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0792 Mild cognitive impairment and dementia: Neuropsychiatric symptoms in Thai elderly
$302
Poster Abstracts
Wednesday, November 9, 2005
Selelder, K 2. Cangtz, B ~. 1Hacettepe University Department of
Psychology, Ankara, Turkey; 2Haeettepe University, Department of Neurology, Ankara, Turkey Background: Daily living impaired in dementia and have to be assessed by standardisedinstruments. Functional Activities Questionnaire (FAQ) as a particularly useful method for initial of functional impairment. The FAQ is a brief, informant-based questionnaire that evaluates performance based on ten complex activities. The FAQ was standardized on Turkish adult sample (Selekler, CangOz & Karako% 2004). The goal of tiffs study was to determine whether neuropsychological test scores are correlated with daily living activities measured by FAQ. Method: Four neuropsychological tests (Auditory Verbal Learning Test-AVLT, Visual-Aural Digit Span Test-VADS, Facial Recognition Test, and WAIS Vocabulary Subtest) and FAQ were adnffnistered to 30 patients with mild cogtfftive impairment (MCI) and 30 healthy controls. Patients with MCI were assessed through extensive neurological examinations. They all scored above 27 on Mini Mental State Examination (MMS E) and no self-reported history of cognitive decline or brain damage. The diagnosis of MCI, the criteria used were consistent with the guidelines established by Petersen et al. (1999). Participants were screened for Geriatric Depression Scale (GDS) (Scheik & Yesavage, 1986). Results: Groups (MCI vs. Control) were compared by t-test and correlations between neuropsychological test scores and FAQ scores computed by Pearson Correlation Coefficient. Control group was a better performance on neuropsychological tests than patients with MCL We have got low correlation between two variables. Conclusion: The results are discussed within the functional activities in MCL MCI group and normal control group showed a similar performance in FAQ. There was not significant correlation between FAQ scores and other neuropsychological test scores in MCI. 0792 Mild cognitive hilpaixulent and dementia: Neuropsyetlialrie symptoms in Thai elderly Senanarong, V ~, Poungvarin, N a, Harnphadungkit, K ~, Wannasaeng, S ~, Jamjumrus, pa, Sujiraschato, U a, Sukhatungka, K ~, Sriboonroung, A a, Udompunthurak, S a, Doody, RS 2, Cunmffngs JL 3.
~Faculty of Medicine Siriraj Hospital Mahidol University, Bangkok, Thailand," 2Alzheimer's Disease Center, Baylor College of Medicine, Houston, Texas, USA; SDepartrnent of Neurology, David Geffen School of Medicine at UCL4, L4, USA Objectives: We investigated the occurrence of neuropsychiatric symptoms in Thai community dwelling elderly. Subjects and Methods: We surveyed conmmtffty dwelling Thai elderly, living in Bangkok, aged 60 and over in 2004 Dementia was diagnosed by DSM IV criteria. MCI was diagnosed by clinical criteria. Neuropsychiatric Inventory (NPI-Q) was used to evaluate neuropsychiatric symptoms. Thai Mental State Examination (TMSE) was utilized at baseline. Results: Of 887 individuals, 172 (10.39%) had MCI and 45 (5.07%) had dementia. The mean ages were 68.72 (6.25) for a coguitively intact group, 71.46 (16.90) for a MCI group, and 77 (8.42) for a dementia group (13 < 0.000). The mean TMSE of those with intact cognition, with MCI, and with dementia was 27.01 (2.31), 23.57(13.77), and 18.80 (16.44) respectively (]3 < 0.000). The prevalence of neuropsychiatric symptoms in those with intact cogtfftion, MCI, and dementia was 50.3%, 63?/;, and 80?/; respectively (13 < 0.000). Post hoc analysis showed significant difference in the prevalence of neuropsychiatric symptoms between a cognitively intact group and a dementia group, and between a cognitively intact group and a MCI group. No difference between the dementia group and the MCI group was found. The mean numbers of neuropsychiatric symptoms were 1.17 (11.68), 1.80 (1.86), and 2.60 (2.52) in those with intact cogtfftion, MCI, and
dementia respectively (i3 < 0.000). The mean NPI-Q severity scores in those with intact cognition, MCI, and dementia were 1.51 (12.76), 2.73 (3.78), and 4.29 (5.39) correspondingly (]3 < 0.000). Conclusion: The presence of neuropsyclffatric symptoms in older individuals with cognitive decline should alert clinicians to further evaluate for MCI or dementia. 0793 Neuropathology in the $305S tau gene mutation Song YJC x, Halliday G M a, Creasey H 2, Morris JGL 3, Brooks WS a, Kril j2. ~University of New South Wales, Prince of IVales Medical
Research Institute, Sydney, Australia; 2University of Sydney, Centrefor Education and Research on Ageing, Sydney, Australia; 3Westmead Hospital Neurology, Sydney, Australia Background: We have previously reported a novel silent ($305S) mutation in the tau gene in two siblings and a history of presenile dementia in their mother 1. One sibling (III-15) had pathologicallyproven progressive supranuclear palsy (PSP). The second affected individual (III-14) recently died at age 63 after a dementing illness lasting seven years and the family consented to an autopsy for research purposes. Tiffs study aimed to investigate the neuropathology of tiffs second fanffly member. Methods: The right half of the brain was frozen and the other half fixed in formalin. Western blot analysis of tau protein using tau-5 antibody and in situ tissue immunohistochernistry for phosphorylated tau using AT8 antibody was performed. Results: III-14 had frontal dementia and eventual PSP-like parkinsonism. Brain atrophy was similar to that of her sister (nffld) and over expression o f soluble 4-repeat tau is similar to that observed in other cases with exon 10 intronic mutations in the tau gene. Hyperphosphorylation of tau occurred in remaining neurons throughout the brain, although silver-positive inclusions and extensive basal ganglia cell loss were absent. Both the clinical and pathological features are incompatible with a diagnosis of PSP. Conclusion: 1) The clinical phenotype, disease severity and rapidity differed between members of this family. 2) The pattern and phosphorylation state of tau deposition in the brain differed between members of this family. 3) The degree of neuronal cell loss differed between members of tiffs family. These differences strongly suggest other factors modify the genetic expression of this disease. 0794 Apoptosis induced neuronal death in Alzheimer's disease
Subhani, F. Student, Quetta, Pakistan Objeel: Apoptosis induced neuronal death in Alzheimer's disease. Purpose: Possible therapeutic regimes and mechanism to prevent apoptosis in Alzheimer's disease. Method: It is a review paper. Papers are studied under topics of. Alzheimer's apoptosis and Alzheimer's neuronal death. Results: Dysfunction of endoplasmic reticuhim by caspase 4 and modulate the Ca signaling. Humanin inlffbit the neuronal death in FAD but not in all cases. Loss o f the nonadrenergic Neurons in the locus ceruleus wlffch send axons to the brain regions suffering neuronal apoptosis. Increase_expression of nitric, oxide synthase 3 gene lead to increase p53, p21, Wal (not found), Bax and CD95 to mediated cell death by mitochondrial dysfunction. The protein levels of caspase-3, 8, and 9, D N A fragmentation factor 45, were decreased, whereas those of apoptosis repressor with caspase recruitment domain and Receptor interacting protein like interacting C L A R P kinase increased in AD, cytochrome c unchanged. Cysteine proteases of the caspase family are activated in neurons undergoing apoptosis by blocking the K + and N a + channels, enhanced by nitric oxide (NO). The decrease of CD7 and CD8 while increase of CD4, CD25 and CD28 were observed. Estrogen sigtffficantly increases the expression of the antiapoptotic protein Bcl-xL and p53 in cultured hippocampal neurons.
Poster Abstracts
Wednesday, November 9, 2005
Selelder, K 2. Cangtz, B ~. 1Hacettepe University Department of
Psychology, Ankara, Turkey; 2Haeettepe University, Department of Neurology, Ankara, Turkey Background: Daily living impaired in dementia and have to be assessed by standardisedinstruments. Functional Activities Questionnaire (FAQ) as a particularly useful method for initial of functional impairment. The FAQ is a brief, informant-based questionnaire that evaluates performance based on ten complex activities. The FAQ was standardized on Turkish adult sample (Selekler, CangOz & Karako% 2004). The goal of tiffs study was to determine whether neuropsychological test scores are correlated with daily living activities measured by FAQ. Method: Four neuropsychological tests (Auditory Verbal Learning Test-AVLT, Visual-Aural Digit Span Test-VADS, Facial Recognition Test, and WAIS Vocabulary Subtest) and FAQ were adnffnistered to 30 patients with mild cogtfftive impairment (MCI) and 30 healthy controls. Patients with MCI were assessed through extensive neurological examinations. They all scored above 27 on Mini Mental State Examination (MMS E) and no self-reported history of cognitive decline or brain damage. The diagnosis of MCI, the criteria used were consistent with the guidelines established by Petersen et al. (1999). Participants were screened for Geriatric Depression Scale (GDS) (Scheik & Yesavage, 1986). Results: Groups (MCI vs. Control) were compared by t-test and correlations between neuropsychological test scores and FAQ scores computed by Pearson Correlation Coefficient. Control group was a better performance on neuropsychological tests than patients with MCL We have got low correlation between two variables. Conclusion: The results are discussed within the functional activities in MCL MCI group and normal control group showed a similar performance in FAQ. There was not significant correlation between FAQ scores and other neuropsychological test scores in MCI. 0792 Mild cognitive hilpaixulent and dementia: Neuropsyetlialrie symptoms in Thai elderly Senanarong, V ~, Poungvarin, N a, Harnphadungkit, K ~, Wannasaeng, S ~, Jamjumrus, pa, Sujiraschato, U a, Sukhatungka, K ~, Sriboonroung, A a, Udompunthurak, S a, Doody, RS 2, Cunmffngs JL 3.
~Faculty of Medicine Siriraj Hospital Mahidol University, Bangkok, Thailand," 2Alzheimer's Disease Center, Baylor College of Medicine, Houston, Texas, USA; SDepartrnent of Neurology, David Geffen School of Medicine at UCL4, L4, USA Objectives: We investigated the occurrence of neuropsychiatric symptoms in Thai community dwelling elderly. Subjects and Methods: We surveyed conmmtffty dwelling Thai elderly, living in Bangkok, aged 60 and over in 2004 Dementia was diagnosed by DSM IV criteria. MCI was diagnosed by clinical criteria. Neuropsychiatric Inventory (NPI-Q) was used to evaluate neuropsychiatric symptoms. Thai Mental State Examination (TMSE) was utilized at baseline. Results: Of 887 individuals, 172 (10.39%) had MCI and 45 (5.07%) had dementia. The mean ages were 68.72 (6.25) for a coguitively intact group, 71.46 (16.90) for a MCI group, and 77 (8.42) for a dementia group (13 < 0.000). The mean TMSE of those with intact cognition, with MCI, and with dementia was 27.01 (2.31), 23.57(13.77), and 18.80 (16.44) respectively (]3 < 0.000). The prevalence of neuropsychiatric symptoms in those with intact cogtfftion, MCI, and dementia was 50.3%, 63?/;, and 80?/; respectively (13 < 0.000). Post hoc analysis showed significant difference in the prevalence of neuropsychiatric symptoms between a cognitively intact group and a dementia group, and between a cognitively intact group and a MCI group. No difference between the dementia group and the MCI group was found. The mean numbers of neuropsychiatric symptoms were 1.17 (11.68), 1.80 (1.86), and 2.60 (2.52) in those with intact cogtfftion, MCI, and
dementia respectively (i3 < 0.000). The mean NPI-Q severity scores in those with intact cognition, MCI, and dementia were 1.51 (12.76), 2.73 (3.78), and 4.29 (5.39) correspondingly (]3 < 0.000). Conclusion: The presence of neuropsyclffatric symptoms in older individuals with cognitive decline should alert clinicians to further evaluate for MCI or dementia. 0793 Neuropathology in the $305S tau gene mutation Song YJC x, Halliday G M a, Creasey H 2, Morris JGL 3, Brooks WS a, Kril j2. ~University of New South Wales, Prince of IVales Medical
Research Institute, Sydney, Australia; 2University of Sydney, Centrefor Education and Research on Ageing, Sydney, Australia; 3Westmead Hospital Neurology, Sydney, Australia Background: We have previously reported a novel silent ($305S) mutation in the tau gene in two siblings and a history of presenile dementia in their mother 1. One sibling (III-15) had pathologicallyproven progressive supranuclear palsy (PSP). The second affected individual (III-14) recently died at age 63 after a dementing illness lasting seven years and the family consented to an autopsy for research purposes. Tiffs study aimed to investigate the neuropathology of tiffs second fanffly member. Methods: The right half of the brain was frozen and the other half fixed in formalin. Western blot analysis of tau protein using tau-5 antibody and in situ tissue immunohistochernistry for phosphorylated tau using AT8 antibody was performed. Results: III-14 had frontal dementia and eventual PSP-like parkinsonism. Brain atrophy was similar to that of her sister (nffld) and over expression o f soluble 4-repeat tau is similar to that observed in other cases with exon 10 intronic mutations in the tau gene. Hyperphosphorylation of tau occurred in remaining neurons throughout the brain, although silver-positive inclusions and extensive basal ganglia cell loss were absent. Both the clinical and pathological features are incompatible with a diagnosis of PSP. Conclusion: 1) The clinical phenotype, disease severity and rapidity differed between members of this family. 2) The pattern and phosphorylation state of tau deposition in the brain differed between members of this family. 3) The degree of neuronal cell loss differed between members of tiffs family. These differences strongly suggest other factors modify the genetic expression of this disease. 0794 Apoptosis induced neuronal death in Alzheimer's disease
Subhani, F. Student, Quetta, Pakistan Objeel: Apoptosis induced neuronal death in Alzheimer's disease. Purpose: Possible therapeutic regimes and mechanism to prevent apoptosis in Alzheimer's disease. Method: It is a review paper. Papers are studied under topics of. Alzheimer's apoptosis and Alzheimer's neuronal death. Results: Dysfunction of endoplasmic reticuhim by caspase 4 and modulate the Ca signaling. Humanin inlffbit the neuronal death in FAD but not in all cases. Loss o f the nonadrenergic Neurons in the locus ceruleus wlffch send axons to the brain regions suffering neuronal apoptosis. Increase_expression of nitric, oxide synthase 3 gene lead to increase p53, p21, Wal (not found), Bax and CD95 to mediated cell death by mitochondrial dysfunction. The protein levels of caspase-3, 8, and 9, D N A fragmentation factor 45, were decreased, whereas those of apoptosis repressor with caspase recruitment domain and Receptor interacting protein like interacting C L A R P kinase increased in AD, cytochrome c unchanged. Cysteine proteases of the caspase family are activated in neurons undergoing apoptosis by blocking the K + and N a + channels, enhanced by nitric oxide (NO). The decrease of CD7 and CD8 while increase of CD4, CD25 and CD28 were observed. Estrogen sigtffficantly increases the expression of the antiapoptotic protein Bcl-xL and p53 in cultured hippocampal neurons.