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1.
Neuropathological stageing of Alzheimer-related changes   总被引:61,自引:5,他引:56  
Summary Eighty-three brains obtained at autopsy from nondemented and demented individuals were examined for extracellular amyloid deposits and intraneuronal neurofibrillary changes. The distribution pattern and packing density of amyloid deposits turned out to be of limited significance for differentiation of neuropathological stages. Neurofibrillary changes occurred in the form of neuritic plaques, neurofibrillary tangles and neuropil threads. The distribution of neuritic plaques varied widely not only within architectonic units but also from one individual to another. Neurofibrillary tangles and neuropil threads, in contrast, exhibited a characteristic distribution pattern permitting the differentiation of six stages. The first two stages were characterized by an either mild or severe alteration of the transentorhinal layer Pre- (transentorhinal stages I–II). The two forms of limbic stages (stages III–IV) were marked by a conspicuous affection of layer Pre- in both transentorhinal region and proper entorhinal cortex. In addition, there was mild involvement of the first Ammon's horn sector. The hallmark of the two isocortical stages (stages V–VI) was the destruction of virtually all isocortical association areas. The investigation showed that recognition of the six stages required qualitative evaluation of only a few key preparations.Supported by the Deutsche Forschungsgemeinschaft  相似文献
2.
成都地区老年期痴呆患病率调查   总被引:43,自引:17,他引:26  
目的 调查成都地区城乡老年期痴呆和阿尔茨海默病(AD)的患病率.方法 采用分层随机整群抽样方法 ,将成都市19个区市县(总人口972万)分为城区、郊区、近郊和远郊,根据各层人口占总人口比例确定各层应查≥55岁的老人数(5 555人),实查5 353人.调查采用筛查和确诊两阶段法,按美国精神障碍诊断与统计手册第3版修订本的标准诊断痴呆.结果 (1)查出痴呆患者143例,患病率为2.67%.其中AD为2.05%,血管性痴呆(VD)为0.37%,其他痴呆为0.24%.(2)女性患病率(3.14%)高于男性(2.16%;P<0.05).(3)痴呆患者的平均年龄[男(80±9)岁,女(82±7)岁]高于正常老年人[男女均为(67±8)岁;P<0.001],且痴呆患病率随年龄增长而上升.(4)农业人口的患病率(2.79%)高于非农业人口(2.40%),但差异无显著性.(5)文盲老人的患病率(4.45%)较小学(1.48%)和初中及其以上(0.17%)文化程度者高(P<0.001).结论 AD是成都地区老人中主要的痴呆类型,VD次之.文盲老人的痴呆患病率高,老年期痴呆患病率随年龄的增长而升高.  相似文献
3.
Life's Journey If life is indeed a journey, then poetry must be the map that reveals all its topographic possibilitiesellipsis while science is the compass that keeps us from getting lost. -R. T. Bartus, Simple Words for Complex Lives, (c) 1998 In the nearly 20 years since the cholinergic hypothesis was initially formulated, significant progress has been achieved. Initial palliative treatments for Alzheimer's disease (AD) have proven beneficial and have gained FDA approval, the use of animal models for studying AD and other neurodegenerative diseases has achieved wider acceptance, and important insight into the potential causes and pathogenic variables associated with various neurodegenerative diseases continues to increase. This paper reviews the current status of the cholinergic hypothesis in the context of continuing efforts to improve upon existing treatments for AD and explores the role that animal models might continue to play. Using the benefit of hindsight, particular emphasis is placed on an analysis of the approaches, strategies, and assumptions regarding animal models that proved useful in developing the initial treatments and those that did not. Additionally, contemporary issues of AD are discussed within the context of the cholinergic hypothesis, with particular attention given to how they may impact the further refinement of animal models, and the development of even more effective treatments. Finally, arguments are presented that, despite the deserved enthusiasm and optimism for identifying means of halting the pathogenesis of AD, a clear need for more effective palliative treatments will continue, long after successful pathogenic treatments are available. This review, therefore, focuses on issues and experiences intended to: (a) facilitate further development and use of animal models for AD and other neurodegenerative diseases, and (b) accelerate the identification of newer, even more effective treatments.  相似文献
4.
阿尔茨海默病病理行为评分表信度和效度   总被引:33,自引:1,他引:32  
目的 :评定阿尔茨海默病 (AD)病理行为评分表 (BEHAVE- AD)的信度和效度。 方法 :8名医生对 6例痴呆病人进行联合测定。对 6 3例痴呆病人进行 BEHAVE- AD和简明精神病评定量表 (BPRS)评定 ,48小时后重复 BEHAVE- AD评定。 结果 :同质性信度系数 Cronbach'sα=0 .770 3。联合检测一致性系数 ICC=0 .95 95 ,重测一致性系数 r=0 .96 1,P均 <0 .0 1。与 BPRS评分相比 ,相关系数 r=0 .475 ,P<0 .0 1。根据医生总体评定结果 ,将病人分组 ,各组病人的量表评分有显著差异。 结论 :BEHAVE- AD中译本有较好的信度和效度 ,值得推广应用  相似文献
5.
Interleukin 1 in the brain: biology, pathology and therapeutic target   总被引:32,自引:0,他引:32  
The cytokine interleukin 1 (IL-1) has diverse actions in the brain. In normal brain the IL-1 system is expressed at low levels and is upregulated rapidly in response to local or peripheral insults. IL-1 mediates host defence responses to local and systemic disease and injury (e.g. fever, slow-wave sleep, appetite suppression and neuroendocrine responses) and to neuroinflammation and cell death in neurodegenerative conditions, such as stroke and head injury. It has also been implicated in chronic degenerative diseases, in particular, multiple sclerosis, Parkinson's and Alzheimer's diseases. The mechanisms regulating the expression and action of IL-1 are poorly understood, but involve multiple effects on neuronal, glial and endothelial cell function. Thus, the IL-1 system provides an attractive and intensely competitive target for therapeutic intervention.  相似文献
6.
Cell death in Alzheimer's disease evaluated by DNA fragmentation in situ   总被引:28,自引:0,他引:28  
Loss of nerve cells is a hallmark of the pathology of Alzheimer's disease (AD), yet the patterns of cell death are unknown. By analyzing DNA fragmentation in situ we found evidence for cell death not only of nerve cells but also of oligodendrocytes and microglia in AD brains. In average, 30 times more brain cells showed DNA fragmentation in AD as compared to age-matched controls. Nuclear alterations suggestive of apoptosis were rare in degenerating cells. Even though the majority of degenerating cells were not located within amyloid deposits and did not contain neurofibrillary tangles, neurons situated within areas of amyloid deposits or affected by neurofibrillary degeneration revealed a higher risk of DNA fragmentation and death than cells not exposed to these AD changes.  相似文献
7.
Alzheimer disease and cerebrovascular pathology: an update   总被引:27,自引:0,他引:27  
Summary. Recent epidemiological and clinico-pathologic data suggest overlaps between Alzheimer disease (AD) and cerebrovascular lesions that may magnify the effect of mild AD pathology and promote progression of cognitive decline or even may precede neuronal damage and dementia.Vascular pathology in the aging brain and in AD includes: 1. cerebral amyloid angiopathy (CAA) with an incidence of 82–98% often associated with ApoEε2 and causing a) cerebral mass hemorrhages (around 70%, mainly in the frontal and parieal lobes), b) multiple or recurrent microhemorrhages (15%), and c) ischemic (micro-)infarcts or lacunes (around 20%). The frequency of these lesions increases with the severity of CAA and shows no correlation with that of senile amyloid plaques. CAA, significantly more frequent in patients with cerebral hemorrhages or infarcts than in aged controls, is an important risk factor for cerebrovascular lesions in AD. 2. Microvascular changes with decreased density and structural abnormalities causing regional metabolic and blood-brain barrier dysfunctions with ensuing neuronal damage. In large autopsy series of demented aged subjects, around 80% show Alzheimer type pathology, 20–40% with additional, often minor vascular lesions, 7–10% “pure” vascular dementia, and 3–5% “mixed” dementia (combination of AD and vascular encephalopathy). AD cases with additional minor cerebrovascular lesions have significantly more frequent histories of hypertension or infarcts than “pure” AD patients. Vascular lesions in AD include cortical microinfarcts, subcortial lacunes, white matter lesions / leukoencephalopathy, small hemorrhages and corticosubcortical infarcts, while in mixed type dementia multiple larger or hemispheral infarcts are more frequent. Small infarcts in AD patients have no essential impact on global cognitive decline which mainly depends on the severity of Alzheimer pathology, but in early stage of AD they may influence and promote the development of dementia. Recent studies showed lower density of plaques and tangles in brains with cerebrovascular lesions, and similar severity of dementia was related to fewer AD lesions in brains with than in those without small vascular lesions. Further studies will help to elucidate the risk factors and impact of cerebrovascular lesions on the development and progression of dementia in AD. Received November 2, 2001; accepted January 16, 2002  相似文献
8.
9.
安理申治疗轻中度阿尔茨海默病有效性及安全性的临床研究   总被引:23,自引:0,他引:23  
目的 评价安理申 (aricept)治疗轻、中度阿尔茨海默病 (Alzheimerdisease ,AD)的有效性及安全性。方法 对 188例轻、中度AD[简易智能状态量表 (MMSE) 10~ 2 4分 ]患者进行了多中心、随机 12周临床试验 ,其中 89例为单盲、安慰剂对照研究 ,99例为自身对照研究。结果 随机、单盲、安慰剂对照组研究结果表明 ,5mg/d安理申治疗 12周时 ,安理申组较安慰剂组MMSE、临床痴呆程度量表 (CDR)及日常生活自理量表 (ADL)分数显著改善 (P依次 <0 0 1、0 0 5、0 0 1)。自身对照组研究结果显示 ,5mg/d安理申治疗 12周时 ,治疗后较治疗前MMSE、CDR及ADL分数分别改善 3 5、0 6、7 1分(P依次 <0 0 1、0 0 5、0 0 1)。安理申治疗 4周时 ,MMSE分数已有提高 (P <0 0 5 )。 145例服用安理申的患者中 ,7例 (4 8%)出现轻度胆碱能兴奋性不良反应 ,43例安慰剂组中 ,2例 (4 7%)出现头晕、恶心 ,两组差异无显著意义 (P >0 0 5 )。结论 安理申能有效治疗轻、中度AD患者 ,对患者的认知功能、痴呆程度和日常生活自理能力均有改善 ,耐受性好 ,安全性高。  相似文献
10.
目的 探讨阿尔茨海默病 (AD)和血管性痴呆 (VD)患者脑脊液 (CSF)中乙酰胆碱 (ACh)和胆碱 (Ch)含量的异同以及它们与认知障碍的关系。方法 采用简易精神状态量表 (MMSE)对 2 2例AD、2 2例VD和 2 0名对照进行认知功能评分 ,利用高效液相色谱 电化学检测方法 (HPLC ECD)进行CSF的ACh和Ch检测 ,而后进行比较和分析。结果 AD组患者CSF的ACh含量 [(10 .7± 5 .1)nmol/L]低于对照组 [(34 .5± 9.0 )nmol/L](P =0 .0 0 1) ,与MMSE评分呈正相关。VD组患者CSF的ACh含量 [(16 .8± 7.4)nmol/L]也低于对照组 (P =0 .0 0 1) ,与MMSE评分呈正相关。AD组的CSF中Ch含量与对照组相比 [分别为 (6 2 7.6± 145 .1)nmol/L和 (716 .0± 15 9.4)nmol/L],差异无显著意义 ,与MMSE不呈相关关系。VD组患者CSF的Ch含量 [(887.4± 187.4)nmol/L]高于对照组 (P =0 .0 0 2 )和AD组患者 (P =0 .0 0 1)。结论  (1)ACh的降低与认知障碍呈正相关 ,提示ACh是与记忆有关的重要神经递质 ;(2 )VD的ACh降低提示有与AD类似的发病机制 ;(3)AD患者ACh显著降低和VD患者胆碱显著增高有助于两者之间的鉴别 ;(4 )应用胆碱酯酶抑制剂来提高脑内ACh水平 ,不仅适用于AD ,也适用于VD。  相似文献
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