Impact of Alzheimer's Disease in Nine Asian Countries.

BACKGROUND: Asia will soon have the majority of demented patients in the world. OBJECTIVE: To assess dementia using a uniform data system to update the current status of dementia in Asia. METHODS: A uniformed data set was administered in Taiwan, China, Hong Kong, Korea, Japan, Philippines, Thailand, Singapore, and Indonesia to gather data with regard to Alzheimer's disease (AD) and its related issues for these countries. RESULTS: In total, 2,370 AD patients and their caregivers were recruited from 2011 to 2014. The demographic characteristics of these patients and the relationships between patients and caregivers were different among individuals in these countries (p < 0.001). Of note, the family history for having dementia was 8.2% for females in contrast to 3.2% for males. CONCLUSION: Our study highlighted the differences in dementia assessment and care in developing versus developed countries. Greater effort with regard to studying dementia, especially in developing countries, is necessary.

[The clinical study of somatosensory evoked magnetic fields in patients with acute cerebral infarction by magnetoencephalography].

OBJECTIVE: To investigate the characteristics of somatosensory evoked magnetic fields (SEF) in patients with acute cerebral infarction by magnetoencephalgraphy (MEG). METHODS: SEFs were recorded from 17 patients with acute cerebral infarction and 18 healthy volunteers using 306-channel whole-head MEG. The electric stimuli were presented with interstimulus intervals of 0.5 s. The peaks of SEF were estimated by equivalent current dipole (ECD), which were superimposed on MRI. RESULTS: M20 was the most elemental components of SEF in all subjects, originating from the area close to the "hand area" of the primary somatosensory cortex. There appeared several abnormal SEF parameters in the patient group: (1) the value of interhemispheric difference of the M20 positions was (8 +/- 4) mm in the normal group and (11 +/- 3) mm in the patient group (P < 0.01); (2) the peak latency of M20 responses in the healthy group was (20.7 +/- 1.1) ms, significantly shorter than those in both the unaffected hemisphere and affected hemisphere in the patient group, (21.8 +/- 1.2) ms and (23.6 +/- 1.9) ms, (both P < 0.01); (3) the strength of ECD in the affected hemisphere was (17 +/- 10) nAm, significantly smaller than that in the unaffected hemisphere, (26 +/- 10) nAm (P < 0.01). CONCLUSION: Latent cortical impairment may be evaluated by MEG with higher spatial and temporal resolution. MEG provides objective and sensitive indexes to evaluate the function of somatosensory cortex in patients with acute cerebral infarction.

Magnetoencephalography assessment of evoked magnetic fields and cognitive function in subcortical ischemic vascular dementia patients.

OBJECTIVE: To investigate the relationship between cognitive impairment and somatosensory evoked magnetic field and auditory evoked magnetic field changes in elderly male patients with subcortical ischemic vascular dementia (SIVD). METHODS: Magnetoencephalography (MEG) was used to record evoked magnetic field changes from 4 SIVD patients (76-88 years), 3 patients with vascular cognitive impairment with no dementia (VCI-ND; 74-87 years), and 6 healthy volunteers (72-85 years). Latency peaks, equivalent current dipole (ECD) strength, and bilateral ECD position were recorded. The MEG data were superimposed on magnetic resonance imaging to produce magnetic source imaging. RESULTS: Compared to controls, SIVD patients showed increased M20 latency and ECD strength. There were no significant differences in M20 inter-hemispheric positions across diagnostic categories. At M100, SIVD patients showed delayed auditory evoked magnetic field latency compared to controls. However, ECD strength and 3-dimensional inter-hemispheric differences were similar across the groups at the M100 measurement. CONCLUSIONS: Changes in somatosensory and auditory evoked magnetic field changes correlated with cognitive impairment in SIVD patients. Magnetic field latency measures may provide an objective and sensitive index for early dementia detection and monitoring of cognitive function.

[The changes of cAMP and adenylyl cyclase mRNA level in hippocampus of mice with ischemia/reperfusion].

AIM: To observe the cAMP and adenylyl cyclase (AC) mRNA level in hippocampus of mice with vascular dementia (ischemia/reperfusion), and explore the molecular pathogenesis of ischemia/reperfusion. METHODS: The mice were subjected for ischemia/reperfusion three times on bilateral common carotid arteries by knots to establish models of ischemia/reperfusion and the changes of learning and memory were tested on 29 d/30 d after operation. Sham-operation mice were introduced as control group. The cAMP level was evaluated by the radioimmunoassay (RIA), AC mRNA positive neurons of hippocampus CA1 area were dyed through in-situ hybridization (ISH). RESULTS: Compared with sham-operation group, the learning and memory of model group was worse (P < 0.05), the cAMP level in hippocampus was lower (P < 0.05) and the surface density (Sv) of AC mRNA positive neurons reduced (P < 0.05). CONCLUSION: The lower cAMP and AC mRNA level in hippocampus might participate in the molecular pathogenesis of ischemia/reperfusion.

[Study of the gene deletions and the immunofluorescence of muscle in patients with DMD/BMD].

AIM: To detect the deletion distribution of dystrophin gene and dystrophin changes in muscle cells of the patients with Duchenne/Becker muscular dystrophy (DMD/BMD), furthermore to investigate the relationship between them and clinical symptoms. METHODS: 42 patients with DMD/BMD were screened by 9 primers multiplex PCR. The patients from 5 DMD and 2 BMD were detected by immunofluorescence technique for analyzing dystrophin located in muscle cell membrane, compared with 2 normal males. RESULTS: The deletion of one or more exons was found in 21 patients. 16 cases (76.2%) were detected in the central region and 5 patients (23.8%) in the 5' extreme region, especially in exon 48 (6 patients). Negative result of staining was seen in 5 DMD patients. Of these, one case of DMD had no detectable levels of dystrophin, but no deletion of DMD gene. Dystrophin immunostaining from two BMD patients consisted of a discontinuous staining pattern around most fibers. CONCLUSION: It might be possible that some correlation existed between the type of gene deletion and the degree of severity of the disease. The amount and size of exon deletion may not affect the symptoms. DMD/BMD are highly heterogeneous in clinical manifestation and in inheritance pattern. The pathologic foundation of DMD and BMD is the absence or abnormal expression of dystrophin. The consequence of that depends not only on the degree, but also on the function.

[The changes of resting [Ca2+]i level and expression of CaM mRNA, CaMPK II mRNA in hippocampal neurons of the mice with vascular dementia].

AIM: To investigate the resting [Ca2]i level and expression of calmodulin (CaM), calmodulin-dependent protein kinase II (CaMPKII) mRNA in hippocampal neurons of the mice with vascular dementia (VD) and their roles in the pathogenesis of VD. METHODS: The mice were subjected for ischemia/reperfusion repeatedly on bilateral common carotid arteries by knots to establish the VD models. Animals with the sham-operation were taken as control group. The changes of behavior were observed through the step-down avoidance test and water maze test on the day 29, 30 after the operations. The hippocampal neurons were obtained immediately after mice were sacrificed and the resting [Ca2+]i was measured using laser scanning confocal microscopy with Fluo-3/AM as fluorescence indicator. RT-PCR technique was used to measure the mRNA expression of CaM, CaMPKII in hippocampal neurons. RESULTS: (1) The abilities of learning and memorizing in model group were inferior to those of sham-operation group( P < 0.05). (2) The resting [Ca2]i level in model group was significantly higher than sham-operation group (P < 0.05), while the expression of CaMmRNA, CaMPKIImRNA in VD group was significantly reduced than sham-operation group (P < 0.01). CONCLUSION: Our study indicates that excessive resting[Ca2+ ]i level and lower CaM, CaMPKII expression in hippocampal neurons might participate in the pathogenesis of VD.