Tuyển tập báo cáo các nghiên cứu khoa học quốc tế ngành hóa học dành cho các bạn yêu hóa học tham khảo đề tài: Neuroinflammation in Alzheimer’s disease wanes with age | Hoozemans et al. Journal of Neuroinflammation 2011 8 171 http content 8 1 171 JJOURNAL1 OF. NEUROINFLAMMATION RESEARCH Open Access Neuroinflammation in Alzheimer s disease wanes with age 1 1 1 2 3 Jeroen JM Hoozemans Annemieke JM Rozemuller Elise S van Haastert Piet Eikelenboom and Willem A van Gool3 Abstract Background Inflammation is a prominent feature in Alzheimer s disease AD . It has been proposed that aging has an effect on the function of inflammation in the brain thereby contributing to the development of age-related diseases like AD. However the age-dependent relationship between inflammation and clinical phenotype of AD has never been investigated. Methods In this study we have analysed features of the neuroinflammatory response in clinically and pathologically confirmed AD and control cases in relation to age range 52-97 years . The mid-temporal cortex of 19 controls and 19 AD cases was assessed for the occurrence of microglia and astrocytes by immunohistochemistry using antibodies directed against CD68 KP1 HLA class II CR3 43 and glial fibrillary acidic protein GFAP . Results By measuring the area density of immunoreactivity we found significantly more microglia and astrocytes in AD cases younger than 80 years compared to older AD patients. In addition the presence of KP1 CR3 43 and GFAP decreases significantly with increasing age in AD. Conclusion Our data suggest that the association between neuroinflammation and AD is stronger in relatively young patients than in the oldest patients. This age-dependent relationship between inflammation and clinical phenotype of AD has implications for the interpretation of biomarkers and treatment of the disease. Keywords Alzheimer s disease microglia astrocyte aging Background Alzheimer s disease AD is a chronic neurodegenerative disease and is the most common cause of dementia. Two hallmarks of the disease are senile plaques which are mainly composed of extracellular deposits of amyloid
