Lack Of Glucose And Neuromotor Diseases
Neuromotor diseases are also known as motor neuron diseases. This name is due to the fact that they affect the performance of this region of the nervous system. Lack of glucose was not always linked to these pathologies, but new discoveries point in that direction.
Motor neurons can be higher or lower. The superior ones are those that are located in the brain and command the orders for the movements. Lower down in the spinal cord are the lower ones, who finally execute the movement itself.
The actions commanded by motor neurons are multiple, however, they always involve movement. Stretching an arm, taking a step, or chewing all depend on this part of the nervous system.
Although there has always been a tendency to link proteins and lipids as determining factors in neuronal growth, now the lack of glucose appears as a possible risk factor for neuromuscular diseases. This changes the perception of glucose as a source of energy only.
If in motor neuron diseases the problem is the destruction of these cells, the question would be to find the cause of the destruction. Including nutritional aspects in the equation makes the subject interesting from the point of view of prevention.
UIC Barcelona research
The research group on neurolipids at UIC Barcelona is dedicated to studying lipid metabolism and cellular signals in the nervous system. Along these lines, they have found that a lack of glucose can be a determining factor in neuromuscular diseases.
So far, the origin of motor neuron diseases is unknown. Risk groups and factors are known, and specific cases have been thoroughly studied to track genetic alterations, but nothing can be said for sure.
Neurologists classify causes as environmental, toxic, hereditary, and even viral. Neuronal degeneration can also come from another underlying disease that, collaterally, degrades neurons; like brain cancer, for example.
The UIC Barcelona research group, studying the CPT1C protein for its role with lipids, was able to attribute sensor functions to it. This means that CPT1C can measure glucose levels and force the neuron to act accordingly.