Plaque-induced neurite abnormalities: Implications for disruption of neural networks in Alzheimer’s disease
AUTOR(ES)
Knowles, Roger B.
FONTE
The National Academy of Sciences
RESUMO
The brains of Alzheimer’s disease patients contain extracellular Aβ amyloid deposits (senile plaques). Although genetic evidence causally links Aβ deposition to the disease, the mechanism by which Aβ disrupts cortical function is unknown. Using triple immunofluorescent confocal microscopy and three-dimensional reconstructions, we found that neuronal processes that cross through an Aβ deposit are likely to have a radically changed morphology. We modeled the electrophysiological effect of this changed morphology and found a predicted delay of several milliseconds over an average plaque. We propose that this type of delay, played out among thousands of plaques throughout neocortical areas, disrupts the precise temporal firing patterns of action potentials, contributing directly to neural system failure and dementia.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=21854Documentos Relacionados
- Plaque-independent disruption of neural circuits in Alzheimer’s disease mouse models
- Effect of Bulgarian propolis on the oral microflora in adolescents with plaque-induced gingivitis
- Involvement of oxidative stress-induced abnormalities in ceramide and cholesterol metabolism in brain aging and Alzheimer's disease
- Referral patterns and diagnosis in presenile Alzheimer's disease: implications for general practice.
- Interactions of laminin with the amyloid ß peptide: Implications for Alzheimer's disease