French researchers claim immune system linked to development of PD
 

Here's the link:

http://www.eurekalert.org/pub_releas...-icc121808.php

Thank you for this interesting paper. PD very clearly has the features of an autoimmune disease and a few years ago we had discussions about it at the other forum. Its nice to see such "out of the box" ideas being experimentally proven. Auto immune responses, leaky BBB, role of vitamin D, Infections and inflammation and stress as contributing factors to PD are discussed here before they are experimentally proven in the labs. There may be many more, but these are a few I remember. And that says a lot about why patients' views and input are important in the pursuit of cure for PD.

girija

White blood cell count
 

Interesting. I know my WBC is always low (2.4 when it should be 4.5 to 10 approximately.) Low WBC indicates a weakened immune system.

It seems like it could be at least in my case
 

It is very timely that you posted this article just a few days back. I was to the endocrinologist yesterday for my hypothyroidism that I have in addition to the PD. I have also been having the most irritated eyes in the past few months. Now he suspects I could have Sjogren's syndrome. Says it runs sometimes with people who have hypothyroidism. I have lots of allergies, borderline high blood sugar. Some kind of swelling and pain and spasms in my left foot, but no injury. The skin on my lower arms looks a little splotchy, almost like vitiligo. My mom had Rhematoid athritis,grandma diabetic, brain disorders in the family. Nephew with some sort of immune deficiency. All these things :)are autoimmune. So,, I got to thinking that my PD is likely the same. Anyone else here have some of these other disorders? It makes sense to me. Thanks FG

I have hypothyroidism, chronic sinusitis....

A note about hypothyroidism
 

Forgive me going off topic, but one of the alleged benefits of coconut oil is improved thyroid function and it seems to be true. My wife (non-PWP) has long dealt with what seemed to be low thyroid function including being sensitive to cold temperature as well as a basal body temperature of 96.7 F.

After two months of the oil she has no problem with the room temperature and her body temp has risen a full degree. Also, she has lost 75% of the grey from her hair.

how much oil?
 

That is incredible, I think you mentioned it helped with anxiety/depression as well, so wonderful for her.

I was wondering, how much of the oil is she taking every day? One can only take so much of the stuff, healthy though it may be.

My first neuro thought I might have an autoimmune problem, especially when he found my biopsy from 1984 that diagnosed discoid lupus. I had several symptoms of systemic lupus, but my ANA was always negative.

I also have many allergies. My lupus resolved itself after a few years, don't know why. I wonder if osteoarthritis is autoimmune related, too.

And where do cytokines fit in?

What is the best kind of coconut oil to take, please?

Journal of Experimental Medicine, Vol 180, 1961-1966, Copyright © 1994 by Rockefeller University Press

ARTICLES

Cytokine-induced immune deviation as a therapy for inflammatory autoimmune disease

MK Racke, A Bonomo, DE Scott, B Cannella, A Levine, CS Raine, EM Shevach and M Rocken
Neuroimmunology Branch, National Institute of Neurological Diseases and Stroke, National Institutes of Health, Bethesda, Maryland 20892.

The properties and outcome of an immune response are best predicted by the lymphokine phenotype of the responding T cells. Cytokines produced by CD4+ T helper type 1 (Th1) T cells mediate delayed type hypersensitivity (DTH) and inflammatory responses, whereas cytokines produced by Th2 T cells mediate helper T cell functions for antibody production.

To determine whether induction of Th2-like cells would modulate an inflammatory response, interleukin 4 (IL-4) was administered to animals with experimental allergic encephalomyelitis (EAE), a prototypic autoimmune disease produced by Th1-like T cells specific for myelin basic protein (MBP). IL-4 treatment resulted in amelioration of clinical disease, the induction of MBP-specific Th2 cells, diminished demyelination, and inhibition of the synthesis of inflammatory cytokines in the central nervous system (CNS).

Modulation of an immune response from one dominated by excessive activity of Th1- like T cells to one dominated by the protective cytokines produced by Th2-like T cells may have applicability to the therapy of certain human autoimmune diseases.

http://jem.rupress.org/cgi/content/abstract/180/5/1961

********************

Nature Reviews Immunology 2, 37-45 (January 2002) | doi:10.1038/nri702

Cytokines and autoimmunity
John J. O'Shea1, Averil Ma2 & Peter Lipsky1 About the authors


Cytokines have crucial functions in the development, differentiation and regulation of immune cells. As a result, dysregulation of cytokine production or action is thought to have a central role in the development of autoimmunity and autoimmune disease. Some cytokines, such as interleukin-2, tumour-necrosis factor and interferons — ostensibly, the 'bad guys' in terms of disease pathogenesis — are well known for the promotion of immune and inflammatory responses. However, these cytokines also have crucial immunosuppressive functions and so, paradoxically, can also be 'good guys'. The balance between the pro-inflammatory and immunosuppressive functions of these well-known cytokines and the implications for the pathogenesis of autoimmune disease is the focus of this review.

"Emerging data indicate that, as the Dave Mason song goes, "there ain't no good guys, there ain't no bad guys", but rather a combination of cytokines exert variable effects at different times during the evolution of autoimmune disease. The complex role of cytokines in autoimmunity, especially their unanticipated immunosuppressive functions, is the focus of the this review. We have focused on interleukin-2 (IL-2), but will also draw on lessons learned from interferons (IFNs) and tumour-necrosis factor (TNF) to illustrate these points."

http://www.nature.com/nri/journal/v2/n1/abs/nri702.html

REVIEW


Nature Immunology 5, 575 - 581 (2004)
Published online: 26 May 2004; | doi:10.1038/ni1078
Elaborate interactions between the immune and nervous systems

Lawrence Steinman


Correspondence should be addressed to Lawrence Steinman steinman@stanford.edu

http://www.nature.com/ni/journal/v5/n6/full/ni1078.html

"In the neurodegenerative diseases Alzheimer disease and Parkinson disease, it has been difficult to identify the main target of the adaptive immune response. Instead, aspects of an innate immune response, including the presence of molecules of the MHC, complement components and cytokines such as TNF are present in the CNS67, 68. The lack of adaptive immunity in Alzheimer and Parkinson disease thus contrasts with its presence in diseases such as myasthenia, multiple sclerosis, Rasmussen encephalitis and stiff-man syndrome."

******************

Distribution of major histocompatibility complex class II-positive microglia and cytokine profile of Parkinson's disease brains

Kazuhiro Imamura1 , Nozomi Hishikawa2

Abstract

There are numerous observations confirming that microglia expressing major histocompatibility complex (MHC) class II molecules are associated with the central nervous system (CNS) in aging and pathological conditions. In this study, we investigated the distribution of MHC class II-positive microglia in Parkinson''s disease (PD) brains.

The number of MHC class II-positive microglia in the substantia nigra (SN) and putamen increased as the neuronal degeneration of the SN proceeded. These cells were also ICAM-1 (CD54) and LFA-1 (CD11a) positive.

The number of activated microglia not only in the SN and putamen but also in the hippocampus, transentorhinal cortex, cingulate cortex and temporal cortex in PD was significantly higher than that in the normal control.

Most activated microglia persisted regardless of the presence or absence of Lewy bodies. They were frequently associated not only with -synuclein-positive Lewy neurites, but also with TH-16-positive dopaminergic and WH-3-positive serotonergic neurites, as well as MAP-2- and SMI-32-positive neurites.

These activated microglia were also positive for TNF- and interleukin-6, which are known to have a neuroprotective function. We conclude that MHC class II-positive microglia are a sensitive index of neuropathological change and are actively associated with damaged neurons and neurites.