Regulation of the Postsynaptic Compartment of Excitatory Synapses by the Actin Cytoskeleton in Health and Its Disruption in Disease

Figure 2

Amyloid- disrupts the actin cytoskeleton and receptor trafficking through multiple pathways. There are many conflicting pathways through which A is proposed to alter the actin cytoskeleton. These may involve both up- and downregulation of cofilin activity. Activation of RhoA by A [204] antagonistically inhibits Rac1 [206], both leading to increased cofilin activity. In contrast, A can cause decrease in cofilin activity via activation of Cdc42 [211]. Both active and inactive cofilin are thought to be required for the formation of cofilin rods, which lead to impairment of intracellular transport [215]. Alternatively or in addition to this, altered expression and/or processing of actin filament stabilizing proteins [217, 218] may impact the trafficking of neurotransmitter receptors.