"This new study highlights the importance of certain soluble proteins, called cytokinesi, in Alzheimer’s disease. The study focuses on one of these cytokines, tumor necrosisi factor-alpha(TNF), a critical component of the brain’s immunei system."
"The new study documents a dramatic and unprecedented therapeutic effect in an Alzheimer’s patient: improvement within minutes following delivery of perispinal etanercept, which is etanercept given by injection in the spine. Etanercept (trade name Enbrel) binds and inactivates excess TNF."
http://www.sciencedaily.com/releases/2008/01/080109091102.htm
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GFAi - asthmai, sinusitis/rhinitis, tendonitis, low back pain, hypothyroid. Started azi 1000mg/week Jan 9, '08. Increased azi to 250mg/day, added 20mg Benicar daily Mar 13, '08. First Flagylii pulse started June 30, '08. Added Doxyii 200mg/day Aug 16.
This is very interesting.
This is very interesting. Especially given the recent study by Balin, et al noted in this post http://www.cpnhelp.org/study_inhibition_of_apopt and that TNF is one of the immunei agents used to kill Cpn. I can readily believe that blocking TNFalpha would lower inflammationi, but it could also allow Cpn to run rampant in the brain. The researchers assume (at least apparently) that the inflammation in the brain is an autoimmune or accidental thing, and don't seem to be aware of the solid body of work done by Balin and others of possible infectious causes to Alzheimer's. Any of our more science minded care to speculate on the end results of blocking TNFalpha in an infected brain?
CAPi for Cpn 11/04. Dx: 25yrs CFSi & FMSi. Protocol: 200mg Doxyi, 500mg MWF Azith, Tinii 1000mg/day pulses; Vit D1000 units, INH 150mg, Magnascent Iodine 20 drps/day, T4 & T3
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CAPi for Cpni 11/04. Dx: 25yrs CFSi & FMSi. Currently: 150mg BID Roxithromycin, Doxycycline 100mg BID, Tinii 1000mg/day pulses; Vit D2000 units, T4 & T3
Kind of like the idea that
Kind of like the idea that in order to end war, rather than even looking to see who the enemy is, they take the ammunition away from our own troops. That always seems to be the approach to any perceived "autoimmune" disorder. Puzzling, isn't it?
Asthma, chronic sinusitis/rhinitis, chronic tendonitis, hypothyroid. Jan 9, '08 started Azithromycin 1000mg/week.
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GFAi - asthmai, sinusitis/rhinitis, tendonitis, low back pain, hypothyroid. Started azi 1000mg/week Jan 9, '08. Increased azi to 250mg/day, added 20mg Benicar daily Mar 13, '08. First Flagyli pulse started June 30, '08. Added Doxyi 200mg/day Aug 16.
Kind of like the idea that
Sort of... but remember: the possibilities for infectious pathogenesis do not end at the bounds of the classical infectious diseasesi. Some diseases might depend on infectionsi which are not significantly harmful per se; some might not even be harmful during therapeutic immune suppression. Bechet's, for example, has been found to respond to both antibacterials and anti-TNFs, and the apparent paradox therein has been noted.
Likewise, I don't think anti-TNFs have been associated so far with long-term deterioration of RA or psoriasis, even though anti-TNFs have now been in use for several years. We don't know yet what happens after 20 years of anti-TNF use. Both RA and psoriasis have been formally shown to be responsive to antibacterials, though I believe the information is more preliminary for psoriasis, and is not that impressive in degree for RA (perhaps because mostly monotherapies have been tried).
Of the diseases widely termed autoimmune, not all are as poorly evidenced as autoimmune as MS is. There is little evidence that any of the autoreactivities in MS cause disease - though they certainly could - there are many autoreactivities which do not cause disease. For many diseases, including Graves', myasthenia gravis, pemphigus, etc, the evidence for the disease being caused by autoreactivities is excellent. As with infectious disease, the best way to show this is by adoptive transfer: add the proposed harmful agent (in this case autoreactive antibodies or T cells) to human tissue explants, or to animals, and see if disease is produced.
However, the question then becomes, what causes the autoreactivity; one possibility is that persistent infection is required to sustain the autoreactivity, and many other possibilities exist. In short, a single disease could be (in some or all of its cases) both autoimmune and infectious at the same time - just as a disease can be infectious and inflammopathic at the same time, or infectious and toxic at the same time.
We do know, however not
We do know, however not surprisingly, that anti-TNFs have been associated with infectionsi. Here's a quick search through pubmed on "etanercept+infection" alone.
Pubmed Search: etanercept+infection
12 pages returned. And some of those infections look kind of nasty...
On Combined Antibiotic Protocol for Cpni in Rosaceai 01/06 - 07/07, On Vit D3 + NACi since 07/07 and daily FIRi Sauna since 08/07
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On Combined Antibiotic Protocol for Cpni in Rosaceai 01/06 - 07/07, On Vit D3 + NACi since 07/07 and daily FIRi Sauna since 08/07