Study

[Guest guest]

Immune system cause of multiple sclerosis questioned

Study shows evidence that myelin-producing cells die before there is any immune

system activity

http://www.mult-sclerosis.org

March 18, 2004

All About Multiple Sclerosis

Prevailing medical wisdom says that multiple sclerosis is an autoimmune disease

- a disease in which the body's immune system turns in on itself. Specifically,

it attacks the myelin sheaths that insulate the nerve cells in the brain and

spinal cord. This immune system activity produces inflammation similar to what

happens in the skin when we get a pimple.

Crucially, the inflammation also kills the cells responsible for producing and

maintaining the myelin. These cells are called oligodendrocytes and they have

long been known to die in large numbers during attacks of MS.

The majority of existing treatments for the disease and a fair proportion of new

treatments currently in research focus on reducing the inflammation or disabling

the immune system cells responsible for it.

However, a dramatic piece of new research published in The ls of Neurology

threatens to turn this understanding of multiple sclerosis on its head.

The study examined twelve brains of people with multiple sclerosis,

concentrating on newly forming areas of disease activity called lesions. It

found that the oligodendrocytes in these lesions were dying before there were

any signs of inflammation.

This implies that it is not the inflammation that causes the death of the

oligodendrocytes in multiple sclerosis but the other way around. The

inflammation occurs in response to the oligodendrocyte cell death.

The authors, Barnett and Prineas of the Institute of Clinical

Neurosciences at the University of Sydney, Australia don't deny that the

inflammation might cause some of the damage seen in multiple sclerosis but they

do paint a radically new picture of of the disease.

They suggest that the first stage of the development of a new multiple sclerosis

lesion is mass suicide of the oligodendrocytes over a relatively small area.

This process is called apoptosis or programmed cell death and is a normal

response in the human body during growth and repair. If cells were allowed to

grow and divide without limits, they would form a cancer. Similarily, cells

infected by viruses or cells that are no longer needed by the body will often

cell kill themselves.

Barnett and Prineas observed oligodendrocytes in which the central nucleus was

shrivelling up - a typical sign of a cell committing suicide. Other cells in the

brain were also changing. Microglia, another type of maintenance cell which can

swallow up dead and dying cells, were forming long extensions ready to engulf

the dead and dying oligodendrocytes. Additionally, a group of proteins, called

complement, which are responsible for activating the body's rubbish-collecting

cells, had collected on the myelin. Crucially, the rubbish-collecting cells of

the immune system, the macrophages, had not yet appeared in the lesion.

Within one or two days of lesion formation, all the oligodendrocytes had

disappeared. The authors suggest that they had been swallowed up by the

microglia. The spaces that they had once occupied were now full of liquid

forming what is known as edema.

The next stage seems to be the invasion of immune system cells. Macrophages now

start to appear, together with T cells, the orchestrators of the immune

response. These initiate and take part in inflammation. The macrophages start to

gobble up the myelin left over by the vanished oligodendrocytes.

The final stage would appear to be regeneration. Oligodendrocyte precursor

cells, cells that have the ability to develop into new oligodendrocytes, move in

to replace the lost cells. They are fed special chemicals called trophic factors

by the macrophages and the process of remyelination can begin.

It is important to bear in mind that this was a study of only 12 brains and

further work needs to be done to validate the studies findings. However, if this

work reflects what is actually happening in multiple sclerosis, then its

implications are earth shattering:

a.. Multiple sclerosis will no longer be an autoimmune disease. A lot of text

books are going to have to be rewritten.

a.. Treatments that target inflammation will not not addressing the root cause

of the diease. This does not mean that they are not effective to some degree but

that they can never be as good as treatments that target the death of the

oligodendrocytes.

a.. All the animal models of multiple sclerosis are poor representations of

the disease in that they are all primarily autoimmune models. Perhaps this is

why so many treatments that are so effective in mouse models prove to make no

difference to multiple sclerosis in humans. For animal models to be valid, they

would need to show the kind of disease process described by Barnett and Prineas.

a.. Researchers will need to change direction. Whilst work on oligodendrocyte

precursor cells becomes more important than ever, work on describing the

inflammation process in multiple sclerosis needs to take a back-seat.

Importantly, researchers need to find out why oligodendrocytes are dying and

what can be done to stop them.

Quite how the world of multiple sclerosis research will react to this paper is

unclear. Thus far, Barnett and Prineas's paper seems to have been met with a

deafening silence which is why I decided to write this piece.

Source:

Relapsing and remitting multiple sclerosis: Pathology of the newly forming

lesion

H. Barnett, MBBS, W. Prineas, MBBS *

ls of Neurology, Feb 23, 2004

http://www3.interscience.wiley.com/cgi-bin/abstract/107629227/ABSTRACT

Copyright © 2004, All About Multiple Sclerosis

Hugs,

[Guest guest]

Haven't posted to this group before, but have enjoyed reading the posts thus

far.

I wanted to thank Jeff for posting the negative side of statins. I can't tell

you how aggravating it gets (although I'm sure you all know!) when well meaning

family and friends call/email/write to tell the latest " miracle " MS cure. It's

good to have at hand reasons for my rejecting mainstream drug treatments. I'm

going to be printing Jeff's post up to reference in my defense :-)

Personally, I'm doing well with keeping my toxin exposures low, eating organic,

and other dietary/natural regimen. The last thing I want to do is further

pollute my body with more " medicine " .

ZombieDogg

----------------

Planning is useless. Survival is as good as it gets.

-- 28 Days Later

[Guest guest]

This study makes no sense to me because of two things, first I am

already " dangerously low in Cholesterol " per my GP and my Dr. of

Internal Medicine. Lowering my Cholersterol with a statins would be

a disaster. In fact, the Internal Medicine Dr. thinks my low

Cholesterol may be a contributing factor in my developing MS.

Second, I recently read a report by an independent group who were

studying the increasing number of patients who are on various

statins who are developing severe MS like symptoms because of the

drug therapy. (The report was given to me by a co-worker who has

high Cholesterol and is on a statin and very upset about the

possible side-effects.)

Whatever, I'm happy to let the uber drug companies battle it out

over profit and product that is ineffective while I happily take LDN.