How does axonal transport dysfunction contribute to neurodegenerative diseases?
Axonal transport dysfunction impairs the movement of essential proteins, organelles, and nutrients along neurons, leading to cellular stress and damage. This disruption may contribute to the accumulation of toxic proteins and neuronal death, seen in neurodegenerative diseases like Alzheimer's, Parkinson's, and amyotrophic lateral sclerosis (ALS).
What mechanisms are involved in axonal transport?
Axonal transport involves two main mechanisms: fast and slow transport. Fast axonal transport uses motor proteins like kinesin (anterograde) and dynein (retrograde) to move organelles and vesicles along microtubules. Slow axonal transport relies on the cytoskeleton and motor proteins to transport proteins and cytoskeletal elements. These processes ensure efficient communication and maintenance within neurons.
What are the differences between fast axonal transport and slow axonal transport?
Fast axonal transport moves materials at rates of 200-400 mm per day, carrying membrane-bound organelles and proteins rapidly along microtubules. Slow axonal transport moves cytoskeletal elements and soluble proteins at rates of 0.1-10 mm per day, ensuring structural maintenance and protein turnover in neurons.
What are the main proteins involved in axonal transport?
The main proteins involved in axonal transport are kinesins, dyneins, and cytoplasmic dynein, which mediate anterograde and retrograde transport along microtubules, respectively, as well as actin and myosin for movement and stability.
How is axonal transport measured in laboratory settings?
Axonal transport is measured in laboratory settings using techniques like live-cell imaging with fluorescent markers, radioactive labeling of transported molecules, and tracking of labeled proteins in axons. Advanced microscopy, such as confocal and electron microscopy, can also be used to visualize and quantify transport dynamics in neuronal cultures or tissue slices.