痴呆是导致中风后存活人群自理能力降低的重要因素。中风后痴呆（PSD）包括发生在中风后的所有类型的痴呆，不论其痴呆的原因为何，如血管性痴呆(VD)，阿尔茨海默氏症(AD)以及混合型痴呆。由于中风致死率的降低和人口老龄化的到来，有可能在未来几十年，全世界范围内中风后痴呆的发病率将大幅增加。在此，我们将报告中风后早期出现的痴呆及长期的认知功能下降的发病率和危险因素，并通过使用PIB正电子扫描确定中风后痴呆中合并脑部淀粉样变的发病率。了解中风后痴呆的发病机制和危险因素，将有利于我们寻求治疗和预防措施，从而减低中风后痴呆的发生。 / 研究目的 / 研究1：中风后早期痴呆的发病率及危险因素 / 早期PSD及长期认知功能下降的发病机制甚为复杂。我们在中国中风存活者中建立了名为 STroke Registry IVEstigating COGnitive decline (STRIVE-COG) 的研究。此研究将报告早期PSD的危险因素。 / 研究2：中风后长期（15-18个月）认知功能下降的发病率及预测因素中风会增加远期痴呆的发生。但是，中风后远期认知功能下降的发病机制还未确定。我们的研究旨在观察中风后远期认知功能下降的危险因素。 / 研究方法 / 研究1：我们连续纳入一年的在我院中风中心留院的中风及短暂性缺血发作病人。在病人中风发生后的3-6个月后，对其进行多个认知领域的神经心理学检查。我们观察了患者的临床特征及结构影像学改变与早期PSD的相关性。我们还对部分早期PSD的病人进行了PIB正电子发射扫描（PIB-PET）检查。 / 研究2：在完成中风后3-6个月认知检查后的1年，即中风后的15-18个月，我们完成了认知心理学的随访检查。我们将认知功能下降定义为简易精神状态评分降低3分及以上，或者临床痴呆评分增加1分及以上。我们观察了认知功能下降和基线期临床、认知心理学和影像学特征（包括白质病变严重程度、陈旧性腔梗、全脑萎缩、额叶萎缩、顶叶萎缩、中颞叶萎缩）。在一组（n=18）早期PSD患者中，我们观察了脑部有类似阿尔茨海默氏病变表现的患者的认知功能下降的发病率。 / 结果 / 研究1：在所有入组的患者中（n=549），早期PSD的发病率为15.3%（n=84）。多因素回归分析显示，除了年龄和性别，早期PSD的危险因素包括急性腔隙性梗死灶(危险比[OR] 2.725, 95% 可信区间[CI] 1.364-5.434, P=0.004)及急性非腔隙性梗死灶(OR 2.809, 95%CI 1.124-6.410, P=0.014)比上无急性梗死灶的病人，还包括白质病变严重度（OR 1.120, 95% CI 1.037-1.210, p=0.004），额叶萎缩（OR 2.596, 95% CI 1.080-6.241, p=0.033），由脑室-大脑比表示的全脑萎缩（4th 四分卫区间 vs 1st区间, OR 3.096, 95% CI 1.374-6.993, p=0.006）。在19个完成了PIB-PET扫描的病人中，6人（31.6%）具有类似AD的脑部淀粉样物聚集的表现。 / 研究2：在452（82.3%）个完成了中风后15-18个月随访检查的病人中，认知功能下降的患者有73个（16.2%）。而年龄、受教育年限、多发陈旧性腔隙性梗死是其独立性预测因素。随访过程中中风复发的患者只有5.1%并且与认知功能下降无相关性。进展性的认知功能下降在PIB阴性（n=12）和PIB阳性（n=6）的患者中分别为41.7%和33.3%，而两者之间显著差别（p=0.731）。 / 结论 / 研究 1: 早期PSD的危险因素除了包括年龄、性别及脑部急性梗死灶之外，还包括脑部的慢性改变，包括白质病变、全脑萎缩、额叶萎缩及合并AD样病变特征。 / 研究 2: 年龄、受教育水平和多发陈旧性腔隙梗死是中风后15-18个月认知功能下降的独立危险因素。而合并AD样病变并不是导致中风后远期认知功能下降的必要因素。 / Dementia is a main cause of dependency in stroke survivors. Poststroke dementia (PSD) includes any dementia after a stroke, irrespective of its causes, e.g. vascular dementia (VD), Alzheimer’s disease (AD) or mixed dementia. A huge increase in prevalence and burden of PSD is likely to happen because of the decline in mortality after stroke and ageing of populations in the coming decades worldwide. In this thesis, we reported the risk factors for early PSD and delayed poststroke cognitive decline, and the prevalence of concurrent amyloid pathology as identified by Pittsburgh compound B (PIB) positron emission tomography (PET) in PSD. Understanding the risk factors of PSD will help to devise preventive and treatment strategies that may reduce the burden of PSD. / Objectives / Study1: Risk factors of early PSD / Mechanisms explaining poststroke early and delayed cognitive decline are complex. We set up a STroke Registry IVEstigating COGnitive decline (STRIVE-COG) among Chinese stroke survivors. Study 1 reported the findings on risk factors for early PSD. / Study 2: Prevalence and predictors for delayed (15-18 months) cognitive decline after stroke / Having a stroke increases the risk of delayed dementia. However, mechanisms accounting for the cognitive decline are uncertain. We investigated the predictors for delayed poststroke cognitive decline. / Subjects and Methods / Study 1：We recruited consecutive stroke or transient ischemic attack (TIA) patients admitted to our acute stroke unit over 1 year. We performed neuropsychological assessment 3-6 months poststroke. We investigated the association between clinical and structural neuroimaging features with early PSD. We performed PIB positron PET among a subset of subjects with early PSD. / Study 2: We performed neuropsychological assessment at baseline (i.e. 3-6 months poststroke) and at 15-18 months poststroke. We defined cognitive decline as a drop of ≥ 3 points in the mini-mental state examination and/or increment in ≥ 1 grading of the clinical dementia rating scale. We investigated the association between cognitive decline with baseline clinical, neuropsychological, and neuroimaging features (white matter changes [WMC] severity, old lacunar infarct, global atrophy, frontal lobe atrophy [FLA], parietal lobe atrophy, medial temporal lobe atrophy). Among a subset of subjects (n=18) with PSD at baseline, we investigated the influence of AD-like PIB retention upon the rate of cognitive decline. / Results / Study 1: Prevalence of early PSD among all recruited subjects (n=549) was 15.3% (n=84). Apart from age and female gender, multivariate regression analyses showed that risk factors for early PSD were presence of acute lacunar (odds ratio [OR] 2.725, 95% confidence interval [CI] 1.364-5.434, P=0.004) or non-lacunar infarct (OR 2.809, 95%CI 1.124-6.410,P=0.014) over no acute infarct apparent on neuroimaging, WMC severity (OR 1.120, 95% CI 1.037-1.210, p=0.004), FLA (OR 2.596, 95% CI 1.080-6.241, p=0.033), and global brain atrophy (4th quartile vs 1st quartile, OR 3.096, 95% CI 1.374-6.993, p=0.006). Among 19 subjects with early PSD who had PIB PET, 6 (31.6%) had AD-like PIB retention. / Study 2: Among 452(82.3%) subjects who had completed the study, cognitive decline occurred in 73 (16.2%) subjects. Age, education, and multiple old lacunar infarcts independenty predicted cognitive decline. Recurrent stroke occurred only in 5.1% and was not associated with cognitive decline. Progressive cognitive decline occurred in 41.7% and 33.3% of PIB negative (n=12) and PIB positive (n=6) PSD patients, respectively (p=0.731). / Conclusion / Study 1: Apart from age, female gender, and presence of acute infarct evident in neuroimaging, chronic brain changes (WMC, global brain atrophy, FLA, and concurrent AD pathology) are associated with early PSD. / Study 2: Age, education, and multiple old lacunar infarcts predicted cognitive decline at 15-18 months poststroke. Concurrent AD-like lesion is not necessary associated with a rapid cognitive decline. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Yang, Jie. / Thesis (Ph.D.)--Chinese University of Hong Kong, 2012. / Includes bibliographical references (leaves 93-109). / Abstract also in Chinese. / Chapter PART I --- LITERATURE REVIEW --- p.1 / Chapter Chapter 1 --- Introduction --- p.2 / Chapter 1.1 --- An overview of stroke --- p.2 / Chapter 1.2 --- Introduction of poststroke dementia --- p.5 / Chapter Chapter 2 --- Poststroke Dementia --- p.6 / Chapter 2.1 --- Defining poststroke dementia --- p.6 / Chapter 2.2 --- Classification of poststroke dementia --- p.7 / Chapter 2.3 --- Frequency, incidence, and clinical determinants of poststroke dementia --- p.20 / Chapter 2.4 --- Imaging methods and imaging features in poststroke dementia --- p.22 / Chapter 2.5 --- Mechanisms of stroke-associated dementia --- p.24 / Chapter 2.6 --- Influence of poststroke dementia on stroke outcome --- p.28 / Chapter PART II --- STUDIES ON EARLY POSTSTROKE DEMENTIA AND DELAYED COGNITIVE DECLINE --- p.31 / Chapter Chapter 3: --- Stroke Registry Investigating Cognitive decline (STRIVE-COG): Risk Factors for Early Poststroke Dementia (Study 1) --- p.32 / Chapter 3.1 --- Abstract --- p.32 / Chapter 3.2 --- Introduction --- p.33 / Chapter 3.3 --- Methods --- p.35 / Chapter 3.4 --- Results --- p.45 / Chapter 3.5 --- Discussion --- p.48 / Chapter Chapter 4 --- Stroke Registry Investigating Cognitive decline (STRIVE-COG): Predictors for Delayed Poststroke Cognitive decline (Study 2) --- p.63 / Chapter 4.1 --- Abstract --- p.63 / Chapter 4.2 --- Introduction --- p.64 / Chapter 4.3 --- Methods --- p.66 / Chapter 4.4 --- Results --- p.76 / Chapter 4.5 --- Discussion --- p.78 / Chapter PART III --- CONCLUSION --- p.88 / Chapter Chapter 5 --- Strengths and Limitations --- p.89 / Chapter Chapter 6 --- Summary and Future Directions --- p.91 / References --- p.93

No description available.

Diss. (sammanfattning) Stockholm : Karolinska institutet, 2005. / Härtill 5 uppsatser.

Diss. (sammanfattning) Stockholm : Karolinska institutet, 2006. / Härtill 5 uppsatser.

Diss. (sammanfattning) Stockholm : Karolinska institutet, 2002. / Härtill 5 uppsatser.

Vascular dementia (VaD), the second most common cause of dementia, causes substantial distress to patients and represents a significant burden to their families and communities. Currently, there is no effective treatment to reverse the brain damage associated with VaD. In general the drugs available for the management of cognitive problems in VaD are expensive and outcomes are uncertain. It is, therefore, important to seek out alternative approaches, which may prove effective, cheaper and safer. Chinese herbal medicine (CHM) has been used for the treatment of dementia-like disorders for centuries. Data from many preclinical studies and some clinical studies have suggested the potential effectiveness of CHM for the treatment of VaD. Based on the literature review conducted as part of this thesis, however, most of the studies were published in Chinese literature and failed to demonstrate methodological rigour or to report sufficient methodological detail. Randomised controlled trials (RCTs) using scientific methods of diagnosis and outcome measures are urgently needed. Wei Nao Kang (WNK) is a three-herb formula developed by Xi Yuan Hospital, China Academy of Chinese Medical Sciences. Preclinical experiments of WNK have demonstrated significant improvement in learning and memory function in VaD animal models in rats and mice. Human case studies have also signalled the potential value of WNK in VaD. Although the results of these studies were encouraging, strong scientific evidence from a well-designed RCT is still required. A rigorous clinical trial methodology, including scientific diagnostic criteria and outcome measures, was designed and applied to the evaluation of WNK for VaD. The trial was successfully conducted over a two-year period. Cognitive functions, as evidenced by the ADAS-cog, were significantly improved in the study group taking WNK herbal medication compared with the placebo group. The ADAS-cog was simultaneously validated as a measure of cognitive function in VaD. Blinding was verified and no major adverse effects were found related to WNK treatment. However, neither group demonstrated long-lasting effect on a 16 weeks follow-up after completion of treatment. WNK demonstrated a significant effect on quality of life (measured by SF-36) and some effect on activities of daily living (measured by ADCS-ADL) in VaD patients. The SF-36 was validated as a measure of general health status and the ADCS-ADL as a measure of activities of daily living in patients with VaD. Both scales were proven sensitive to the presence of VaD, and provided useful supplementary outcome measures for VaD. A cerebral perfusion study was conducted to identify changes in cerebral blood flow and its relationship with clinical symptoms. The study showed that WNK had marked increases in blood flow in the inferior frontal and anterior temporal regions, both of which are closely related to cognitive function in human brains. This study has provided scientific evidence in support of the clinical effect of WNK on VaD. In addition, it validated several outcome measures in assessing improvements in cognitive functions, activities of daily living and quality of life in VaD patients. One of the highlights of this study is the application of SPECT scans as an outcome measure. This provided an excellent objective parameter for assessing the effects of WNK. To the best of our knowledge, SPECT scanning has never been used in VaD trials of herbal medicines. / Doctor of Philosophy (PhD)

Thesis (Ph.D.)--University of Western Sydney, 2008. / A thesis presented to the University of Western Sydney, College of Health and Science, Centre for Complementary Medicine, in fulfilment of the requirements for the degree of Doctor of Philosophy. Includes bibliographies.

A literatura científica vem debatendo sobre a existência de uma associação entre diabetes mellitus (DM) e demência, doença de Alzheimer (DA) e demência vascular (DV). O DM é um conhecido fator de risco para a doença cerebrovascular (DCV) e DV, porém não há consenso até o momento do real papel do DM no desenvolvimento das alterações neuropatológicas da DA. Objetivos: verificar a associação entre DM e demência, DM e alterações neuropatológicas da DA e DV. Métodos: os dados foram coletados do Banco de Encéfalos Humanos do Grupo de Estudos em Envelhecimento Cerebral da FMUSP estudados de 2004 a 2015. A amostra foi dividida em dois grupos: não diabéticos e diabéticos. Os diagnósticos de DM e de demência foram estabelecidos post-mortem mediante entrevista com informante. O diagnóstico de demência exigiu escore >= 1 na Escala de Avaliação Clínica da Demência (CDR) e Questionário sobre Declínio Cognitivo no Idoso (IQCODE) >= 3,42. O diagnóstico etiológico da demência foi determinado por exame neuropatológico por imuno-histoquímica. A proporção de casos de demência, de DA e de DV de não diabéticos e diabéticos foi determinada, assim como a relação entre DM e placas neuríticas (PN) e emaranhados neurofibrilares (ENF), e neuropatologia vascular. As análises estatísticas empregadas foram o teste de Mann-Whitney e regressão linear múltipla para variáveis quantitativas, teste de ?2, teste exato de Fisher e regressão logística múltipla para variáveis categóricas. Resultados: amostra total foi de 1.037 indivíduos, sendo 758 não diabéticos (73,1%) e 279 diabéticos (26,9%). Demência foi constatada em 28,7% em diabéticos. O DM não se associou à frequência mais elevada de demência (OR: 1,22; IC 95%: 0,81-1,82; p=0,34). O DM não está associado com ENF (p=0,81), PN (p=0,31), grupo infarto (p=0,94), angiopatia amiloide (p=0,42) e arteriolosclerose hialina (p=0,07). Após o ajuste para variáveis demográficas e para os fatores de risco vascular, o diagnóstico de DM não se associou ao diagnóstico neuropatológico de DA e vascular. Conclusão: o DM não está associado à demência e às alterações neuropatológicas da DA e de DV / The scientific literature has been debating the existence of an association between diabetes mellitus (DM) and dementia, Alzheimer\'s disease (AD) and vascular dementia (VaD). DM is a known risk factor for cerebrovascular disease (CVD) and VaD, but there is still no consensus on the real role of DM in the development of AD neuropathology. Objectives: to investigate the association among DM and dementia, neuropathology (NP) of AD and VaD. Methods: Data were collected from the cases included in the Brain Bank of the Brazilian Aging Brain Study Group between 2004 and 2015. Cases were divided into 2 groups: no diabetics and diabetics. Clinical diagnosis of dementia was determined by the scores >= 1.0 in the Clinical Dementia Rating (CDR) and >= 3.42 in the Informant Questionnaire on Cognitive Decline in the Elderly (IQCODE). Etiological diagnoses of dementia were determined by neuropathological examination, using immunohistochemistry. The proportion of dementia cases, AD and VaD of no diabetics and diabetics were investigated as well as the relationship among DM and neuritic plaques (NPq) and neurofibrillary tangles (NFT). Mann-Whitney test and multiple linear regression for quantitative variables, and chi-square test and multiple logistic regression for categorical variables were the statistical analyses applied. Results: Total sample included 1037 subjects, divided in 758 (73.1%) no diabetics and 279 diabetics (26.9%). Dementia was present in 27.8% of diabetics. DM did not increase the frequency for dementia (OR: 1.22; IC 95%: 0.81-1.82; p=0.34). DM was not associated with NFT (p=0.81), NPq (p=0.31), infarct group (0.94), cerebral amyloid angiopathy (0.42) and hyaline arteriolosclerosis (p=0.07). After adjustment for demographic variables and vascular risk factors, DM was not associated with DA and vascular NP. Conclusion: DM is not associated with dementia, AD and vascular neuropathology

A literatura científica vem debatendo sobre a existência de uma associação entre diabetes mellitus (DM) e demência, doença de Alzheimer (DA) e demência vascular (DV). O DM é um conhecido fator de risco para a doença cerebrovascular (DCV) e DV, porém não há consenso até o momento do real papel do DM no desenvolvimento das alterações neuropatológicas da DA. Objetivos: verificar a associação entre DM e demência, DM e alterações neuropatológicas da DA e DV. Métodos: os dados foram coletados do Banco de Encéfalos Humanos do Grupo de Estudos em Envelhecimento Cerebral da FMUSP estudados de 2004 a 2015. A amostra foi dividida em dois grupos: não diabéticos e diabéticos. Os diagnósticos de DM e de demência foram estabelecidos post-mortem mediante entrevista com informante. O diagnóstico de demência exigiu escore >= 1 na Escala de Avaliação Clínica da Demência (CDR) e Questionário sobre Declínio Cognitivo no Idoso (IQCODE) >= 3,42. O diagnóstico etiológico da demência foi determinado por exame neuropatológico por imuno-histoquímica. A proporção de casos de demência, de DA e de DV de não diabéticos e diabéticos foi determinada, assim como a relação entre DM e placas neuríticas (PN) e emaranhados neurofibrilares (ENF), e neuropatologia vascular. As análises estatísticas empregadas foram o teste de Mann-Whitney e regressão linear múltipla para variáveis quantitativas, teste de ?2, teste exato de Fisher e regressão logística múltipla para variáveis categóricas. Resultados: amostra total foi de 1.037 indivíduos, sendo 758 não diabéticos (73,1%) e 279 diabéticos (26,9%). Demência foi constatada em 28,7% em diabéticos. O DM não se associou à frequência mais elevada de demência (OR: 1,22; IC 95%: 0,81-1,82; p=0,34). O DM não está associado com ENF (p=0,81), PN (p=0,31), grupo infarto (p=0,94), angiopatia amiloide (p=0,42) e arteriolosclerose hialina (p=0,07). Após o ajuste para variáveis demográficas e para os fatores de risco vascular, o diagnóstico de DM não se associou ao diagnóstico neuropatológico de DA e vascular. Conclusão: o DM não está associado à demência e às alterações neuropatológicas da DA e de DV / The scientific literature has been debating the existence of an association between diabetes mellitus (DM) and dementia, Alzheimer\'s disease (AD) and vascular dementia (VaD). DM is a known risk factor for cerebrovascular disease (CVD) and VaD, but there is still no consensus on the real role of DM in the development of AD neuropathology. Objectives: to investigate the association among DM and dementia, neuropathology (NP) of AD and VaD. Methods: Data were collected from the cases included in the Brain Bank of the Brazilian Aging Brain Study Group between 2004 and 2015. Cases were divided into 2 groups: no diabetics and diabetics. Clinical diagnosis of dementia was determined by the scores >= 1.0 in the Clinical Dementia Rating (CDR) and >= 3.42 in the Informant Questionnaire on Cognitive Decline in the Elderly (IQCODE). Etiological diagnoses of dementia were determined by neuropathological examination, using immunohistochemistry. The proportion of dementia cases, AD and VaD of no diabetics and diabetics were investigated as well as the relationship among DM and neuritic plaques (NPq) and neurofibrillary tangles (NFT). Mann-Whitney test and multiple linear regression for quantitative variables, and chi-square test and multiple logistic regression for categorical variables were the statistical analyses applied. Results: Total sample included 1037 subjects, divided in 758 (73.1%) no diabetics and 279 diabetics (26.9%). Dementia was present in 27.8% of diabetics. DM did not increase the frequency for dementia (OR: 1.22; IC 95%: 0.81-1.82; p=0.34). DM was not associated with NFT (p=0.81), NPq (p=0.31), infarct group (0.94), cerebral amyloid angiopathy (0.42) and hyaline arteriolosclerosis (p=0.07). After adjustment for demographic variables and vascular risk factors, DM was not associated with DA and vascular NP. Conclusion: DM is not associated with dementia, AD and vascular neuropathology

Demenzformen sind in Deutschland und in der Welt eine der verbreitetsten Erkrankungen der Bevölkerung des hohen Alters, welche mit hohem medizinischem Aufwand und hohen Kosten verbunden sind sowie mit einer hohen psychischen Belastung sowohl für die Patienten als auch für deren Angehörigen und des betreuenden medizinischen Personals einher geht. Daher ist eine schnelle und zuverlässige Diagnosestellung wichtig, wofür Testverfahren mit hoher Sensitivität und Spezifität erforderlich sind. Es muss eine klare Differenzierung zwischen den Demenzarten wie des Alzheimertyps, des vaskulären Typs, des Mischformtyps und weiteren Formen sowie den sekundären Demenztypen möglich sein. Die klinisch relevanten Methoden zur Erfassung der Demenz sind neben der Erhebung einer spezifischen Anamnese und des klinisch neurologischen Status, bildgebenden Verfahren und die Anwendung neuropsychologischer Testverfahren. Des Weiteren gehören Blut- und Liquoruntersuchungen zum Diagnostikspektrum. Der MMSE unterscheidet signifikant zwischen dementen und nicht dementen Patienten, daher musste eine vorgesehene Kontrollgruppe negiert werden, da kein signifikanter Unterschied des Demenzschweregrads zu den eingeschlossenen dementen Patienten bestand. In dieser retrospektiv ausgewerteten, anonymisierten Studie wurden immunologische Blutparameter untersucht, die eine Differenzierung zwischen der Alzheimer-Demenz, der vaskulären Demenz und dem Mischtyp ermöglichen sollten. Zur Überprüfung des Ergebnisses ist der HIS sehr gut geeignet, da er signifikant zwischen den drei Demenzformen separiert. In der Bildgebung finden sich signifikante Unterschiede zwischen der vaskulären Demenz zur Alzheimerdemenz bezogen auf ausgeprägte Stenose in arteriellen Gefäßen und daraus resultierende mikro-/makropathische Veränderungen und dadurch sich entwickelnde fokalneurologische Defizite sowie Schlaganfälle. Wohingegen eine Kombination aus allgemeiner und regionaler Atrophie signifikant häufiger bei Patienten mit Alzheimer- auftreten als bei Patienten mit vaskulärer Demenz. Die grundlegende Hypothese bestand darin, dass aktivierte autoreaktive T-Zellen die BlutHirn-Schranke passieren können und die Mikroglia aktivieren und damit eine immunotoxische Immunantwort erzeugen. Dies führt zu einer überschießenden Apoptose mit dadurch bedingtem Zelluntergang. Für den Nachweis einer entsprechenden Immunreaktion wurden die Moleküle CD 25, CD 54, CD 95 und das Annexin-V im peripheren Blut bestimmt und mit den üblichen Demenzdiagnostikverfahren verglichen. Dabei ist eine signifikante Trennung zwischen den Patienten mit Alzheimer Demenz bezogen auf das CD 25 und das Verhältnis CD25*10/CD95*10 gegenüber der vaskulären Demenz zu sehen. Die Lymphozyten 95 kommen signifikant häufiger im Blut der Patienten mit vaskulärer Demenz vor gegenüber der AD. Bei den anderen Parametern finden sich keine signifikanten Unterschiede. Mittels der genannten Punkte lässt sich eine gute Differenzierung zwischen Alzheimerdemenz und vaskulärer Demenz vornehmen. Dies muss mittels weiterer Studien und einer größeren Patientenzahl sowie Kontrollgruppe validiert werden.:Abkürzungsverzeichnis 5 1. Wissenschaftliche Aufgabenstellung und Zielsetzung 12 2. Einführung zur Thematik 13 2.1 Epidemiologie 13 2.2 Diagnostik 23 2.3 Therapie 42 3. Problemstellung 47 3.1 Immunologische Testmethodik 47 4. Material und Methoden der Patienten 59 4.1 Statistische Grundlagen 60 5. Ergebnisse 63 5.1 Patienten und klinische Diagnosezuordnung 63 5.2 Diagnosegruppen 64 5.3 Immunologischer Bluttest 80 5.4 Modell Alzheimer- zu vaskulärer Demenz 90 5.5 Zusammenfassung Blutuntersuchung 92 5.6 Zusammenfassende Ergebnisstabelle 93 6. Diskussion 95 6.1 Demographischen Variablen 95 6.2 Klinik 96 6.3 Neuropsychologische Testverfahren 97 6.4 Apparative Diagnostik (Ultraschall, CT, MRT, PET) 97 6.5 Immunologie 99 7. Zusammenfassung 103 8. Summary 105 9. Abbildungsverzeichnis 106 10. Tabellenverzeichnis 108 11. Literaturverzeichnis 110 12. Danksagung 128