A breach in the scaffold: the possible role of cytoskeleton dysfunction in the pathogenesis of major depression

Abstract

Depression is one of the most common psychiatric disorders with inadequately understood disease mechanisms. It has long been considered that dendritic regression and decrease in the number of dendritic spines are involved in depression. Dendrites made up of microtubules and actin filaments form synapses with neighboring neurons, which come together as an important communication network. Cytoskeletal proteins undergo post-translational modifications to define their structure and function. In depression and other psychiatric disorders, post-translational modifications may be disrupted that can result in altered cytoskeletal functions. The disruption of microtubule and actin in terms of morphology and functions may be a leading cause of dendritic regression and decrease in dendritic spine in depression.