Alzheimer’s disease (AD) involves the progressive deterioration of mental faculties including cognition, rational thinking, and memory. At times, this disease can become debilitating and can increase the risk for other health issues. Poor memory, for example, can cause an AD patient to lose a significant amount of weight because this person may have forgotten to eat at regular mealtimes. Those affected by AD progress in their disease differently, and patients with AD also vary in regard to the level of disease severity. Medications are available to help slow the progression of AD; however, a cure for the disease remains elusive.
Currently, many researchers are focusing their efforts on amyloid plaques which are typically found as deposits in the brains of AD patients. The main component of these plaques is Aβ peptide, and aggregation of these peptides are what cause the plaque formation.
Research has consistently found a correlation between AD pathogenesis and the generation of reactive oxygen species (ROS) and soluble Aβ oligomers. Additional research has also found that within many AD patients, high concentrations of zinc (Zn) and copper (Cu) exist within the amyloid deposits. The interaction between Cu2+-Aβ can result in significant brain toxicity for AD patients, a discovery that has recently facilitated more attention toward chelation therapy of Cu2+ from Cu2+-Aβ aggregates as an approach to AD. Specifically, researchers believe the Cu2+-Aβ interactions are reversible and Cu2+ binding to Aβ peptides have the potential to be regulated by chelation.
Catalytic photooxygenation has previously been discovered to reduce the effect of neurotoxicity and aggregation of amyloid β (Aβ) peptides. In a study by Xiongwei Dong et al, the effect of ultraviolet (UV) exposure ≤400 nm on chelator-treated and -untreated Cu-bound aggregates was examined.