老年癡呆症的病患者，在美國超過三百萬人，全世界則有一仟七百萬到二仟萬人之多，人口統計資料預測老年癡呆症患者，正在增加，為了照顧這些病人，美國社會每年要花費1,000億美元。台灣方面，65歲的人當中，患得老年癡呆症的人數是5-10%，85歲的人群增加到25%，90歲的人群就高達半數（50%），患者本身痛苦憂傷，對於患者家人╱庭，在親情與錢財上的負擔也是相當大的打擊與折磨、老年癡呆症患者的腦部上的主要病理病徵（特點）是腦神經組織內出現大量的神經原纖維纏結（Neurofibrillary tangles，由含有TAU蛋白質的paried helical filaments組成）。也出現大量的神經炎斑（老年斑，Neuritic plague /amyloid，含有Amyloidβ蛋白質的Amyloid fibers組成）。醫生可以經由綜合病者在臨床上的病情資料與腦部切片（biopsy）或解剖（Autopsy）病理上的顯微鏡檢視結果，可以很準確地診斷老年癡呆症。至於利用活體皮膚（Skin Biopsy）組織切片檢視以及利用腦脊髓液（Cerebrospinal fluid）的ELISA對於抗體（Antibody） 的測試反應結果，只能當作對於老年癡呆症，診斷上的補助參考。老年癡呆症的致病原因目前還不清楚，或許與患者的遺傳基因組合，慢性長期的病毒感染，以及諸如腦部內外傷，唐氏病症（Down Syndrome），還有帶有Apolipoprtoin E4基因60歲以後晚年發病的等等致病因子有密切關連。唐氏病患者，腦部出現老年癡呆症的病理病徵，通常要比一般老年癡呆症提早20年左右，主要原因是唐氏病患具有三個第21號染色體（Trisomy 21），就因為多了這個額外的染色體，也就是Amyliodβ-precursor蛋白質基因的所在地，就大幅增加患老年癡呆症的危機，這項遺傳基因與老年癡呆症有關連的觀察，提供了人造老年癡呆症老鼠（Transgenic mice of Alzheimer's Disease）基因移換的合理的基礎，目前用來治療老年癡呆症的藥物Tacrine或Aricept雖然對某些病患者有效（非痊癒），但利用基因轉殖成功的老年癡呆症老鼠，會加速篩選出對老年癡呆症更有效的新藥。

Alzheimer's disease (AD) strikes more than 3 million people in the United States and 17 to 20 million people world-wide, respectively. Demography predicts that the number of AD-affected persons is rising. The cost to American society for taking care of individuals with AD is currently estimated to be close to $100 billion, annually. In Taiwan, 5-10% of people at the age of 65,25% of 85 year-old people, and 50% of 90 year-old people have AD. The emotional and financial hardships to families can be unbearable and the stress impact on individuals with AD is devastating. The major pathological lesions in the brains of AD patients are neurofibrillary tangles (NFT) consisting of paired helical filaments (PHF) and neuritic plaques (NP)/amyloid plaques (AP) containing amyloid β-protein (Aβ). A confident diagnosis of AD can be made by a combination of clinical evaluation of dementia status and histopathological examination of brain biopsy/autopsy sections. Skin biopsy testing and enzyme linked immunosorbent assay (ELISA) tests of CSF with corresponding antibodies to Aβ and PHF can only be used as a complementary aid for AD diagnosis. The causesof AD are unknown, but may be related to susceptible genetic-make up, slow viral infection, and other risk factors such as brain injury/trauma, Down Syndrome (DS) and with the presence of apolipoprotein E4 gene in those individuals over 60. Since DS (trisomy 21) individuals have an extra copy of the amyloid β-precursor protein gene, the risk for getting AD increases substantially, as evidenced by the appearance/onset of the major AD-pathological hallmark lesions such as NFT and AP in DS approximately 20 years earlier than in those individuals with AD alone. This observa-tion has provided the rationale for generating the transgenic mouse models of AD. The treat-ment of AD with drugs such as Tacrine or Aricept represents a certain degree of success (not a cure), but the transgenic AD mice may facilitate the development and screening of more effec-tive new drugs for AD.