[reverett123]

From my blog-A Matter of Balance

Today’s London “Telegraph” reported on a study in the current issue of the journal “Neurology” that pretty much seals the case for neuroinflammation as causal in both Alzheimer’s and Parkinson’s Diseases.

Beginning with a group of 222 AD patients with an average of 83, they obtained baseline data via blood work and cognitive testing. For the next six months they monitored the patients general health by periodic examination and reports from caregivers. Of the group, 110 had either accidents or infections with inflammation. Their memory loss as measured by the cognitive testing was double that of those who had remained healthy.

Further, of those whose initial blood work had shown high levels of the proinflammatory cytokine TNF-a,, showed memory loss at a rate of four times the healthy group. And, finally, those of this already inflamed group who had the ill-luck to suffer an additional infection during the period lost memory at a rate TEN times the rate of those in their the healthy group. (More)

[Teana]

Great job Professor Rick,

I don't understand everything I just read but what does make sense make me feel good. Can anyone interpret for me?

Thanks,
Tina

[girija]

Rick,
You might find this work interesting,
http://researchnews.osu.edu/archive/allerglas.htm

Drs. Glasers are pioneers in neuroimmunology. What they say about stress leading to altered immune functions and your report that inflammation as a key component of progression of PD fit perfectly well together and explain some aspects of PD.

girija

[girija]

Tina,

Beginning with a group of 222 AD patients with an average of 83, they obtained baseline data via blood work and cognitive testing. For the next six months they monitored the patients general health by periodic examination and reports from caregivers. Of the group, 110 had either accidents or infections with inflammation. Their memory loss as measured by the cognitive testing was double that of those who had remained healthy.

Interpretation: This study published in the Journal of Neurology was briefly reviewed by someone for the Telegraph.
What the researchers have done is as follows:

They selected 222 Alzhemeirs Patients of different ages and the average age was 88,
Doctors collected blood samples as well as evaluated their cognitive abilities using standard tests. Examples of Standard tests are word association, memory testing etc.,
These patients' health was monitored for 6months, by hospital check ups and/or by what their care givers told the doctors.
About half 110 of these patients got some infection or a wound that caused inflammation. Fever, chills, and swelling of tissue around the wound as well redness around the wound are indications of inflammation.
People who got sick or hurt and the others were tested for memory function after 6 months. Patients who remained healthy had better memory function while those that got "fevers" had deteriorated i.e, memory loss was more.

urther, of those whose initial blood work had shown high levels of the proinflammatory cytokine TNF-a,, showed memory loss at a rate of four times the healthy group. And, finally, those of this already inflamed group who had the ill-luck to suffer an additional infection during the period lost memory at a ate TEN times the rate of those in their the healthy group. (More)

Blood work these patients showed the following:
TNF alpha is a protein made by the blood cells and it goes up whenever there are infections and is an indicator of inflammation. Blood test of TNF divided patients into two groups: one presumably with normal TNF levels and the others with high amount of a protein TNF (that is pro-inflammatory) in their blood. people wiht high TNF, i.e, wiht inflammation showed faster memory loss than the patients wiht low TNF. When the TNF high patients got more infections, their memory functions deteriorated even further, 10 times worse than those remained healthy.

This shows if thee is inflammation, AD progresses faster and it might be true for PD too. This is the reason neuro-inflammation is a big thing in PD research.

I apologize if I made it too simple, I just wanted to make it as clear as possible, hope it helps>

Originally Posted by Teana

Great job Professor Rick,

I don't understand everything I just read but what does make sense make me feel good. Can anyone interpret for me?

Thanks,
Tina

[reverett123]

There is a response by our immune system that has been noted by numerous researchers. It involves an immune cell type called microglia that turn on when a threat is detected and then turn off. But under certain conditions the "off" order is ignored and the inflammatory response continues. In one example, a mouse was given a shot of a bacterial toxin in a limb that triggered inflammation. A few hours later, the toxin was eliminated and the immune system packed its bags and called it a day in the affected limb.

But in the animal's brain the immune system kept rolling at full speed and was still going *ten months* later. And the majority of the rodent's substanta nigra had been wiped out. The chemicals produced in the process are cytokines and TNF-alpha mentioned is one of these.

In a sense, our brains really are on fire. In slow motion, yes, but a new infection throws more fuel on as in the case of the AD patients.

[Teana]

Thank you so much for taking the time to write this in simple terms, it really does make sense. There is a real difference between looking at Parkinson's and looking into Parkinson's, I'm so thankful for people like you both.

As a side note;

Does anyone know anything about thyroid antibodies and if or how they could effect PD.
I used to have Graves disease so they check my thyroid every once in a while but in Nov. of last year my new doctor had the antibodies checked. The thyroid function is normal but the antibodies were over 1000. Normal range is 30. They said there is nothing to worry about if the thyroid function is normal.

If you have any insight I would love to hear it.
Thanks so much,
Tina

[jinglelady4]

reverett123, taking this one step further:

wouldn't this infection issue also be a good argument for the need for good dental coverage being an essential necessity provision by Social Security Disability for PD and Altzheimer's patients?

jingle

[reverett123]

Once an immune system is "primed" to over react,an infection outside the BBB can trigger the destruction within it. Periodontal disease should constitute a chronic, always present trigger. So the microglia are always active. There is another side to this as well. The cytokines produced by the microglia are themselves destructive and perpetuate inflammation. But they are also, themselves, neurotransmitters. Even in normal folk, when your immune system starts cranking up the cytokines, your brain takes a vacation and your immune system takes over and sends you to bed. The chemistry is not neutral.

Finally, your body has a response to inflammation. It releases a chemical that signals the immune system to cut back and start to wind things down. Unfortunately, the chemical is cortisol which, as a chronic problem, is destructive in its own right. PWP typically have elevated cortisol.

So, all from inflammation, we have self destructive action of the microglia plus interference with normal function plus elevated cortisol.

Originally Posted by jingle belle

reverett123, taking this one step further:

wouldn't this infection issue also be a good argument for the need for good dental coverage being an essential necessity provision by Social Security Disability for PD and Altzheimer's patients?

jingle

[pegleg]

Yep, I have been saying PD and inflammationnn are too cozy for there not to be some relationshhip.

I wish I c ould find that book written by a researcher y ears ago claiming this very thing. I'll keep searching.

thanks, Rick

[Teana]

Is it called "The fungus factor"?
Tina