Abstract: Alzheimer’s disease is a devastating neurodegenerative disorder affecting millions worldwide, with current treatments offering only limited benefits. Central to emerging research is the role of autophagy and endolysosomal pathways, which are essential for clearing misfolded proteins and damaged organelles. Bridging integrator 1 (BIN1), traditionally recognized for its role in membrane remodeling and endocytosis, has recently emerged as a top genetic risk factor for Alzheimer’s disease, linking cellular clearance mechanisms to the development of toxic amyloid-beta plaques and tau tangles. In this review, we provide an accessible overview of how disruptions in autophagy and endolysosomal trafficking contribute to the neurodegeneration process in Alzheimer’s disease, positioning BIN1 as a central mediator within this complex network. Recent advances have shown that alterations in BIN1 expression and isoform distribution are associated with increased tau pathology and changes in amyloid-beta processing. Moreover, BIN1 appears to also influence synaptic transmission, neuroinflammation, and overall cellular homeostasis. The integration of recent findings not only deepens our understanding of Alzheimer’s disease pathology but also opens new avenues for the development of targeted treatments. This timely perspective underscores the potential of modulating BIN1 activity to enhance cellular clearance mechanisms and offers hope for more effective interventions for Alzheimer’s disease.

Key words: Alzheimer’s disease, amyloid-beta, autophagy, bridging integrator 1, cellular clearance, endolysosomal network, genetic risk factors, membrane dynamics, neurodegeneration, neuroinflammation, synaptic transmission, tau