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Titolo:
AGES in brain ageing: AGE-inhibitors as neuroprotective and anti-dementia drugs?
Autore:
Dukic-Stefanovic, S; Schinzel, R; Riederer, P; Munch, G;
Indirizzi:
Univ Leipzig, IZKF Neurosci Grp, D-04103 Leipzig, Germany Univ Leipzig Leipzig Germany D-04103 rosci Grp, D-04103 Leipzig, Germany Univ Wurzburg, Bioctr, D-97074 Wurzburg, Germany Univ Wurzburg Wurzburg Germany D-97074 Bioctr, D-97074 Wurzburg, Germany Univ Wurzburg, Dept Psychiat, D-97080 Wurzburg, Germany Univ Wurzburg Wurzburg Germany D-97080 ychiat, D-97080 Wurzburg, Germany
Titolo Testata:
BIOGERONTOLOGY
fascicolo: 1, volume: 2, anno: 2001,
pagine: 19 - 34
SICI:
1389-5729(2001)2:1<19:AIBAAA>2.0.ZU;2-U
Fonte:
ISI
Lingua:
ENG
Soggetto:
GLYCATION END-PRODUCTS; PAIRED HELICAL FILAMENTS; ENDOTHELIAL GROWTH-FACTOR; ALZHEIMERS-DISEASE BRAIN; MONOCYTIC THP-1 CELLS; PROTEIN-CROSS-LINKING; NECROSIS-FACTOR-ALPHA; NF-KAPPA-B; MAILLARD-REACTION; OXIDATIVE STRESS;
Keywords:
advanced glycation endproducts; Alzheimer's disease; ss-amyloid; inflammation; neurofibrillary tangles;
Tipo documento:
Review
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
83
Recensione:
Indirizzi per estratti:
Indirizzo: Munch, G Univ Leipzig, IZKF Neurosci Grp, D-04103 Leipzig, Germany Univ Leipzig Leipzig Germany D-04103 , D-04103 Leipzig, Germany
Citazione:
S. Dukic-Stefanovic et al., "AGES in brain ageing: AGE-inhibitors as neuroprotective and anti-dementia drugs?", BIOGERONTOL, 2(1), 2001, pp. 19-34

Abstract

In Alzheimer's disease, age-related cellular changes such as compromised energy production and increased radical formation are worsened by the presence of AGEs as additional, AD specific stress factors. Intracellular AGEs (most likely derived from methylglyoxal) crosslink cytoskeletal proteins and render them insoluble. These aggregates inhibit cellular functions including transport processes and contribute to neuronal dysfunction acid death. Extracellular AGEs, which accumulate in ageing tissue (but most prominently on long-lived protein deposits like the senile plaques) exert chronic oxidative stress on neurons. In addition, they activate glial cells to produce free radicals (superoxide and NO) and neurotoxic cytokines such as TNF-alpha. Drugs, which inhibit the formation of AGEs by specific chemical mechanisms(AGE-inhibitors), including aminoguanidine, carnosine, tenilsetam. OPB-9195 and pyridoxamine, attenuate the development of (AGE-mediated) diabetic complications. Assuming that carbonyl stress' contributes significantly to the progression of Alzheimer's disease, AGE-inhibitors might also become interesting novel therapeutic drugs for treatment of AD.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 21/09/20 alle ore 15:39:11