Idioma:

Sub-lethal levels of amyloid β-peptide oligomers decrease non-transferrin-bound iron uptake and do not potentiate iron toxicity in primary hippocampal neurons

SanMartín, C. D. ; Paula-Lima, A. C. ; Hidalgo, C. ; Núñez, M. T.

Biometals, 2012-08, Vol.25 (4), p.805-813 [Periódico revisado por pares]

Dordrecht: Springer Netherlands

Texto completo disponível

Citações Citado por

Enviar para

Título:
Sub-lethal levels of amyloid β-peptide oligomers decrease non-transferrin-bound iron uptake and do not potentiate iron toxicity in primary hippocampal neurons
Autor: SanMartín, C. D. ; Paula-Lima, A. C. ; Hidalgo, C. ; Núñez, M. T.
Assuntos: Amyloid beta-Peptides - pharmacology ; Animals ; Biochemistry ; Biological Transport - drug effects ; Biomedical and Life Sciences ; Cation Transport Proteins - genetics ; Cation Transport Proteins - metabolism ; Cell Biology ; Cell Survival - drug effects ; Cell Survival - genetics ; Cells, Cultured ; Female ; Hippocampus - cytology ; Iron - metabolism ; Life Sciences ; Medicine/Public Health ; Microbiology ; Neurons - drug effects ; Neurons - metabolism ; Pharmacology/Toxicology ; Plant Physiology ; Pregnancy ; Rats ; Rats, Sprague-Dawley ; Reverse Transcriptase Polymerase Chain Reaction
É parte de: Biometals, 2012-08, Vol.25 (4), p.805-813
Notas: ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
Descrição: Two major lesions are pathological hallmarks in Alzheimer’s disease (AD): the presence of neurofibrillary tangles formed by intracellular aggregates of the hyperphosphorylated form of the cytoskeletal tau protein, and of senile plaques composed of extracellular aggregates of amyloid beta (Aβ) peptide. Current hypotheses regard soluble amyloid beta oligomers (AβOs) as pathological causative agents in AD. These aggregates cause significant calcium deregulation and mediate neurotoxicity by disrupting synaptic activity. Additionally, the presence of high concentrations of metal ions such as copper, zinc, aluminum and iron in neurofibrillary tangles and senile plaques, plus the fact that they accelerate the rate of formation of Aβ fibrils and AβOs in vitro, suggests that accumulation of these metals in the brain is relevant to AD pathology. A common cellular response to AβOs and transition metals such as copper and iron is the generation of oxidative stress, with the ensuing damage to cellular components. Using hippocampal neurons in primary culture, we report here the effects of treatment with AβOs on the (+)IRE and (−)IRE mRNA levels of the divalent metal transporter DMT1. We found that non-lethal AβOs concentrations decreased DMT1 (−)IRE without affecting DMT1 (+)IRE mRNA levels, and inhibited non-transferrin bound iron uptake. In addition, since both iron and AβOs induce oxidative damage, we studied whether their neurotoxic effects are synergistic. In the range of concentrations and times used in this study, AβOs did not potentiate iron-induced cell death while iron chelation did not decrease AβOs-induced cell death. The lack of synergism between iron and AβOs suggests that these two neurotoxic agents converge in a common target, which initiates signaling processes that promote neurodegeneration.
Editor: Dordrecht: Springer Netherlands
Idioma: Inglês;Holandês

Links

View this record in MEDLINE/PubMed

Voltar para lista de resultados

Realização: Logos de Redes Sociais:

Sub-lethal levels of amyloid β-peptide oligomers decrease non-transferrin-bound iron uptake and do not potentiate iron toxicity in primary hippocampal neurons

SanMartín, C. D. ; Paula-Lima, A. C. ; Hidalgo, C. ; Núñez, M. T.

Dordrecht: Springer Netherlands

Buscando em bases de dados remotas. Favor aguardar.