were used for dose-response relationships. RESULTS: Significant age-stratified interactions were found when exploring the associations between nap frequency or duration and CVD events (P interaction = 0.001, 0.036 respectively). Individuals younger than 65 years with higher nap frequency or longer nap duration had a significantly increased risk of CVD events (P < 0.001, P = 0.001 respectively). The age group of 65-74 years showed significant associations between CVD events and nap frequency or nap duration (P = 0.017, 0.016 respectively), together with nap duration and CVD deaths (P = 0.008). In the subgroup of females aged 65-74, significant associations were found between nap frequency or duration and CVD events (P = 0.006, 0.002 respectively). Nap frequency or duration was also significantly associated with CVD deaths (P =0.005, 0.010 respectively). CONCLUSIONS: This study underscores a noteworthy correlation between a higher frequency or longer duration of daytime nap and an increased susceptibility to CVD among individuals aged 65-74 years, particularly in females. However, further research is needed to better understand the underlying mechanisms.

Leptin alleviates endoplasmic reticulum stress induced by cerebral ischemia/reperfusion injury via the PI3K/Akt signaling pathway.

BACKGROUND: Cerebral ischemic/reperfusion injury (CIRI) is a key factor for the prognosis of ischemic stroke (IS), the leading disease in terms of global disability and fatality rates. Recent studies have shown that endoplasmic reticulum stress (ERS) may be a target against CIRI and that leptin, a peptide hormone, has neuroprotective activity to mitigate CIRI. METHODS: An in vitro CIRI model was induced in primary cortical neurons by oxygen-glucose deprivation and reoxygenation (OGD/R) after pretreatment with LY294002 (10 µmol/L) and/or leptin (0.4 mg/L), and cell viability, neuronal morphology and endoplasmic reticulum (ER) dysfunction were evaluated. An in vivo CIRI model was established in rats by middle cerebral artery occlusion and reperfusion (MCAO/R) after the injection of LY294002 (10 µmol/L) and/or leptin (1 mg/kg), and neurological function, infarct volume, cerebral pathological changes, the expression of ERS-related proteins and cell apoptosis were examined. RESULTS: In vitro, leptin treatment improved the cell survival rate, ameliorated neuronal pathological morphology and alleviated OGD/R-induced ERS. In vivo, administration of leptin significantly reduced the infarct volume, neurological deficit scores and neuronal apoptosis as well as pathological alterations. In addition, leptin suppressed MCAO/R-induced ERS and may decrease apoptosis by inhibiting ERS-related death and caspase 3 activation. It also regulated expression of the antiapoptotic protein Bcl-2 and the proapoptotic protein Bax in the cortex. Furthermore, the inhibitory effect of leptin on ERS was significantly decreased by the effective phosphatidylinositol 3-kinase (PI3K) inhibitor LY294002. CONCLUSIONS: These results confirm that ERS plays an important role in CIRI and that leptin can inhibit the activation of ERS through the PI3K/Akt pathway, thereby alleviating CIRI. These findings provide novel therapeutic targets for IS.

The independent risks and specific biomarker of breast cancer-related ischemic stroke.

AIM: This retrospective study was designed to investigate the independent risks and specific biomarker for breast cancer-related ischemic stroke (BCRS). METHODS: Clinical features and laboratory findings were compared between BCRS group and breast cancer group without stroke, and further multivariate analyses were performed to predict independent risks factors for BCRS patients. A receiver operator characteristic (ROC) curve analysis was configured to estimate the diagnostic efficacy of each independent risk and the product of these risks and to obtain the optimal cut-off value of diagnosis, which was termed the BCRS Index. RESULTS: BCRS patients had elevated plasma D-dimer and CA153 levels and platelet-to-lymphocyte ratio (PLR), as well as more patients received endocrine therapy (all p ＜ 0.05). Moreover, multivariate analysis revealed that D-dimer levels (odds ratio [OR]: 1.002; 95% confidence interval [CI]: 1.001-1.003; p = 0.000), CA153 levels (OR: 1.005; 95% CI: 1.001-1.008; p = 0.007), PLR (OR: 1.010; 95% CI: 1.004-1.015; p = 0.001), and endocrine therapy (OR: 1.268; 95% CI: 1.087-1.479; p = 0.003) were identified as independent risks of BCRS. Furthermore, ROC analysis displayed that the product of risks had the best diagnostic efficacy, of which the area under the curve was 0.846 ± 0.28. The optimum cut-off point was 2.37 × 106/mL, which was termed the BCRS Index with higher diagnostic accuracy and validity. CONCLUSIONS: Endocrine therapy, as well as elevated plasma D-dimer and CA153 levels and PLR values may be independent risks for BCRS. Furthermore, BCRS Index should be served as a novel specific biomarker for BCRS, which is useful to distinguish BCRS for clinicians.

Recurrent episodes of reversible posterior leukoencephalopathy in three Chinese families with GJB1 mutations in X-linked Charcot-Marie-tooth type 1 disease: cases report.

BACKGROUND: The X-linked form of Charcot-Marie-Tooth disease type 1 (CMTX1) is an inherited peripheral neuropathy that arises in patients with mutations in the gap-junction beta-1 gene (GJB1). CASE PRESENTATION: Three young male patients from Southern China with pes cavus experienced multiple episodes of transient central nervous system (CNS) dysfunction. Three patients all had reversible posterior leukoencephalopathy as detected by brain diffusion-weighted magnetic resonance imaging (MRI-DWI). Nerve conduction velocity (NCV) showed sensorimotor polyneuropathy with mixed demyelinating and axonal features. Genetic testing indicated a c.425G > A (p.Arg142Glu) or c.563 C > T (p.Thr188Ile) or c.103G > C (p.Val35Leu) mutation in GJB1. The unique feature of this report is the identification of two novel mutations: c.563 C > T and sc.103G > C of the GJB1 gene detected in two families respectively. Another unique feature is that peripheral neuropathy symptoms in the three patients were insidious and found at the onset of CNS symptoms. CONCLUSIONS: Posterior leukoencephalopathy is involved in CMTX1 patients. The white matter changes in MRI of CMTX1 patients are reversible and recover later than CNS symptoms.

Specific Biomarkers of Prostate Cancer-Associated Ischemic Stroke: A Case-Control Study.

BACKGROUND Ischemic stroke in cancer patients is associated with poor prognosis. However, the specific biomarkers of cancer-associated ischemic stroke (CaIS) have not been well defined. MATERIAL AND METHODS A retrospective study was conducted on PCaIS patients. Clinical data and laboratory and imaging findings were collected. Multivariable logistic regression analysis was used to analyze the independent risk factors for PCaIS. A multiple model combining the independent risk factors of PCaIS was developed using the receiver operating characteristic (ROC) and area under the ROC curve (AUC). RESULTS A total of 83 PCaIS patients and 83 prostate cancer (PCa) patients were included. PCaIS patients had higher levels of D-dimer, neutrophil-to-lymphocyte ratio (NLR), and total prostate-specific antigen (T-PSA). In the multivariate analysis, D-dimer [OR=1.001, 95% CI: 1.00,1.00, P=0.002], NLR [OR=1.12, 95% CI: 1.04,1.22, P=0.005], and T-PSA [OR=6.275, 95% CI: 2.57,15.31, P<0.001] were independent risk factors of PCaIS. Additionally, the AUC of the multiple model of PCaIS was 0.815 (95% CI, 0.750-0.869), with sensitivity of 81.71% and specificity of 70.21%. CONCLUSIONS Elevated levels of D-dimer and T-PSA and increased NLR are independent risk factors of PCaIS. The multiple model of PCaIS can be a specific biomarker and is a reliable predictor of development of PCaIS.

Leptin attenuates cerebral ischemic injury in rats by modulating the mitochondrial electron transport chain via the mitochondrial STAT3 pathway.

BACKGROUND: According to recent studies, leptin may exert a neuroprotective function by affecting the phosphorylation of signal transducer and activator of transcription 3 (STAT3). During stress, STAT3 regulates mitochondrial oxidative stress and reduces apoptosis. OBJECTIVE: In the present study, we hypothesized that leptin increases STAT3 phosphorylation in the mitochondria and protects against mitochondrial oxidative stress in rats subjected to permanent middle cerebral artery occlusion (MCAO). RESULTS: Leptin reduced reactive oxygen species (ROS) production, and we confirmed that the mechanism underlying this change involved the enzymatic activities of mitochondrial respiratory chain complexes I and II. In addition, leptin increased the level of STAT3 Ser727 phosphorylation in the mitochondria. CONCLUSIONS: Based on these results, leptin may regulate mitochondrial respiratory chain enzymatic activities via mitochondria-targeted STAT3 to reduce ROS production and protect brain tissues from mitochondrial oxidative stress during cerebral ischemia.

Cerebral hemorrhage as the initial manifestation in patients with systemic cancer.

BACKGROUND: Cerebral hemorrhage as well as ischemic stroke is one of the common complications among patients with cancer. Ischemic stroke could be the initial manifestation in some patients with cancer. Meanwhile, some patients with cancer also could present cerebral hemorrhage as the initial manifestation, and further studies are required to determine whether these patients have their unique clinical features. AIM: To investigate the clinical features and underlying pathogenesis of concealed systemic cancer patients with cerebral hemorrhage as the initial manifestation. METHODS: The clinical data of patients with concealed systemic cancer who presented cerebral hemorrhage as the initial manifestation registered at the First Affiliated Hospital of Guangxi Medical University from January 2010 to December 2015 were prospectively collected and analyzed. RESULTS: Seventeen systemic cancer patients with cerebral hemorrhage as the initial manifestation (0.02%) were ultimately enrolled from 8,326 patients with cerebral hemorrhage. Three patients had traditional risk factors, but the other 14 patients did not. The common subtypes of malignancy were lung cancer, liver cancer, gastric carcinoma, rectal cancer and melanoma. Most patients (11/17, 64.7%) had elevated plasma levels of cancer biochemical markers, including cancer antigen (CA)125, CA153 and CA199, carcino-embryonic antigen, and alpha fetal protein. Coagulopathy was observed in 15 patients. CONCLUSION: The concealed systemic cancer patients with cerebral hemorrhage as the initial manifestation may lack conventional vascular risk factors but did present coagulopathy and elevated plasma levels of cancer biochemical markers. Coagulopathy might be responsible for the cerebral hemorrhage.

Potential Pathogenesis and Biomarkers of Kidney Cancer-Related Stroke.

BACKGROUND Stroke risk and stroke recurrence are increased in cancer patients, but the pathogenesis and biomarkers of kidney cancer-related stroke (KCS) are generally unclear. The aim of the present research was to investigate the pathogenesis and plasma biomarkers of kidney cancer-related stroke. MATERIAL AND METHODS A retrospective review was conducted on acute stroke patients with kidney cancer (KC) who were admitted to the hospital between January 2006 and December 2015. A total of 106 patients with KCS (active KC patients with acute stroke but without conventional vascular risks) were identified. In addition, 106 age- and sex-matched patients with KC alone were recruited. RESULTS KCS patients had higher plasma D-dimer, cancer antigen (CA) 125, and CEA levels and greater proteinuria levels than did KC patients. Multiple logistic regression analysis showed that the risk of stroke in patients with KC increased independently by 0.8% (odds ratio [OR] 1.008; 95% confidence interval [CI] 1.002, 1.013; p=0.004) with a 1 ng/mL increase in D-dimer levels, by 1.2% (OR 1.012; 95% CI 1.007, 1.018; p=0.000) with a 1 U/mL increase in CA125, by 2.5% (OR 1.025; 95% CI 1.012, 1.038; p=0.000) with a 1 U/mL increase in CEA by 1.4% (OR 1.014; 95% CI 1.005, 1.024; p=0.004) with a 1 mg increase in urine protein in 24 hours. CONCLUSIONS Elevated plasma D-dimer, CA125 and CEA levels, and increased urine protein levels might lead to hypercoagulability and then KCS; however, they may also be biomarkers of KCS.

Associations of TNFα-308G/A and TNFα-238G/A Polymorphisms with Ischemic Stroke in East Asians and Non-East Asians: A Meta-Analysis.

AIMS: Two well-characterized polymorphisms in the tumor necrosis factor (TNF) gene, TNFα-308G/A and TNFα-238G/A, are thought to play important roles in the etiology and pathogenesis of ischemic stroke. Due to ethnic diversity, studies of the associations between these polymorphisms and ischemic stroke are inconclusive. Thus, we conducted a meta-analysis to derive more precise estimates of these associations in East Asians and non-East Asians. MATERIALS AND METHODS: We searched relevant publications in the PubMed, Embase, and Medline databases. A total of 18 studies with 8075 patients and 8217 controls were included. The odds ratios (OR) and 95% confidence intervals (CIs) were evaluated to identify associations. RESULTS: Analyses of the full dataset failed to identify any significant association between ischemic stroke and the TNFα-308G/A (A vs. G: OR = 0.86, 95% CI: 0.72-1.02, p = 0.08) or TNFα-238G/A (A vs. G: OR = 0.94, 95% CI: 0.67-1.32, p = 0.72) polymorphism. In subgroup analysis by ethnicity, TNFα-308G/A was found to be a protective factor (A vs. G: OR = 0.69, 95% CI: 0.56-0.85, p = 0.01) against ischemic stroke in the East Asians. No significant association was detected between ischemic stroke risk and TNFα-238G/A in the East Asians (A vs. G: OR = 0.82, 95% CI: 0.57-1.16, p = 0.26) or non-East Asians (A vs. G: OR = 1.61, 95% CI: 0.90-2.88, p = 0.11). CONCLUSIONS: The results of this meta-analysis suggest that there is no significant relationship between ischemic stroke and TNFα-308G/A or TNFα-238G/A. However, according to subgroup analysis of East Asians, TNFα-308G/A is a protective factor against ischemic stroke.

Association between the rs112735431 polymorphism of the RNF213 gene and moyamoya disease: A case-control study and meta-analysis.

Ring finger protein 213 (RNF213) gene polymorphisms are thought to be significant in the etiology and pathogenesis of moyamoya disease (MMD). Due to the rarity of MMD patients, their ethnic diversity, and the use of varying methodologies, studies of the association between these polymorphisms and MMD have not been repeatable. This lack of reproducibility affects the strength of the conclusions drawn from their results. We conducted the present case-control study and meta-analysis to provide more precise estimates of the association between the rs112735431 (c.14576G>A) polymorphism and the risk of MMD. A total of 81 MMD patients and 100 healthy controls were enrolled in our case-control study. The RNF213 rs112735431 (c.14576G>A) polymorphism was genotyped using Sanger sequencing after amplification with polymerase chain reaction (PCR). The genetic algorithm (GA) genotype and A allele frequencies of RNF213 rs112735431 (c.14576G>A) (odds ratio, OR=7.10, 95% confidence interval, CI=1.51-33.43, p=0.006; OR=9.37, 95% CI=2.10-41.84, p<0.001, respectively) were significantly higher in the MMD group than those in the control group. In our meta-analysis, we assessed a total of eight case-control studies, including 985 patients and 2335 controls. Pooled ORs indicated a significant association between the presence of the rs112735431 (c.14576G>A) polymorphism and MMD risk (dominant model: OR=74.55, 95% CI=35.86-154.98, p<0.00001). Subgroup analysis based on country and sensitivity analysis verified these results. Our case-control study and meta-analysis both provide evidence of an association between the rs112735431(c.14576G>A) polymorphism in the RNF213 gene and MMD risk.

Clinical Features of Liver Cancer with Cerebral Hemorrhage.

BACKGROUND Cerebral hemorrhage is common in patients with cancer, but the clinical features and pathogenesis of liver cancer patients with cerebral hemorrhage are not well known. MATERIAL AND METHODS Liver cancer patients who developed cerebral hemorrhage were recruited from the First Affiliated Hospital of Guangxi Medical University between January 2003 and December 2014. We retrospectively analyzed clinical presentations, results of laboratory tests, and imaging examinations. The clinical features and pathogenesis were summarized. RESULTS Among 11133 patients with liver cancer, 9 patients (0.08%), including 3 females and 6 males met the inclusion criteria. The age range was 48-73 years and the average age was 61.67±8.97 years. Five patients did not have traditional hemorrhage risk factors and 4s had the risk factors; however, all had developed hepatocellular carcinoma, and 3 had developed metastasis. All 9 patients showed elevated tumor markers: an increased AFP level was detected in 6 patients, coagulation dysfunctions in 8 patients, and abnormal liver functions in 6 patients. Five patients had developed cerebral hemorrhagic lesions in the lobes of their brains, while hemorrhagic lesions in the basal ganglia occurred in 3 patients and in the brainstem in only 1 patient. Four patients had clear consciousness, while 5 patients were in coma and showed poor prognosis. CONCLUSIONS Patients who have liver cancer complicated with cerebral hemorrhage usually lack traditional risk factors of cerebral hemorrhage. The site of cerebral hemorrhage is often detected in the lobes of the brain. Coagulation dysfunctions might be the main pathogenesis of liver cancer complicated with cerebral hemorrhage.

[Clinical characteristics of acute cerebral hemorrhage in patients with systemic malignancy].

OBJECTIVE: To investigate the clinical features of systemic malignancy patients with acute cerebral hemorrhage as well as its underlying mechanism. METHODS: The clinical data, including presentation, lab tests and neurological images, of systemic malignancy patients with acute cerebral hemorrhage at the First Affiliated Hospital of Guangxi Medical University between January 2003 and December 2014 were collected and analyzed. RESULTS: Among 61 326 systemic malignancy patients, 25 patients(0.04%)were found with acute cerebral hemorrhage and were enrolled. Out of these 25 patients, age ranged from 31 to 77 years old, with an average age of 61 years, 18 patients were males. The clinical features of the systemic malignancy patients with acute cerebral hemorrhage were found that most patients (14/25, 54.0%) lacked traditional risk factors, with sudden symptom onset and some degree of neurologic deficiency in all patients, and most hemorrhagic lesions (19/25, 76.0%) involved the hemicerebrum, for most patients (16/25, 60.0%) cerebral hemorrhage occurred after 3 days to 3 years of the malignancy diagnosis, and some malignancy patients (8/25, 32.0%) presented with cerebral hemorrhage as the first presentation. The common subtypes of malignancy found were lung cancer (8/25, 32.0%), liver cancer (7/25, 28.0%), and then gastric carcinoma (6/25, 24.0%). Most patients (22/25, 88.0%) had elevated plasma level of cancer biochemical marks (including one or more than one of cancer antigen 125, 153 and 199, carcino-embryonic antigen, and alpha fetal protein), most patients (16/25, 64.0%) were found to have coagulation disorder. CONCLUSIONS: The unique clinical features of the systemic malignancy patients with acute cerebral hemorrhage are most patients lacking traditional risk factors, with coagulation disorder and with hemorrhagic lesions in hemicerebrum. And coagulation disorder might be responsible for the cerebral hemorrhage.

Clinical features and biological markers of lung cancer-associated stroke.

Objective To identify the unique clinical features and biological markers of lung cancer-associated stroke. Methods We recruited 102 patients with lung cancer plus stroke, 102 with lung cancer, and 102 with stroke. Detailed information was analysed and compared among groups. Results The groups were age-matched. Patients with lung cancer plus stroke showed multiple lesions involving multiple cerebral artery territories on magnetic resonance imaging, compared with stroke-alone patients. These patients also had a poorer modified Rankin Scale score at 30 days, and high mortality (18.6%). Patients with lung cancer plus stroke had a higher incidence of metastasis, and higher blood levels of D-dimer, CA125 and CA199 compared with patients with lung cancer alone. Multivariate logistic regression analysis showed that levels of D-dimer, CA125 and CA199 were independently related to lung cancer-associated stroke. Conclusion Elevated plasma D-dimer, CA125 and CA199 may be independent risk factors for and biomarkers of lung cancer-associated stroke.

[Clinical features of ischemic stroke in patients with nasopharyngeal carcinoma].

OBJECTIVE: To investigate the clinical features of ischemic stroke in patients with nasopharyngeal carcinoma. METHODS: The clinical data of the nasopharyngeal carcinoma patients with ischemic stroke treated at the First Affiliated Hospital of Guangxi Medical University between January 2006 and December 2013 were collected. RESULTS: Among 3 822 patients with nasopharyngeal carcinoma 10 patients suffered from acute ischemic stroke. The 10 patients were males and their age ranged from 39 to 70 years old, with an average age of 51 years. All of the patients were found with squamous cell carcinoma, with metastasis in 7 of them. Among the 10 patients, only 3 patients had with traditional risk factors for ischemic stroke, but no traditional risk factor was found in other 7 patients; 2 patients showed single lesion in brain and 8 patients with two or more lesions due to the blockage of multiple cerebral arteries; 7 patients showed an elevated plasma D-dimer level. CONCLUSION: It is suggested that the acute ischemic stroke occurring in the patients with nasopharyngeal carcinoma commonly lacks traditional risk factors, with elevated plasma D-dimer levels and multiple lesions due to involvement of several cerebral arteries.

Motivational interviewing for improving recovery after stroke.

BACKGROUND: Psychological problems are common complications following stroke that can cause stroke survivors to lack the motivation to take part in activities of daily living. Motivational interviewing provides a specific way for enhancing intrinsic motivation, which may help to improve activities of daily living for stroke survivors. OBJECTIVES: To investigate the effect of motivational interviewing for improving activities of daily living after stroke. SEARCH METHODS: We searched the Cochrane Stroke Group's Trials Register (November 2014), the Cochrane Central Register of Controlled Trials (CENTRAL; 2015, Issue 1), MEDLINE (1948 to March 2015), EMBASE (1980 to March 2015), CINAHL (1982 to March 2015), AMED (1985 to March 2015), PsycINFO (1806 to March 2015), PsycBITE (March 2015) and four Chinese databases. In an effort to identify further published, unpublished and ongoing trials, we searched ongoing trials registers and conference proceedings, checked reference lists, and contacted authors of relevant studies. SELECTION CRITERIA: Randomised controlled trials (RCTs) comparing motivational interviewing with no intervention, sham motivational interviewing or other psychological therapy for people with stroke were eligible. DATA COLLECTION AND ANALYSIS: Two review authors independently selected studies for inclusion, extracted eligible data and assessed risk of bias. Outcome measures included activities of daily living, mood and death. MAIN RESULTS: One study involving a total of 411 participants, which compared motivational interviewing with usual care, met our inclusion criteria. The results of this review did not show significant differences between groups receiving motivational interviewing or usual stroke care for participants who were not dependent on others for activities of daily living, nor on the death rate after three-month and 12-month follow-up, but participants receiving motivational interviewing were more likely to have a normal mood than those who received usual care at three-months and 12-months follow-up. AUTHORS' CONCLUSIONS: There is insufficient evidence to support the use of motivational interviewing for improving activities of daily living after stroke. Further well designed RCTs are needed.

Overexpression of 14-3-3 protein protects pheochromocytoma cells against 1-methyl-4-phenylpyridinium toxicity.

Objective To investigate the effects of 14-3-3 protein overexpression on the 1-methyl-4-phenylpyridinium (MPP(+)) induced pheochromocytoma (PC12) cell death and the potential mechanisms. Methods pcDNA3.1(+)-14-3-3 plasmids, which could be expressed in mammalian cell, were constructed and transfected into PC12 cells with Lipofectamine 2000. The expression of 14-3-3 protein, Bcl-2 protein, and BAD protein were determined by western blot. 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) assay, microplate reader, and flow cytometric analysis were used to measure cell viability, the caspase activity, and apoptotic ratio respectively. Results (1) The expression of 14-3-3 protein increased significantly three weeks after pcDNA3.1 (+)-14-3-3 plasmids transfected into PC12 cells. (2) MPP(+) caused a decrease of cell viability in a dose-dependent manner. At 100 mu mol/L MPP(+), cell viability reduced approximately 50%. (3) The caspase activity increased along with the MPP(+) concentrations rising and reached its maximum value (0.34 mu mol/mg protein) at 100 mu mol/L MPP(+). However caspase activity decreased significantly when the MPP(+) concentration exceeded 100 mu mol/L. (4) Overexpression of 14-3-3 protein decreased the apoptosis ratio of PC12 cells treated with 100 mu mol/L MPP(+) from 26.5% to 8.6%. (5) Bcl-2 protein tended to decrease but BAD protein tended to increase after treatment of PC12 cells with 100 mu mol/L MPP(+). Overexpression of 14-3-3 protein significantly increased the cellular level of Bcl-2 protein and decreased that of BAD protein. Conclusion Overexpression of 14-3-3 protein may reduce MPP(+)-induced apoptotic cell death in PC12 cells by up-regulating the Bcl-2 expression and down-regulating the BAD expression. These results may provide a promising target for treatment of Parkinson' s disease.