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Volumn 76, Issue 4, 2001, Pages 1050-1056

Neurotoxic Aβ peptides increase oxidative stress in vivo through NMDA-receptor and nitric-oxide-synthase mechanisms, and inhibit complex IV activity and induce a mitochondrial permeability transition in vitro

Author keywords

Alzheimer's disease; Beta amyloid; Complex IV; Mitochondrial permeability transition; Neurotoxicity; Oxidative stress

Indexed keywords

AMYLOID BETA PROTEIN; CHLORPROMAZINE; CYCLOSPORIN A; CYTOCHROME C OXIDASE; N METHYL DEXTRO ASPARTIC ACID RECEPTOR; OXYGEN RADICAL; RUTHENIUM RED; AMYLOID BETA PROTEIN (1 28); AMYLOID BETA PROTEIN (25 35); AMYLOID BETA PROTEIN (35 25); AMYLOID BETA PROTEIN[1-40]; AMYLOID BETA-PROTEIN (1-28); AMYLOID BETA-PROTEIN (25-35); AMYLOID BETA-PROTEIN (35-25); CYCLOSPORIN; NITRIC OXIDE SYNTHASE; PEPTIDE FRAGMENT; REACTIVE OXYGEN METABOLITE;

EID: 0034745636     PISSN: 00223042     EISSN: None     Source Type: Journal    
DOI: 10.1046/j.1471-4159.2001.00112.x     Document Type: Article
Times cited : (191)

References (37)
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    • Beta-amyloid stimulation of inducible nitric-oxide synthase in astrocytes is interleukin-1beta- and tumor necrosis factor-alpha (TNFalpha)-dependent, and involves a TNFalpha receptor-associated factor- and NFkappaB-inducing kinase-dependent signaling mechanism
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    • Akama, K.T.1    Van Eldik, L.J.2
  • 3
    • 0029115555 scopus 로고
    • The structure of the presenilin 1 (S182) gene and identification of six novel mutations in early onset AD families
    • (1995) Nature Genet. , vol.11 , pp. 219-222


* 이 정보는 Elsevier사의 SCOPUS DB에서 KISTI가 분석하여 추출한 것입니다.