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Titolo:
Active glycation in neurofibrillary pathology of Alzheimer disease: N-epsilon-(carboxymethyl) lysine and hexitol-lysine
Autore:
Castellani, RJ; Harris, PLR; Sayre, LM; Fujii, J; Taniguchi, N; Vitek, MP; Founds, H; Atwood, CS; Perry, G; Smith, MA;
Indirizzi:
Case Western Reserve Univ, Inst Pathol, Cleveland, OH 44106 USA Case Western Reserve Univ Cleveland OH USA 44106 Cleveland, OH 44106 USA Case Western Reserve Univ, Dept Chem, Cleveland, OH 44106 USA Case WesternReserve Univ Cleveland OH USA 44106 Cleveland, OH 44106 USA Osaka Univ, Sch Med, Dept Biochem, Osaka, Japan Osaka Univ Osaka JapanOsaka Univ, Sch Med, Dept Biochem, Osaka, Japan Duke Univ, Med Ctr, Div Neurol, Durham, NC 27710 USA Duke Univ Durham NC USA 27710 , Med Ctr, Div Neurol, Durham, NC 27710 USA Alteon Inc, Ramsey, NJ 07446 USA Alteon Inc Ramsey NJ USA 07446Alteon Inc, Ramsey, NJ 07446 USA
Titolo Testata:
FREE RADICAL BIOLOGY AND MEDICINE
fascicolo: 2, volume: 31, anno: 2001,
pagine: 175 - 180
SICI:
0891-5849(20010715)31:2<175:AGINPO>2.0.ZU;2-W
Fonte:
ISI
Lingua:
ENG
Soggetto:
PAIRED HELICAL FILAMENTS; INDUCED DIABETIC RATS; END-PRODUCTS; MAILLARD REACTION; LIPID-PEROXIDATION; AMADORI PRODUCT; GLYCOXIDATION; PROTEINS; ACCUMULATION; STRESS;
Keywords:
advanced glycation end products; Alzheimer disease; N-epsilon-(carboxymethyl) lysine; hexitol-lysine; oxidative stress; free radicals;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
33
Recensione:
Indirizzi per estratti:
Indirizzo: Perry, G Case Western Reserve Univ, Inst Pathol, 2085 Adelbert Rd, Cleveland, OH 44106 USA Case Western Reserve Univ 2085 Adelbert Rd Cleveland OH USA 44106
Citazione:
R.J. Castellani et al., "Active glycation in neurofibrillary pathology of Alzheimer disease: N-epsilon-(carboxymethyl) lysine and hexitol-lysine", FREE RAD B, 31(2), 2001, pp. 175-180

Abstract

Advanced glycation end products are a diverse class of posttranslational modifications, stemming from reactive aldehyde reactions, that have been implicated in the pathogenesis of a number of degenerative diseases. Because advanced glycation end products are accelerated by, and result in formation of, oxygen-derived free radicals, they represent an important component of the oxidative stress hypothesis of Alzheimer disease (AD). In this study, we used in situ techniques to assess N-epsilon-(Carboxymethyl)lysine (CML), the predominant advanced glycation end product that accumulates in vivo, along with its glycation-specific precursor hexitol-lysine, in patients with AD as well as in young and aged-matched control cases. Both CML and hexitol-lysine were increased in neurons, especially those containing intracellular neurofibrillary pathology in cases of AD. The increase in hexitol-lysine and CML in AD suggests that glycation is an early event in disease pathogenesis. In addition, because CML can result from either lipid peroxidation oradvanced glycation, while hexitol-lysine is solely a product of glycation,this study, together with studies demonstrating the presence of 4-hydroxy-2-nonenal adducts and pentosidine, provides evidence of two distinct oxidative processes acting in concert in AD neuropathology. Our findings support the notion that aldehyde-mediated modifications, together with oxyradical-mediated modifications, are critical pathogenic factors in AD. (C) 2001 Elsevier Science Inc.

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Documento generato il 25/09/20 alle ore 07:06:50