Research on the Relationship Between Vestibular Migraine With/Without Cognitive Impairment and Brainstem Auditory Evoked Potential.

Background: Vestibular migraine (VM) is the most common cause of spontaneous vertigo with no specific physical and laboratory examinations, and is an under-recognized entity with substantial burden for the individual and the society. In this study, by observing the brainstem auditory evoked potential (BAEP) and cognitive function of VM patients, the possible laboratory diagnostic indicators of VM and the influence of disease on cognitive function were discussed. Method: The study included 78 VM patients, 76 migraine patients, and 79 healthy individuals. The age, gender, and other clinical history of the three groups matched. All participants underwent BAEP examinations, in which patients in the migraine group and outpatients of the VM group were in the interictal period, and inpatients in the VM group were examined during episodes, while all patients tested for the Addenbrooke's cognitive examination-revised (ACE-R) scale were in the interictal period. The differences in BAEP and ACE-R scores between the three groups of members and their relationship with the clinical features of VM patients were analyzed. Result: The peak latency of I, III, and V wave in the BAEP of the VM group was longer than that of the migraine group and the control group (p < 0.05). The peak latency of V wave in the BAEP of the migraine group was longer than that of the control group (p < 0.05). The ACE-R of the VM group scored lower than the migraine group in terms of language fluency and language (p < 0.05), and lower than the control group in terms of total score, language fluency, language, and visuospatial (p < 0.05); and the ACE-R of the migraine group scored lower than the control group in the total score and visuospatial (p < 0.05). Conclusion: Migraine patients have brainstem dysfunction, and VM patients have more severe brainstem dysfunction than migraine patients, suggesting that VM patients have both central nervous system damage and peripheral nerve damage. Migraine patients have cognitive impairment, while cognitive impairment in VM patients is more severe than in migraine patients.

Knockdown of MicroRNA-1 in the Hippocampus Ameliorates Myocardial Infarction Induced Impairment of Long-Term Potentiation.

BACKGROUNDS/AIMS: It has been reported that myocardial infarction (MI) is a risk factor for vascular dementia. However, the molecular mechanism remains largely unknown. METHODS: MI mice were generated by ligation of the left coronary artery (LCA) for 4 weeks. Passive and active avoidance tests were performed to evaluate the cognitive ability of MI mice. A theta-burst stimulation (TBS) protocol was applied to elicit long-term potentiation (LTP) of the perforant pathway-dentate gyrus synapse (PP-DG). Western blot analysis was employed to assess protein levels. RESULTS: In this study, we demonstrated that after 4 weeks of MI, C57BL/6 mice had significantly impaired memory. Compared with the sham group, in vivo physiological recording in the MI group revealed significantly decreased amplitude of population spikes (PS) with no effect on the latency and duration of the stimulus-response curve. The amplitude of LTP was markedly decreased in the MI group compared with the sham group. Further examination showed that the expression of the TBS-LTP-related proteins BDNF, GluA1 and phosphorylated GluA1 were all decreased in the MI group compared with those in the sham group. Strikingly, all these changes were prevented by hippocampal stereotaxic injection of an anti-miR-1 oligonucleotide fragment carried by a lentivirus vector (lenti-pre-AMO-1). CONCLUSION: MI induced cognitive decline and TBS-LTP impairment, and decreased BDNF and GluA1 phosphorylation levels from overexpression of miR-1ated were involved in this process.

A prospective study of the incidence and correlated factors of post-stroke depression in China.

BACKGROUND: Post-stroke depression (PSD) is commonly observed among stroke survivors. However, statistical analysis of such data is scarce in developing countries. The purpose of this study is to examine the incidence of PSD and its relationship with stroke characteristics in China. METHODS: This was a prospective hospital-based study. Stroke patients were assessed within two weeks after acute ischemic stroke onset and then reevaluated at three months. Hamilton Depression Scale (HAMD) was used for screening depression (PSD). Subjects with HAMD score of ≥7 were further assessed with the World Health Organization Composite International Diagnostic Interview. Stroke severity was measured by the National Institutes of Health Stroke Scale (NIHSS). Stroke outcome was measured by the modified Rankin Scale (mRS). RESULTS: One hundred and two stroke patients were recruited, only ninety-one patients completed del period (men = 53, 63.74%), with mean age 60.0±10.4 years (range, 34-82 years). The incidence of PSD was 27.47% two weeks after stroke. The occurrence of PSD was unrelated with age, stroke type, stroke lesion and the history of disease. In univariate analysis gender, PSD was correlated with female gender. In multivariate logistic regression analysis, poor stroke outcome (mRS≥3) (OR 12.113, CI 1.169 to 125.59, P<0.05) was the important predictors of PSD. CONCLUSIONS: The study indicated that gender, functional dependence and stroke outcome are determinants of PSD occurrence during the first 2 weeks after stroke in China.

Protective effect of edaravone against PrP106-126-induced PC12 cell death.

The prion protein peptide PrP106-126 induces cell apoptosis through mechanisms involving production of intracellular reactive oxygen species. The present study investigated the effects of edaravone, a potent free radical scavenger in clinical use, on cell cytotoxicity induced by PrP106-126. Results showed that PrP106-126 decreased PC12 cell viability in a dose- and time-dependent manner. Edaravone significantly antagonized the cytotoxic effects of PrP106-126. Mechanistically, PrP106-126 decreased PC 12 intracellular glutathione (GSH) concentrations, decreased superoxide dismutase (SOD) enzyme activity, increased concentrations of the oxidation end product malondialdehyde (MDA), depolarized the mitochondrial membrane, and increased caspase-3 activity. Edaravone alone did not affect GSH, SOD, or MDA but did effectively reverse all of the intracellular prooxidant effects induced by PrP106-126 and inhibit induced apoptosis in PC12 cells. In conclusion, edaravone may be a viable candidate for the treatment of oxidative stress-induced neurodegenerative disease.

[Study on exons 3 and 4 of alpha-synuclein gene in Chinese familial Parkinson disease patients].

OBJECTIVE: To study the relationship of Chinese familial Parkinson disease with alpha-synuclein gene. METHODS: Polymerase chain reaction-single strand conformational polymorphism (PCR-SSCP) and polymerase chain reaction-heteroduplex analysis(PCR-HA) were employed to detect the abnormal mobilization in the familial Parkinson disease and sporadic Parkinson disease patients, then it was verified by gene sequencing. RESULTS: No mutation was found in alpha-synuclein gene exons 3 and 4 by PCR-SSCP together with PCR-HA. An inserted c and an inserted t were found in intron 4, position 23 and position 67 respectively. CONCLUSION: (1) Exons 3 and 4 of alpha-synuclein gene are not the mutational hot spots of Chinese familial Parkinson disease. (2) Two polymorphisms were found in intron 4 of alpha-synuclein gene. They are 23 ins c and 67 ins t.