Association of intracellular Aβ with endosomal membranes.
Their findings provide evidence that Aβ aggregates building up in synapses are formed locally, within synaptic endosomes, due to disruptions in nascent Aβ proteostasis. This research contributes to our understanding of whether synaptotoxic Aβ is mainly derived from plaques or if it is produced and aggregated locally, within affected synaptic compartments. Filling this knowledge gap is important for the development of an effective treatment for AD, as extracellular and intrasynaptic pools of Aβ may not be equally modulated by immunotherapies or other therapeutic approaches.
