Targeting brain metal homeostasis in Alzheimer's disease
Accumulating evidence indicates that loss of neurons in Alzheimer's disease (AD) is a result of oxidative stress driven by active metal ions such as copper on different amyloid beta peptide aggregates. With many trials on AD drugs failing, scientists of the EU-funded TS4NC project are turning to the regulation of metal homeostasis as a treatment option. The new multifunctional S4N agents constitute promising candidates as not only do they chelate copper away from amyloid plaques and provide neuroprotection, but they also redistribute copper ions into the physiological circulation. The TS4NC proposed approach is expected to help restore brain metal homeostasis and open new drug development paths for AD.
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