Abstract
Due to their enormous surface area compared to other cell types, neurons face unique challenges in properly handling supply and retrieval of the plasma membrane (PM)—a process termed PM turnover—in their distal areas. Because of the length and extensiveness of dendritic branches in neurons, the transport of materials needed for PM turnover from soma to distal dendrites will be inefficient and quite burdensome for somatic organelles. To meet local demands, PM turnover in dendrites most likely requires local cellular machinery, such as dendritic endocytic and secretory systems, dysregulation of which may result in dendritic pathology observed in various neurodegenerative diseases (NDs). Supporting this notion, a growing body of literature provides evidence to suggest the pathogenic contribution of dysregulated PM turnover to dendritic pathology in certain NDs. In this article, we present our perspective view that impaired dendritic endocytic and secretory systems may contribute to dendritic pathology by encumbering PM turnover in NDs.
Highlights
Dendrites are neuronal compartments essential for receiving electrochemical signals from presynaptic neurons through formed synapses
Besides what we have described so far, many other molecules have been identified whose dysregulation interferes with cellular components such as cytoskeletons, mitochondria, endosomes, endoplasmic reticulum (ER), and Golgi that may be linked to dendritic pathology (Jan and Jan, 2010; Lei et al, 2016; Kweon et al, 2017; Kelliher et al, 2019)
Evidence for the Involvement of Local related in brain (Rab)-Mediated Endocytic Pathway in Dendritic Pathology in neurodegenerative diseases (NDs) Several previous studies provide experimental evidence to support a link between endosomal defects and neuronal pathology in NDs, which has been well-reviewed in recent articles (Kiral et al, 2018; Guadagno and Progida, 2019)
Summary
Dendrites are neuronal compartments essential for receiving electrochemical signals from presynaptic neurons through formed synapses.
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