As usual, there were numerous interesting scientific presentations. One
recurring theme this year was the presence of damage to mitochondria as an early and possibly causal event in MS.
Mitochondria supply the energy the cell needs to function, and prevent damage by oxidation. The
role of iron in MS damage was also a frequent topic.
Dr. Stephen Hauser from UCSF received the Charcot award, and gave an interesting talk on the
role of B cells in MS. B cells are present in the brain and spinal fluid, and treatments that reduce the
number of B cells have a marked effect in relapsing MS.
One session addressed the role of gut bacteria in MS. The normal gut has
a large variety of bacteria, and these bacteria affect the activity of the immune system. Studies in mice
show that bacteria in the gut can affect autoimmune diseases. The bacteria change depending on exposure,
antibiotic treatment and diet.
The genetics consortium studying MS has now identified over 100 genetic markers for increased
risk of MS, with another large batch in the confirmation process. These genetic data are being combined
with other types of information to suggest that the immune system (white blood cells) are the main cause of MS.
One of the long-standing arguments in MS has been whether disease is caused by autoimmune attack on normal myelin,
or abnormal myelin causing autoimmunity.
My particular interest is the role of Epstein-Barr virus in causing MS. There
were an unusual number of presentations on EBV and other viruses. Increased antibodies to one EBV protein
predict more disease activity, and there are EBV infected cells in the spinal fluid. Dr. Pender from Australia
presented results from treating a progressive MS patient with cells to increase immunity to EBV. HIV infection
may protect against MS, or HIV treatment may help in MS.