Human body is like a huge robot, which has its movement and electronics. We are partially mechanical and partially electronic, but the most mysterious part is how these two mediums connect together. Scientists from the University of Edinburgh and the University of Oxford found two molecules that are responsible for connecting nerves with muscles.
These contact points between nerves and muscles are known as synapses. Some diseases weaken them and sometimes cause atrophy. The problem is that we still understand those synapses rather poorly. Improving our knowledge on the connecting points between mechanical muscles and electronic nerves could lead scientists to creating new therapies to treat neurodegenerative diseases, such as spinal muscular atrophy (SMA).
Researchers discovered a pair of molecules, one in muscles and one in nerves, that could be responsible to the formation of synapses. Scientists used zebrafish and mice to determine that synapses do not form properly when the function of nerves is disrupted. They followed this to two molecules that have to bond to establish synapses. When synapses cannot form, diseases start, which can affect motor function rendering the patient immobile.
Spinal muscular atrophy affects one in 6000 babies and is also known as the “floppy baby syndrome” due to weak muscles. They simply waste away in a progressive muscle wastage process, which leads patients to loss of mobility and control of their movements. There are new therapies to treat SMA and they are increasingly more effective, but this disease is still incurable and is likely to stay that way for the foreseeable future. However, a better understanding of synapses could help scientists creating new treatments that would help maintaining synapses and at least slowing down the progression of SMA and other similar diseases.
Dr Thomas Becker, one of the authors of the study, said: “Our findings contribute to the fundamental understanding of the components that hold synapses together. This knowledge reveals potential new therapeutic targets for stabilisation of synapses in diseases, such as SMA. In the future, we plan to use the zebrafish model in automated screening experiments to find drugs that stabilise synapses”.
If we think of human as a robot, we can imagine easier ways to fix stuff. However, we didn’t create this mechanism and, therefore, have to spend time getting to know it better. This new discovery may not be groundbreaking, but it will inch scientists at least a little closer to creating new therapies for degenerative diseases.
Source: University of Edinburgh