Litcius/Paper detail

Photo-oxygenation by a biocompatible catalyst reduces amyloid-β levels in Alzheimer’s disease mice

Shuta Ozawa, Yukiko Hori, Y. Shimizu, Atsuhiko Taniguchi, Takanobu Suzuki, Wenbo Wang, Yung Wen Chiu, Reiko Koike, Satoshi Yokoshima, Tohru Fukuyama, Sho Takatori, Youhei Sohma, Motomu Kanai, Taisuke Tomita

2021Brain53 citationsDOIOpen Access PDF

Abstract

Amyloid formation and the deposition of the amyloid-β peptide are hallmarks of Alzheimer's disease pathogenesis. Immunotherapies using anti-amyloid-β antibodies have been highlighted as a promising approach for the prevention and treatment of Alzheimer's disease by enhancing microglial clearance of amyloid-β peptide. However, the efficiency of antibody delivery into the brain is limited, and therefore an alternative strategy to facilitate the clearance of brain amyloid is needed. We previously developed an artificial photo-oxygenation system using a low molecular weight catalytic compound. The photocatalyst specifically attached oxygen atoms to amyloids upon irradiation with light, and successfully reduced the neurotoxicity of aggregated amyloid-β via inhibition of amyloid formation. However, the therapeutic effect and mode of actions of the photo-oxygenation system in vivo remained unclear. In this study, we demonstrate that photo-oxygenation facilitates the clearance of aggregated amyloid-β from the brains of living Alzheimer's disease model mice, and enhances the microglial degradation of amyloid-β peptide. These results suggest that photo-oxygenation may represent a novel anti-amyloid-β strategy in Alzheimer's disease, which is compatible with immunotherapy.

Topics & Concepts

Amyloid (mycology)NeurotoxicityAlzheimer's diseaseP3 peptidePathogenesisAmyloid precursor proteinPeptideImmunotherapyChemistryMicrogliaMedicineNeurosciencePharmacologyDiseaseImmunologyPathologyBiochemistryBiologyImmune systemInternal medicineToxicityInflammationNeuroinflammation and Neurodegeneration MechanismsAlzheimer's disease research and treatmentsCholinesterase and Neurodegenerative Diseases