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Objective To study the relationship between the serum homocysteine ( Hcy ) levels in patients with first-episode depression and event related potentials ( ERP ) P300.Methods 117 first-episode depressive patients were selected as the case group,and 110 healthy volunteers were selected as the health control group,the de-termination of serum Hcy levels in the two groups were detected by enzyme linked immunosorbent assay,measured by the Shenzhen Brain Master brain evoked potential system to complete the visual P300.Results The serum Hcy levels of the case group was (14.0 ±9.8)μmol/L,which was higher than (10.5 ±7.5)μmol/L of the health control group (t=-3.087,P <0.05).The N1,N2 incubation period of the case group were (91.4 ±18.6) ms,(235.4 ± 30.5)ms,respectively,which were longer than (88.6 ±13.0)ms,(204.3 ±20.3)ms of the health control group(t=1.305,8.990,all P<0.01);The P3 incubation period of the case group were (359.5 ±30.0)ms,which was longer than (327.2 ±41.8)ms of the health control group(t=6.685,P<0.05).The target P3,non-target P2 amplitude of the case group were (4.1 ±2.0)μV,(4.2 ±1.9)μV,respectively,which were singnificantly lower than (6.8 ± 3.8)μV,(6.6 ±3.6) μV of the health control group( t=-6.694,-6.485,all P<0.01).The P2 incubation period of Hcy case group was (194.4 ±13.6) ms,which was longer than (163.1 ±21.8) ms of the non Hcy case group(t=8.486,P<0.01).The P3 incubation period of Hcy case group was (357.0 ±24.5)ms,which was longer than (337.1 ±45.5)ms of the non Hcy case group(t=2.645,P<0.05).The target P3,non-target P2 amplitude of the Hcy case group were (5.4 ±1.5)μV,(5.2 ±1.2) μV,which were significantly lower than (5.8 ±3.8)μV, (5.4 ±3.2)μV of the Hcy case group(t=-0.745,-0.208,all P<0.01).Conclusion The serum Hcy levels in patients with first-episode depression increased, and P300 latency, amplitude decreased, the cognitive function is related to Hcy metabolism disorder and depression damage.
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AIM: Currently, there are almost 100 genes related to Alzheimer's disease (AD), and studies have indicated that apolipoprotein E (APO E) ε4 allele is a genetic risk factor of AD. However, there have been no reports of the distributions of APO E genotypes and allele frequencies in Uighur and Han AD patients. METHODS: We analyzed APO E gene polymorphism in 209 AD cases diagnosed based on National Institute of Neurological and Communicative Disorders and Stroke and Alzheimer's Disease and Related Disorders Association and 220 non-dementia controls. We used polymerase chain reaction-restriction fragment length polymorphism methods as the basis of this epidemiological survey. RESULTS: In the AD and control groups, there are no statistically significant differences in APO E genotypes and allele frequency between the Uighur and Han ethnicities (P < 0.05). In the AD group, the ε3/4 genotype (28.2%) and ε4 allele frequency (14.8%) occurred at a higher rate than in the control (13.2% and 8.0%, respectively; P < 0.05). This distinction remained true within each ethnicity; the ε3/4 genotype and ε4 allele frequency are higher in the AD groups (Uighur, 30.6% and 15.8%, respectively; Han, 25.5% and 13.8%, respectively) than in the control groups (Uighur, 14.5% and 9.4%, respectively; Han, 11.7% and 6.3%, respectively; P < 0.05). CONCLUSIONS: The distribution of APO E genotype and allele frequency does not differ between the Uighur and Han ethnicities. The APO E ε4 allele is a risk factor of AD for both populations.
