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Advanced glycation end products in Alzheimer's disease and other neurodegenerative diseases.
Am J Pathol 1998; 153(4):1149-55AJ

Abstract

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.

Authors+Show Affiliations

Department of Neuropsychiatry, Sapporo Medical University, Japan.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

9777946

Citation

Sasaki, N, et al. "Advanced Glycation End Products in Alzheimer's Disease and Other Neurodegenerative Diseases." The American Journal of Pathology, vol. 153, no. 4, 1998, pp. 1149-55.
Sasaki N, Fukatsu R, Tsuzuki K, et al. Advanced glycation end products in Alzheimer's disease and other neurodegenerative diseases. Am J Pathol. 1998;153(4):1149-55.
Sasaki, N., Fukatsu, R., Tsuzuki, K., Hayashi, Y., Yoshida, T., Fujii, N., ... Makita, Z. (1998). Advanced glycation end products in Alzheimer's disease and other neurodegenerative diseases. The American Journal of Pathology, 153(4), pp. 1149-55.
Sasaki N, et al. Advanced Glycation End Products in Alzheimer's Disease and Other Neurodegenerative Diseases. Am J Pathol. 1998;153(4):1149-55. PubMed PMID: 9777946.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Advanced glycation end products in Alzheimer's disease and other neurodegenerative diseases. AU - Sasaki,N, AU - Fukatsu,R, AU - Tsuzuki,K, AU - Hayashi,Y, AU - Yoshida,T, AU - Fujii,N, AU - Koike,T, AU - Wakayama,I, AU - Yanagihara,R, AU - Garruto,R, AU - Amano,N, AU - Makita,Z, PY - 1998/10/20/pubmed PY - 1998/10/20/medline PY - 1998/10/20/entrez SP - 1149 EP - 55 JF - The American journal of pathology JO - Am. J. Pathol. VL - 153 IS - 4 N2 - 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. SN - 0002-9440 UR - https://www.unboundmedicine.com/medline/citation/9777946/Advanced_glycation_end_products_in_Alzheimer's_disease_and_other_neurodegenerative_diseases_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0002-9440(10)65659-3 DB - PRIME DP - Unbound Medicine ER -