作者: Chris Peers , Mark L. Dallas , Hannah E. Boycott , Jason L. Scragg , Hugh A. Pearson
DOI: 10.1111/J.1749-6632.2009.05026.X
关键词: Amyloid beta 、 Homeostasis 、 Cell type 、 Endocrinology 、 Amyloid precursor protein secretase 、 Hypoxia (medical) 、 Extracellular 、 Internal medicine 、 Neuroscience 、 Biology 、 Neurodegeneration 、 In vitro
摘要: Periods of chronic hypoxia, which can arise from numerous cardiorespiratory disorders, predispose individuals to the development dementias, particularly Alzheimer's disease (AD). AD is characterized in part by increased production amyloid beta peptide (Abeta), forms extracellular plaques be identified post mortem. Numerous studies have now shown that even vitro, increase Abeta different cell types. Evidence has been produced indicate hypoxia alters both expression precursor, APP, and also secretase enzymes, cleave APP. Other implicate reduced degradation as a possible means increases levels. Such variability may attributable cell-specific responses hypoxia. Further evidence indicates some, but not all cellular adaptations (including alteration Ca(2+) homeostasis) require formation. However, other aspects hypoxic remodeling function appear occur independently this process. The molecular contribute our understanding clinical association incidence AD. it remains determined whether inhibition one or more effects benefit arresting neurodegenerative disease.