抄録
Increasing evidence suggests that dyshomeostasis of trace elements are implicated in the pathogenesis of various neurodegenerative diseases such as Alzheimer’s disease, prion diseases, and dementia with Lewy bodies. These diseases share similarity in the formation ofβ-sheet containing amyloid fibrils by disease-related proteins includingβ-amyloid protein (AβP), prion protein, α-synuclein, polyglutamine, and the introduction of apoptotic degeneration. Trace elements can bind to these proteins and cause their conformational changes. Furthermore, these proteins are co-localized in synapses and play crucial roles in the regulation of trace elements. Thus, it is possible that the interactions between the disease-related proteins and trace elements are based on the physiological roles of these proteins. We review here the current understanding of the pathology of the neurodegenerative diseases based on the metal-binding to disease-related proteins and on the disruption of metal homeostasis.
