Alzheimer’s disease is a debilitating form of dementia which currently affects at least 30 million people worldwide. For many decades, the prevailing hypothesis on the pathogenesis of Alzheimer’s disease has involved the gradual buildup of β-amyloid plaques in the brain. Recent evidence suggests that soluble oligomers assemblies of β-amyloid are neurotoxic and responsible for the synaptic and memory dysfunction. Herein, we review the main researches on the mechanisms through which β-amyloid oligomers exert their toxic action.
Buy this Article