Study On Apolipoprotein E Gene Polymorphisms And Neuroelectrophysiology In Alzheimer's Disease

Objective: Alzheimer's disease (AD) is one of the reasons that cause elder dementia. Up to date, the definite etiology is not clear, but it is confirmed to be associated with aging and heredity. Finding out the correlated genes is a hot of study on AD. In the present study Apolipoprotein E (ApoE) gene and promoter -491A/T, -427T/C polymorphisms were investigated in order to understand the relationship with AD.Lacking of specific biologic targets causes the difficulty of early diagnosis in AD. In present study, auditory event-related potential, (A-ERP)(P300), visual evoke potential (VEP), auditory brain -stem response (ABR), electroencephalograph (EEG) were investigated, particularly with non-linear Dynamic EEG analysis in order to help for early diagnosis.Part I Study on ApoE gene and promoter polymorphisms1. Diagnostic criteria: DSM-IV-R criteria, NINCDS桝DRDA criteria. 35 probably AD, and 38 age, sex matched healthy elders were chosen by scores ofMMSE,SECF.2. ApoE gene polymorphism was detected by PCR桼ELP. Results: e 4 allelic frequencies are higher in AD than in control(P<0.05). the main genotype is e 3/4. It suggested that e 4 is a risk factor in AD. Carriers with (?4+) have lower onset age than e 4. , female with e 4 have the lower onset age than ?4. . Itsuggested the female with e 4is a risk factor.-491A/T, -427T/C ApoE promoter polymorphisms were detected. Result: there was no difference in the frequency of the ?91A/T, -427T/C allele between the AD subjects and control samples. (P>0.05). But ApoE ?2 and -427 TC have closed relationship. 60% carriers with e 2 are TC, and only 5.3% carriers without e , are TC. It suggested that -491A/T, -427T/C gene polymorphisms are not associated with AD.Part II Study on neuroelectrophysiology in AD23 mild, moderate patients in AD and 21 age, sex matched healthy older were chosen.1. P300P300 was recorded with stimuli target/not target. Observe N,, P:, N:, P3 latency and amplitude. Result: There were significant difference in P3 latency between the controls and AD. P3 latency delays in AD (p<0.01). There was significant difference in P3 latency delay in AD (P<0.01). There were significant group differences in P3 latency and P3 amplitude between mild AD as well as moderate AD and the control (P<0.01). P3 latency delays in mild and moderate AD. P3 amplitude decreases only in moderate AD. P300 latency was significantly correlated with scores of MMSE and SECF.2. VEPPatten reversal -VEP was used. Observe N75, PI00, N135, P200. Compared with control, P200 latency delays (P<0.01). P200 latency was significantly correlated with scores of MMSE and SECF. There was significant group difference in P200 and N135 latency. Between the control, mild, moderate AD. N135 latency delays only in moderate AD. P200 latency delays in both two groups of AD.3. ABRObserve peak I - V latency and amplitude, I -HI > ffl- V , I - V inner-peak latency (IPL). Result: compared with control, peak V , HI-V .. I -V IPL significantly delay. I - V IPL significantly delay. I - V IPL significantly correlated with scores of MMSE and SECF(p<0.01). There was significant difference in I - V, III- V latency delay between the control, mild AD, moderate AD. I~V, EQ-Vlatency delay in moderate AD. It suggests ABR is normal in mild AD.4. EEGEEGs were recorded from 16 electrodes, 91.7% of patients' EEG were abnormal. Non-linear analysis of EEG in AD patients was studied first time in our country. In the study, correlation dimension D2 was used to study local changes in complexity. Result: D2 significantly decrease at many electrodes (except Ol, O2, F8, T6) in AD patient, particularly in left hemisphere (at FP1, FP2, F3, F4). D2 (FP1, F3, T3, C3, C4)(P<0.01) were significantly correlated with scores of MMSE. There was significant difference in D2 between mild AD as well as moderate AD and the control. D2 (T3, T4, C3, C4) significantly decreased in mild AD patients. It's necessary to further the study in non-linear area.Conclusion:...