Research Summary: Rab32 connects ER stress to mitochondrial defects in multiple sclerosis

Mitochondria are often referred to as the ‘powerhouses’ of the cell, as they are largely responsible for the production of energy that our body needs to go about daily life.  There is growing evidence that suggests that problems with mitochondria are common in people with multiple sclerosis (MS), especially those in the more progressed stages of disease that have high levels of neurodegeneration.  When the mitochondria aren’t working properly, the cellular environment changes and inflammation is promoted.

The endoplasmic reticulum (ER) is another component of the cell that is heavily involved in synthesising, processing and packaging proteins.  Similarly to mitochondrial dysfunction, ER stress is also linked to MS.  During these times of ER stress, it has been seen that the ER and mitochondria have much greater interactions within the cell.  It is thought that these interactions may promote the death of neurons.  Therefore, finding out the causes and mechanisms by which the ER and mitochondria communicate may help improve our understanding of the damage caused in MS and lead to a new avenue for treatments.

It has been shown recently that the interaction between the mitochondria and the ER is largely controlled by a protein called Rab32.  Interestingly, this protein has also been found to be increased during inflammation of the brain.  Considering this, researchers from the University of Alberta set out to try and discover what the levels of this protein were like in people with MS and how it might be involved in the disease.

Their results are summarised in this image that we made below:

Rab32

This study has shown that Rab32 is a novel marker of neurodegeneration in people with MS.  It also provides more evidence to the importance of ER stress and mitochondrial dysfunction in the disease process.  It will be important now to confirm these results in larger studies.  If the results hold true, it will then be of interest to determine whether inhibiting the production of Rab32 could be a novel therapy to prevent neurodegeneration in multiple sclerosis.

The abstract for this study can be read in full here.

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