Mutations in the SORLA protein create defective exosomes that fail to properly support neighboring brain cells, revealing a previously unrecognized pathway in Alzheimer's pathogenesis. Cells carrying the faulty protein produce both fewer exosomes and vesicles with diminished neuroprotective capacity. This discovery builds on decades of research into intercellular communication mechanisms, where exosomes have emerged as critical messengers carrying proteins, lipids, and nucleic acids between neurons and glial cells. The finding suggests Alzheimer's may partially stem from communication breakdown rather than solely from amyloid plaques and tau tangles. For aging adults, this represents a potentially actionable target since exosome dysfunction could theoretically be addressed through lifestyle interventions that enhance cellular health or future therapeutics designed to restore vesicle function. However, the research appears early-stage and would require validation in human subjects before clinical applications emerge. The SORLA connection is particularly intriguing because this protein has known roles in neuronal trafficking and has been linked to Alzheimer's risk in genome-wide studies. This cellular communication angle could explain why some individuals develop dementia despite modest plaque burdens.