Despite these contributions, we suggest specific areas of inquiry that warrant further interrogation, including the elucidation mechanisms in recipient cells that are modulated by exosomal miRNAs, the characterization of exosomal contents that are responsible for alterations in neuroinflammation and the examination of other aggregate-prone peptides (e.g., TDP-43, α-synuclein) in exosomes that may synergistically increase risk for late life cognitive impairment. This evidence concerns the gene TARDBP and Cognitive impairment.