The research focuses on the possibility of early detection of AD-specific vascular and atrophic brain changes in families which have a tendency to inherit the disease. The research includedthree families with AD inher...The research focuses on the possibility of early detection of AD-specific vascular and atrophic brain changes in families which have a tendency to inherit the disease. The research includedthree families with AD inheritance. All patientsunderwent: cognitive function assessment(MMSE),determination of dementia severity(CDR) and AD stages (TDR), computed tomography (CT), magnetic resonance imaging (MRI), scintigraphy of the brain (SG), rheoencephalography (REG), and cerebral multigated angiography (MUGA). All patients with different AD stages, as well as their descendants, have specific atrophic changes in the temporal lobes of the brain. The degree of these changes increases as AD becomes more severe and ranges from 4% - 8% (TDR-0) to 33% - 62% (TDR-3) of the total mass of a healthy person’s temporal lobes. Simultaneously, thepatients examined have changes of microcirculation manifested by reduction of the capillarybed in the temporal and frontalparietal regions,the development of multiple arteriovenousshunts in the same areas, early venous dumping, anomalous expansion of venoustrunks that receive blood from the arterialvenous shunts, venous stasis on the frontoparietal boundary. Similar changes are found among AD patients’ descendants aged 8 - 11, the only difference being in the degree of temporal lobes atrophy which is 4.7%. This proves that microcirculatory disorders are primary and atrophic changes of the temporal lobes are secondary in AD development. The data obtained indicate that the examination of AD patients’ relatives should begin well before the possible manifestations of the disease, even in childhood. It will allow to reveal the possibility of inheritance and the signs of the disease at the earliest possible stage and to begin its treatment in time.展开更多
Introduction: The research focuses on the clinical study of cerebral angioarchitectonics and microcirculation disorders in the development of Alzheimer’s disease (AD) in comparison with other neurodegenerative and is...Introduction: The research focuses on the clinical study of cerebral angioarchitectonics and microcirculation disorders in the development of Alzheimer’s disease (AD) in comparison with other neurodegenerative and ischemic lesions. Materials and methods: 1117 patients with different types and stages of neurodegenerative and ischemic lesions were examined, 93 of whom (8.33%) had different stages of AD—Test Group;1024 (91.67%) had cerebral atherosclerosis, Binswanger disease (BD), vascular Parkinsonism (VP)—Control Group. The examination included definition of CDR, MMSE, cerebral CT, MRI, cerebral sciagraphy (SG), rheoencephalography (REG), morphometric detection of AD stages with TDR, and cerebral multi-gated angiography (MUGA). Results: In all patients with AD, regardless of the disease stage, specific сerebral small vessel disease (CSVD), manifested by dyscirculatory angiopathy of Alzheimer’s type (DAAT), was detected in the temporal and fronto-parietal areas. Conclusions: DAAT is an AD-specific lesion of cerebral microvessels that changes hemodynamics, causes cerebral hypoxia, and contributes to impaired amyloid beta metabolism. The combination of deposition of amyloid beta in the cerebral tissue and vascular wall, as well as specific disorders of microcirculation, cause neurodegeneration and AD development. Patients with other neurodegenerative and ischemic lesions had no DAAT manifestations.展开更多
Objective To explore the effect of β-amyloid protein (Aβ) on S100β expression in rat hippocampus and its mechanisms. Methods At 7 days after bilateral stereotaxis injection of different dose of fibrillar Aβ 25-35 ...Objective To explore the effect of β-amyloid protein (Aβ) on S100β expression in rat hippocampus and its mechanisms. Methods At 7 days after bilateral stereotaxis injection of different dose of fibrillar Aβ 25-35 and interluekin-1 receptor antagonist (IL-1ra) into the rat CA1 region, the learning and memory abilities of rats were tested with passive avoidance task. Amyloid deposition was detected by using Congo red staining technique. Nissl staining and immunohistochemical techniques were used to analyze the number of neurons, and GFAP and the S100β expression in hippocampal CA1 region , respectively. Results After fibrillar Aβ injection, the step-through latency of rats was significantly shortened compared to that of the control group. The GFAP positive astrocytes were found surrounding amyloid deposition. Neuronal loss occurred in the pyramidal cell layer of CA1 region. The number of S100β positive cells in Aβ-treated group was significantly increased compared with that in the control group. After IL-1ra injection, the number of S100β positive cells was significantly decreased. Conclusion Intrahippocampal injection of Aβ 25-35 could cause similar pathologic changes of Alzheimer’s disease. Aβ 25-35 was capable of up-regulating S100β expression in a dose-dependent manner. The injection of IL-1ra could attenuate the effect of Aβ on S100β expression.展开更多
Two types of ligands-biphenyl and stilbene derivatives, -which can be labeled with Tc-99m for the diagnosis of Alzheimer' s disease (AD) have been synthesized successfully. The key steps in these two syntheses inv...Two types of ligands-biphenyl and stilbene derivatives, -which can be labeled with Tc-99m for the diagnosis of Alzheimer' s disease (AD) have been synthesized successfully. The key steps in these two syntheses involved Suzuki reaction and Wittig reaction respectively. The new discovered debromination reaction may be expanded to the compounds with double or triple bond adjacent to the carbon atom bearing the bromine atoms. These types of syntheses provide a route to a series of biphenyl and stilbene derivatives that will benefit the search of new imaging agents for AD.展开更多
文摘The research focuses on the possibility of early detection of AD-specific vascular and atrophic brain changes in families which have a tendency to inherit the disease. The research includedthree families with AD inheritance. All patientsunderwent: cognitive function assessment(MMSE),determination of dementia severity(CDR) and AD stages (TDR), computed tomography (CT), magnetic resonance imaging (MRI), scintigraphy of the brain (SG), rheoencephalography (REG), and cerebral multigated angiography (MUGA). All patients with different AD stages, as well as their descendants, have specific atrophic changes in the temporal lobes of the brain. The degree of these changes increases as AD becomes more severe and ranges from 4% - 8% (TDR-0) to 33% - 62% (TDR-3) of the total mass of a healthy person’s temporal lobes. Simultaneously, thepatients examined have changes of microcirculation manifested by reduction of the capillarybed in the temporal and frontalparietal regions,the development of multiple arteriovenousshunts in the same areas, early venous dumping, anomalous expansion of venoustrunks that receive blood from the arterialvenous shunts, venous stasis on the frontoparietal boundary. Similar changes are found among AD patients’ descendants aged 8 - 11, the only difference being in the degree of temporal lobes atrophy which is 4.7%. This proves that microcirculatory disorders are primary and atrophic changes of the temporal lobes are secondary in AD development. The data obtained indicate that the examination of AD patients’ relatives should begin well before the possible manifestations of the disease, even in childhood. It will allow to reveal the possibility of inheritance and the signs of the disease at the earliest possible stage and to begin its treatment in time.
文摘Introduction: The research focuses on the clinical study of cerebral angioarchitectonics and microcirculation disorders in the development of Alzheimer’s disease (AD) in comparison with other neurodegenerative and ischemic lesions. Materials and methods: 1117 patients with different types and stages of neurodegenerative and ischemic lesions were examined, 93 of whom (8.33%) had different stages of AD—Test Group;1024 (91.67%) had cerebral atherosclerosis, Binswanger disease (BD), vascular Parkinsonism (VP)—Control Group. The examination included definition of CDR, MMSE, cerebral CT, MRI, cerebral sciagraphy (SG), rheoencephalography (REG), morphometric detection of AD stages with TDR, and cerebral multi-gated angiography (MUGA). Results: In all patients with AD, regardless of the disease stage, specific сerebral small vessel disease (CSVD), manifested by dyscirculatory angiopathy of Alzheimer’s type (DAAT), was detected in the temporal and fronto-parietal areas. Conclusions: DAAT is an AD-specific lesion of cerebral microvessels that changes hemodynamics, causes cerebral hypoxia, and contributes to impaired amyloid beta metabolism. The combination of deposition of amyloid beta in the cerebral tissue and vascular wall, as well as specific disorders of microcirculation, cause neurodegeneration and AD development. Patients with other neurodegenerative and ischemic lesions had no DAAT manifestations.
文摘Objective To explore the effect of β-amyloid protein (Aβ) on S100β expression in rat hippocampus and its mechanisms. Methods At 7 days after bilateral stereotaxis injection of different dose of fibrillar Aβ 25-35 and interluekin-1 receptor antagonist (IL-1ra) into the rat CA1 region, the learning and memory abilities of rats were tested with passive avoidance task. Amyloid deposition was detected by using Congo red staining technique. Nissl staining and immunohistochemical techniques were used to analyze the number of neurons, and GFAP and the S100β expression in hippocampal CA1 region , respectively. Results After fibrillar Aβ injection, the step-through latency of rats was significantly shortened compared to that of the control group. The GFAP positive astrocytes were found surrounding amyloid deposition. Neuronal loss occurred in the pyramidal cell layer of CA1 region. The number of S100β positive cells in Aβ-treated group was significantly increased compared with that in the control group. After IL-1ra injection, the number of S100β positive cells was significantly decreased. Conclusion Intrahippocampal injection of Aβ 25-35 could cause similar pathologic changes of Alzheimer’s disease. Aβ 25-35 was capable of up-regulating S100β expression in a dose-dependent manner. The injection of IL-1ra could attenuate the effect of Aβ on S100β expression.
基金Project supported by the National Institute of Health(NIH)USA and the Institute for the Study of Aging(ISOA)USA.
文摘Two types of ligands-biphenyl and stilbene derivatives, -which can be labeled with Tc-99m for the diagnosis of Alzheimer' s disease (AD) have been synthesized successfully. The key steps in these two syntheses involved Suzuki reaction and Wittig reaction respectively. The new discovered debromination reaction may be expanded to the compounds with double or triple bond adjacent to the carbon atom bearing the bromine atoms. These types of syntheses provide a route to a series of biphenyl and stilbene derivatives that will benefit the search of new imaging agents for AD.
