New study suggests role of protein Rab32 in multiple sclerosis

Of new work by Professor Paul Eggleton and colleagues in multiple sclerosis, Science Daily reported on 24 April 2017:


The joint Exeter-Alberta research team was the first to combine clinical and laboratory experiments to explain how mitochondria becomes defective in people with MS. Using human brain tissue samples , they found that a protein called Rab32 is present in large quantities in the brains of people with MS, but is virtually absent in healthy brain cells.

Where Rab32 is present, the team discovered that a part of the cell that stores calcium (endoplasmic reticulum or ER) gets too close to the mitochondria. The resulting miscommunication with the calcium supply triggers the mitochondria to misbehave, ultimately causing toxicity for brain cells people with MS.



From MedicalNewsToday:


In their new investigation, the researchers study a protein called Rab32, which is known to be involved in certain mitochondrial processes.

They found that levels of Rab32 are much higher in the brains of people with MS and hardly detectable in brains of people without the disease.

They also discovered that the presence of Rab32 coincides with disruption to a communication system that causes mitochondria to malfunction, causing toxic effects in the brain cells of people with MS.



link: http://www.medicalnewstoday.com/articles/317077.php


The journal citation:

Yohannes Haile, Xiaodan Deng, Carolina Ortiz-Sandoval, Nasser Tahbaz, Aleksandra Janowicz, Jian-Qiang Lu, Bradley J. Kerr, Nicholas J. Gutowski, Janet E. Holley, Paul Eggleton, Fabrizio Giuliani, Thomas Simmen. Rab32 connects ER stress to mitochondrial defects in multiple sclerosis. Journal of Neuroinflammation, 2017; 14 (1) DOI: 10.1186/s12974-016-0788-z


Note also the 2012 paper:

Expression profiling of Rab GTPases reveals the involvement of Rab20 and Rab32 in acute brain inflammation in mice
Neuroscience Letters 527(2):110-4 · August 2012