Advanced Glycation End Products in Alzheimer's Disease and Other Neurodegenerative Diseases

Autor: Nobuyuki Sasaki, Zenji Makita, Yorihide Hayashi, Richard Yanagihara, Naoji Amano, Nobuhiro Fujii, Kayo Tsuzuki, Taku Yoshida, Takao Koike, Ryo Fukatsu, Ralph A. Garruto, Ikuro Wakayama
Rok vydání: 1998
Předmět:
Zdroj: The American Journal of Pathology. 153:1149-1155
ISSN: 0002-9440
DOI: 10.1016/s0002-9440(10)65659-3
Popis: Advanced glycation end products (AGEs) have been implicated in the chronic complications of diabetes mellitus and have been reported to play an important role in the pathogenesis of Alzheimer's disease. In this study, we examined the immunohistochemical localization of AGEs, amyloid beta protein (A beta), apolipoprotein E (ApoE), and tau protein in senile plaques, neurofibrillary tangles (NFTs), and cerebral amyloid angiopathy (CAA) in Alzheimer's disease and other neurodegenerative diseases (progressive supranuclear palsy, Pick's disease, and Guamanian amyotrophic lateral sclerosis/Parkinsonism-dementia complex). In most senile plaques (including diffuse plaques) and CAA from Alzheimer's brains, AGE and ApoE were observed together. However, approximately 5% of plaques were AGE positive but A beta negative, and the vessels without CAA often showed AGE immunoreactivity. In Alzheimer's disease, AGEs were mainly present in intracellular NFTs, whereas ApoE was mainly present in extracellular NFTs. Pick's bodies in Pick's disease and granulovacuolar degeneration in various neurodegenerative diseases were also AGE positive. In non-Alzheimer neurodegenerative diseases, senile plaques and NFTs showed similar findings to those in Alzheimer's disease. These results suggest that AGE may contribute to eventual neuronal dysfunction and death as an important factor in the progression of various neurodegenerative diseases, including Alzheimer's disease.
Databáze: OpenAIRE