Potential Therapeutic Strategies for Alzheimer’s Disease Targeting or Beyond β-Amyloid: Insights from Clinical Trials

Figure 1

β-amyloid hypothesis based therapeutic targets. APP, after sequentially being cleaved by BACE1 and γ-secretase, gives rise to a neuron toxic molecule Aβ42. This peptide can exist as monomers or aggregates into oligomers and plagues. The assembly of Aβ42 triggers downstream effects and induces tau phosphorylation. BACE1 inhibitors and GSI/GSM aim to prohibit the production of pathological Aβ, and vaccines or Aβ antibodies promote clearance mechanism. As for tau, GSK-3β inhibitors and other antiaggregates are potential therapeutics targeting on blocking tau hyperphosphorylation or aggregation.