The majority cases of Alzheimer's disease (AD) are sporadic late-onset form not being linked to APP and PS1 gene mutations. It is believed that the environmental risk factors play an important role in the onset and development of AD. Patients suffering from cerebral ischemia and stroke in which hypoxic conditions occur are much more susceptible to AD. Increasing evidence suggests that hypoxia facilitates the pathogenesis of AD through accelerating the accumulation of Abeta, increasing the hyperphosphorylation of tau, impairing the normal functions of blood-brain barrier, and promoting the degeneration of neurons. Further investigations into the relationship between hypoxia and AD may open the avenue for effective preservation and pharmacological treatments of this neurodegenerative disease.
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