2014-08-012024-05-17https://scholars.lib.ntu.edu.tw/handle/123456789/689236摘要：背景: 近年來失智症生物標記進展提供了在阿茲海默症的早期甚至臨床前診斷的可能性，讓我們在阿茲海默症的早期病理變化剛出現時便開始治療。腦脊髓液中的 Aβ42蛋白濃度的下降與 tau蛋白的上升是目前認為診斷阿茲海默症較為可靠的生物標記。但其血液中的 Aβ42蛋白與 tau蛋白濃度的上升或下降則尚無定論。此外與類澱粉相關之失智症並非只有輕度知能障礙或者阿茲海默症而已，在有些巴金森失智症，路易氏體失智症，進行性失語症額顳葉型失智症和健康老年人身上都有可能存在 。本研究的目的在做為我們之前通過的第一年的計畫完成時間縱向性研究。 研究方法：利用血漿中的生物標記、結構性磁振造影、類澱粉射出斷層造影、去氧氟-18葡萄糖射出斷層造影進行縱貫性演變。我們將使用免疫減磁法來量測血漿中 Aβ40和 Aβ42，以及 tau蛋白濃度。整個三年期間，研究對象包括 30名輕度知能障礙患者，30名早期阿茲海默症，30名巴金森失智症/名路易氏體失智症，30名原發性進行性失語症之額顳葉型失智症和 30名健康老年人。所有受試都接受相同的神經心裡學檢查來評估記憶、注意力、執行功能、視覺空間功能。我們並將在 18個月之後進行如上所述包括神經心理、血漿生化、神經影像與神經心裡學測驗之所有檢查。 預期結果與結論：可得到不同生物標記在各種類澱粉相關之失智症的量化與大腦分佈類型與及隨著時間的演變狀態。 <br> Abstract: Recent advance in biomarkers provides possible early or preclinical diagnosis of Alzheimer’s disease (AD) which implements treating patients at early Alzheimer's pathology. Decreased Aβ42 and increased tau proteins in CSF are considered reliable biomarkers for AD while the issue of plasma tau and amyloid proteins for AD and other dementias remains unsolved. The purpose of this two-year project aims to be an extension (II and III years) for our granted first year project to investigate the longitudinal effect of using plasma biomarkers for AD and other related dementias including Parkinson’s disease dementia (PDD) / Dementia with Lewy’s body (DLB), primary progressive aphasia (APP) subtypes of frontotemporal lobe dementia (FTLD) to explore relation to neuroimaging including amyloid images ie., Pittsburgh compound B positron emission tomography (PiB-PET) and magnetic resonance images. In this 3-year period, we will use immunomagnetic reduction assay to measure amyloid Aβ40, Aβ42 and tau proteins in 30 subjects with MCI, 30 subjects with early AD and 30 controls; and also 30 subjects with APP subtypes of FTLD as well as 30 subjects with PDD / DLB. All subjects will receive 3D MR and DTI studies and received a set of neuropsychological tests assessing memory, executive, attention and visuospatial functions; all subjects with specific consent receive amyloid PiB-PET scans. All subjects receive follow up at an interval of 18 months with a range of +/- one month. All neuroimages will be quantitatively analyzed using softwares such as FSL, Freesurfer and home-made Matlab based programs. The data will be analyzed as a comparison to control subjects. Group specific patterns of the plasma and neuroimaging biomarkers will be established. Correlations between different biomarkers in different group of subjects will be sought. Finally we will use linear regression analyses to explore most potential predictors for each type of dementias.