Chang, RCC

Hugon, J

Suen, KC

Yu, MS

Hong Kong Medical Journal

HKU Scholars Hub

Title Research strategies in molecular signaling of neuronalapoptosis in Alzheimer's diseaseAuthor(s) Chang, RCC; Suen, KC; Yu, MS; Hugon, JCitationThe 8th Medical Research Conference Abstracts, Hong KongMedical Journal, Hong Kong, China, 25-26 January 2003, v. 9 n. 1Supp 1, p. 82Issued Date 2003URL http://hdl.handle.net/10722/45653Rights Creative Commons: Attribution 3.0 Hong Kong License82      HKMJ Vol 9 No 1 February 2003 SupplementClinical features and risk factors of cognitive impairment after stroke in Hong KongChineseLY Zou1, LSW Li2 & RTF Cheung1. 1Division of Neurology, University Department of Medicine, The University of Hong Kongand 2Department of Medicine, Tung Wah Hospital, Hong KongIntroduction: Stroke is recognized as an important cause of dementia. The goal of the present study is to examinea series of clinical features and risk factors of cognitive impairment after stroke.Method: A standard protocol was applied to 185 consecutive unselected stroke patients within two weeks afteronset of their strokes. Demographic and clinical data were collected. Barthel Index was used to assess the activitiesof daily living and Mini Mental Status Examination (MMSE) was used to assess the cognitive function. The cutoffson MMSE score for cognitive impairment were selected according to Crum’s criteria and the education level.Results: Seventy-seven stroke patients (41.6%) had cognitive impairment or worse. Cognitive impairment wasunrelated to age, gender, marital status, handedness, type of stroke (ischaemic/haemorrhagic), side of the lesion,location of stroke, smoking habit, drinking habit, diabetes mellitus, and hyperlipidaemia. Low education level, lowBarthel Index and hypertension were the independent predictors of cognitive impairment in logistic regressionanalysis (P<0.05).Conclusion: The local incidence of cognitive impairment after stroke is high. Education level, functionalimpairment and hypertension may increase the risk of cognitive impairment after stroke.Research strategies in molecular signaling of neuronal apoptosis in Alzheimer’sdiseaseRaymond Chuen-Chung CHANG, Ka-Chun Suen, Man-Shan Yu, Jacques HugonDepartment of Anatomy, Faculty of Medicine, The University of Hong KongIntroduction: Neuronal loss is a key issue in the pathogenesis of Alzheimer’s disease (AD). It is evident thatneuronal apoptosis is one mode of neurodegeneration. Among all the factors leading to neuronal apoptosis,_-amyloid peptides (A_) are the most important toxin in AD pathogenesis. Therefore, the molecular signalingevents of neuronal apoptosis receive much attention in AD research.Methods: Different cell culture models were employed to prove the involvement of a particular protein kinase inA_ neurotoxicity. To verify the involvement of a protein kinase, both the phosphorylation of the kinase and itssubstrate had to be examined. Having done these experiments, the next step was to elucidate how significance of akinase in A_ neurotoxicity by using molecular biology technique to transfect neurons over-expressing wild-type ornegatively mutated kinase. Furthermore, neurons from knockout and the wild-type mice were used to prove thefindings from genetically manipulated neurons. Apart from these experiments, investigation of whether the kinaseinvolved in real clinical case was another important strategy to show the significance of the kinase in the pathogenesisof AD. Afterwards, it is also essential to show how a particular kinase incorporates into other well-known apoptoticpathways.Results and Conclusion: By using these strategies, we have demonstrated that a novel double-strandedRNA-dependent protein kinase (PKR) is significantly involved in A_-induced neuronal apoptosis. It also playssignificant roles in the pathogenesis of AD.Acknowledgement: The study was supported by Seed Funding Grant 2001-2002 to RCCC, and RGC grant(HKU 7305/00M) to JH.NUS-21NUS-22

Research strategies in molecular signaling of neuronal apoptosis in Alzheimer's disease

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Research strategies in molecular signaling of neuronal apoptosis in Alzheimer's disease

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