Axonal transport dysfunction Sample Clauses

Axonal transport dysfunction. ‌ The proper transport of protein and organelle cargoes along the cytoskeleton is a vital process for virtually all mammalian cells. This process is particularly important in neurons, since they are polarized cells with axons and dendrites usually extending over great distances. Since most neuronal proteins are synthesised in the cell body and then transported to their final destination, neurons require highly efficient transport of cargoes to the distal regions of axons and dendrites to permit functioning of synapses. Likewise, trophic factors need to be shipped from the synapse to the cell body. Transport from cell body to the axon terminal is termed anterograde axonal transport and transport from the axon terminal to the cell body is termed retrograde axonal transport. Most long range transport through axons is mediated by kinesin and dynein molecular motors that move along microtubules. Within axons, microtubules are mostly orientated with their plus ends (the ends to which tubulin subunits are added) towards the synapse. Most kinesins move towards the plus end of microtubules (anterograde transport) whereas dynein moves towards the minus end of microtubules (retrograde transport) (Hirokawa and Noda, 2008). A number of lines of evidence suggest that defective axonal transport contributes to neurodegenerative diseases including ALS (for review see (Xx Xxx et al., 2008)). Firstly, mutations in dynactin, a component of the dynein motor, can cause a familial form of ALS (Xxxxx et al., 2004; Xxxx et al., 2003) and mutant dynactin damages dynein function (Xxxx et al., 2006). Secondly, the presence of protein/organelle accumulations in ALS such as neurofilament and mitochondria in the proximal axon suggest that axonal transport is disrupted (Xxxxxxxx et al., 2004; Xxxxxxxxx, 1968; Xxxxxx et al., 1984; Xxxx et al., 1998; Xxxxxx and Xxxxx, 2007). Thirdly, damage to axonal transport has been described in ALS transgenic animals and cellular models. Defective axonal transport of components of the cytoskeleton, mitochondria and vesicles are observed in mutant SOD1 mice that develop ALS (Xxxxxxxx et al., 2010; Xx Xxx et al., 2007; Xxxxxx et al., 2005; Xxxxxxxxxx and Cleveland, 1999; Xxxxx et al., 1997). Also overexpression of neurofilaments can model ALS in mice and damage to axonal transport is seen in these models (Xxxxxxx et al., 1995; Xxxxxxxxxx et al., 2006). Finally, disrupting molecular motor function can model ALS in transgenic mice. The Legs-at-odd-angles a...
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