Some neurodegenerative disorders are pathologically characterized by the deposition of abnormally aggregated proteins, both inside and outside the cells, in various peripheral tissues and the central nervous system (CNS). These diseases are called amyloidosis.
These amyloidogenic proteins are soluble in their healthy state. Yet under some unknown conditions, they can aggregate and form tertiary structures in crossed β sheets, ultimately leading to the onset of each disease. The pathological signs characteristic of Alzheimer's disease are two types of amyloid accumulation, each consisting of Aβ and tau.
Therefore, inhibition of amyloid protein aggregation or efficient clearance of already formed amyloids are considered promising therapeutic strategies. However, this strategy has so far been unsuccessful to improve cognition in Alzheimer's disease, so there is a need to investigate new ideas.
With the aim of treating Alzheimer's disease, scientists have studied the artificial addition of oxygen atoms to amyloid by a photooxygenation catalyst and photostimulation.
Oxygenated Aβ has the ability to inhibit the aggregation and clearance of Aβ in the brain. It was clarified that the clearance of oxygenated Aβ was improved and that microglia are involved in the mechanism. Similar experiments were performed with special attention to astrocytes as cells other than microglia in the brain, but no effect of improving the clearance of oxygenated Aβ was observed. This suggests the specific involvement of microglia.
Scientists have also attempted to develop a non-invasive photooxygenation method with the aim of adapting this method to humans. After developing a new photooxygenation catalyst with cerebral migration properties and performing a non-invasive reaction of intravenous administration of the catalyst and light irradiation from outside the skull, Aβ was able to be oxygenated in the brain of a mouse. alive.