Figure 1.

Illustration of the different hypotheses of Alzheimer's Disease (AD) Development and Progression: Amyloid hypothesis: as disturbed secretase enzymes increase production of Aβ42 eventually forming Aβ plaques that impact synaptic functionality, and neuronal dysfunction. Tau Hypothesis: Where increased production of hyperphosphorylated tau provokes disintegration of microtubules and accumulation of hyperphosphorylated tau fibrils causing neuronal death. Cholinergic hypothesis: where disturbed Acetylcholine (ACH) impacts synaptic function. Inflammation hypothesis: where increased release of inflammatory modulators provoke exaggerated immune response that disrupts synaptic functions and plasticity. Mitochondrial hypothesis: where disrupted mitochondrial functions causes glucose hypometabolism, poor ATP production and increased production of ROS, eventually causing synaptic dysfunction. (Created with BioRender.com).