Signs and Symptoms                      Treatment                                                         Effect Senile Plaque Formation β-secretase inhibitor Decreases the formation of Aβ by inhibiting cleavage of APP by β-secretase [51]   γ-secretase inhibitor Decreases the formation of Aβ by inhibiting cleavage of APP by γ-secretase [52]   PKC activator Decreases the formation of Aβ by increasing cleavage of APP within the Aβ domain by α-secretase via upregulation by PKC activation [53]   Antiaggregant Inhibits aggregation of Aβ into oligomers [54,55]   Vaccination Causes an immune response by which the body targets Aβ for degredation [56-58]   ApoE inhibitor Allows for removal of Aβ by blocking attachment of ApoE to Aβ [59] Neurofibrillary Tangles CDK5 inhibitor Inhibits phosphorylation of tau protein by CDK5 [60]   GSK-3 inhibitor Inhibits phosphorylation of tau protein by GSK-3 [61]   ApoE inhibitor May inhibit phosphorylation of tau protein by GSK-3 via signal blocking [62,63]   Antiaggregant Inhibits aggregation of tau protein [64] Low Acetylcholine Levels AChE inhibitor Increases levels of acetylcholine by inhibiting its degredation by AChE [45-48] Oxidative Stress Antioxidant Breaks or inhibits free radical chain reactions by scavenging unpaired electrons [65,66]

Table 2: A summary of current treatment options for AD and their effects. (Aβ = amyloid beta peptide; AChE = acetylcholinesterase; ApoE = apolipoprotein E; APP = amyloid precursor protein; CDK5 = cyclin-dependent kinase 5; GSK-3 = glycogen synthase kinase 3; PKC = protein kinase C).