Exploring lysosomal defects and rescue strategies for Alzheimer’s disease using human transdifferentiated neurons

Aging is the critical factor of Alzheimer’s disease (AD), the most common neurodegenerative disease. Among the pathological changes in the brain associated with AD, protein aggregates are the characteristic pathological hallmark that is composed of misfolded and toxic proteins. A decline in lysosomal proteolytic activity has been linked to protein aggregation and neuronal death, whereas how the lysosomes become defective and exacerbate neurodegeneration in the brain of AD patients is not well understood.