G.Y. Wen


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 causes of 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 in 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 observation has provided the rationale for generating the transgenic mouse models of AD. The treatment 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 effective new drugs for AD.