The abnormal aggregation of beta-amyloid (A beta) peptides is a hallmark of Alzheimer's disease (AD) that affects more than 10% of the people over the age 60 world-wide. While the exact mechanism of neuronal loss and cognitive decline has not been elucidated yet, the amyloid hypothesis about the causative role of A beta aggregation in AD pathology has been widely supported by the numerous in vivo and in vitro data. In this respect, many efforts have been made to explore therapeutic agents that can modulate the aggregation of A beta, but none of the efforts succeeded in producing effective anti-A beta drugs for treating AD. This article provides an overview of recent attempts that have employed light energy to intervene with the self-assembly process of A beta peptides via the generation of oxidative stress by photosensitizers, such as natural or synthetic dyes, light-responsive nanomaterials, and photoelectrochemical platforms. The underlying mechanism of photodynamic reactions suppressing A beta aggregation and the dilemma in generating long-been-blamed oxidative stress are discussed by addressing the positive role of oxidative stress produced by the photosensitizers in the light-induced suppression of A beta-mediated neurotoxicity. We have summarized current challenges and strategies to advance photo-induced inhibition and modulation of A beta aggregation as a therapeutic option for treating AD in the future.