Fig. 3
From: Therapeutic potential of ADAM10 modulation in Alzheimer’s disease: a review of the current evidence
The cross-talk between intracellular pathway involved in synaptic plasticity and ADAM10 availability. LTP induces the activation of the PI3K/AKT pathway which regulates GSK-3 activity negatively. This process contributes to inhibit LTD followed by GSK-3 inhibition. On the other hand, activated AKT induces clathrin-mediated ADAM10 endocytosis via its role in regulation of AP2. Aβ can inhibit mentioned pathways through activation of caspase-3. Aβ: amyloid β; ADAM10: a disintegrin and metalloproteinase domain-containing protein 10; APP: amyloid precursor protein; GSK-3: glycogen synthase kinase; LTD: long-term depression; LTP: long-term potentiation; PI3K: Phosphatidylinositide 3-kinase;