摘要
The Alzheimer’s disease (AD) is the most widespread chronic, insidious neurodegenerative disease causing dementia in elderly and leading to a massive burden on AD individuals, their families, and on social and health care systems. Its diagnosis is subjective, definite AD can only be diagnosed after pathological brain specimens are examined by either biopsy or autopsy, and it covers 50%-70% of all dementia cases. It is estimated that, by 2050, the number of people aged 80 years or older will approach 370 million worldwide and that 50 percent of those aged 85 years or older will be afflicted with AD. Causes of the disease are multifactorial;where genetics and environmental risk factors work in harmony to cause the disease. Neuropathological features of AD depend on finding of extracellular deposits of β-amyloid peptides (Aβ) that lead to senile plaque formation and intracellular neurofibrillary tangles of hyperphosphory lated tau. However, increasing evidence has suggested that inflammation may play a critical role in AD pathogenesis as well. In the era of genome and sophisticated technology, AD early diagnosis still indecisive and valid biomarkers for AD to be used in routine clinical practice have met with dissatisfaction. Indeed, the relatively unchanged levels of plasma β-amyloid in AD, and a lack of analytical sensitivity for assays for the axonal damage marker have increased the effort to find an alternative ultra-sensitive assay for pathological markers in peripheral blood. We believe that early presymptomalogical practical inexpensive strategies, for characterizing a potential surrogate marker in blood and CSF for AD is warranted, are of interest because they: 1) confirm diagnosis;2) enable epidemiological screening;3) identify distinct groups of patients (predictive testing);4) monitor progression and response to treatment and aid in design/implementation of optimal therapeutic regimens;5) further the study of the brain-behaviour relationship underlying neurodegeneration.
The Alzheimer’s disease (AD) is the most widespread chronic, insidious neurodegenerative disease causing dementia in elderly and leading to a massive burden on AD individuals, their families, and on social and health care systems. Its diagnosis is subjective, definite AD can only be diagnosed after pathological brain specimens are examined by either biopsy or autopsy, and it covers 50%-70% of all dementia cases. It is estimated that, by 2050, the number of people aged 80 years or older will approach 370 million worldwide and that 50 percent of those aged 85 years or older will be afflicted with AD. Causes of the disease are multifactorial;where genetics and environmental risk factors work in harmony to cause the disease. Neuropathological features of AD depend on finding of extracellular deposits of β-amyloid peptides (Aβ) that lead to senile plaque formation and intracellular neurofibrillary tangles of hyperphosphory lated tau. However, increasing evidence has suggested that inflammation may play a critical role in AD pathogenesis as well. In the era of genome and sophisticated technology, AD early diagnosis still indecisive and valid biomarkers for AD to be used in routine clinical practice have met with dissatisfaction. Indeed, the relatively unchanged levels of plasma β-amyloid in AD, and a lack of analytical sensitivity for assays for the axonal damage marker have increased the effort to find an alternative ultra-sensitive assay for pathological markers in peripheral blood. We believe that early presymptomalogical practical inexpensive strategies, for characterizing a potential surrogate marker in blood and CSF for AD is warranted, are of interest because they: 1) confirm diagnosis;2) enable epidemiological screening;3) identify distinct groups of patients (predictive testing);4) monitor progression and response to treatment and aid in design/implementation of optimal therapeutic regimens;5) further the study of the brain-behaviour relationship underlying neurodegeneration.
