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Alzheimer's disease - a neurospirochetosis?
Anonymous
Posted: Saturday, January 7, 2012 7:55 AM
Originally posted by: onward

In an article quoted above -
of 13 essential oils tested, "Cinnamomum verum bark" was found to have "the highest antimicrobial activity, particularly against resistant strains."


According to Wikipedia:

quote:
"Cinnamomum verum ("True cinnamon", Sri Lanka cinnamon or Ceylon cinnamon)"


So isn't it interesting that Ceylon cinnamon, which some on this discussion board have already chosen as the best cinnamon supplement for their AD LOs, turns out to have notable antimicrobial activity. Hmmm...

And cinnamon has been reported in a number of cases (on this discussion board) to produce at least a temporary improvement in AD symptoms.

And maybe this result is due to a variety of functions of cinnamon, antibacterial (anti-spirochete) being an important one of them?
Anonymous
Posted: Saturday, January 7, 2012 7:55 AM
Originally posted by: onward

If it turns out to be true that spirochetes are a/the chief cause of AD, what are the best ways to combat it? I guess the primary approach would be extensive testing to determine which specific spirochetes and accompanying infections are involved in each case, then targeting those culprits with prescription meds. But I wonder what, if any, OTC possibilities may exist.
Anonymous
Posted: Saturday, January 7, 2012 7:55 AM
Originally posted by: onward

John, thanks.

Here's another helpful quote from that paper you cited:

quote:
Cinnamon and its extract, irrespective of source, have been associated with a variety of health beneficial effects, including anti-microbial, anti-viral, antioxidant, and insulin-like activities.

Many of the corresponding bioactivities are possibly attributed to cinnamaldehyde, a major constituent of the essential oil responsible for the flavor and aroma of whole cinnamon.

In addition, a number of polymeric polyphenol molecules known as proanthocyanidins are present in the aqueous extract that are likely responsible for the majority of the antioxidant properties of cinnamon.


http://www.diabetesaction.org/...ers_09.pdf?docID=781


I wonder, is there a safe and effective way to administer Ceylon cinnamon oil, and how would the effects differ from those of the powder capsules or the tea?
Anonymous
Posted: Saturday, January 7, 2012 7:55 AM
Originally posted by: swarfmaker

I'm thinking that while an infection may be the root cause of some portion of cases, maybe even most of the cases, there will probably be other causes.

I'm also thinking that while having tooth/gum problems may be a sign of severe infection, it probably doesn't take a huge colony of the bacteria to cause AD, but rather a few getting into the wrong place. I'm thinking this because no doubt there will be people who say that their LO had dentures or never had a problem with their teeth or gums. This may also be where "genetic predisposition" comes into play, not a predisposition to AD, but to a spirochete infection. There are probably people who are immune.
Anonymous
Posted: Saturday, January 7, 2012 7:55 AM
Originally posted by: onward

Needs-help: Sorry, I don't know the answer to your question.

__________________________________________


In case anyone's interested:

The article posted at the beginning of this thread ("Alzheimer's disease - a neurospirochetosis") was also posted (not by me) in another large discussion forum, generating an ongoing discussion with now more than 200 posts. (Needless to say, no one would agree with all that's posted there.)

Part of that discussion (see especially post 1, and also its follow-ups) is a commentary about oral spirochetes, their possible connection to AD, and suggestions about what does and doesn't work when one is trying to get rid of oral spirochetes.

Another part of the discussion is an informative, back-and-forth argument (still ongoing) over whether AD really is a spirochetosis or not.

http://www.freerepublic.com/fo...f-chat/2769347/posts
Anonymous
Posted: Saturday, January 7, 2012 7:55 AM
Originally posted by: john1943

Onward,

If you look through the discussions on "Cinnamon Really Helps" (and perhaps digressions on it to other topics), there is mention the bad effects of Cassia cinnamon mainly because of its high coumarin content.

Ceylon cinnamon has much less coumarin than Cassia. One person takes a spoonful of the powder several times a day.

Another complication is that oily substances cross the blood brain barrier much more readily than aqueous ones. Thus, if we can tolerate oil from Ceylon cinnamon, it has better odds of success.
Anonymous
Posted: Saturday, January 7, 2012 7:55 AM
Originally posted by: john1943

Onward,

I found this in a post of yours regarding Cynthia's success with cinnamon:

"or Ceylon cinnamon powder (from Penzey’s Spices or mountainroseherbs.com)-
3 rounded teaspoons per day (in coffee or straight from the spoon)."

http://alzheimers.infopop.cc/e...=410304334#410304334

I had tried the Ceylon cinnamon from Penzeys, but I used only the aqueous extract! Perhaps I'll get some more and see if my wife will take it right off the spoon.
Anonymous
Posted: Saturday, January 7, 2012 7:55 AM
Originally posted by: onward

More about the pathogen hypothesis of AD, from the Alzheimer Research Forum:

______________________________________________

Q. From Joy K.—Posted 20 July 2004

Has anyone tested the use of antibiotics for Alzheimer's patients? My mother was diagnosed with the disease more than seven years ago. Although she quit after the diagnosis, she was a heavy smoker most of her life, which resulted in congestion problems. Over the last seven years she was given antibiotics several times. Each time her condition improved dramatically. When she stopped the medication she reverted back to the way she was before. She is now in the last stages of her disease and refuses to eat or drink. She was sent to the emergency room and not expected to survive the night. They gave her and antibiotic drip and by the next day she was fighting to go home. She recognized us, was able to put three words together, and understood and responded to everything we said to her. She even played a little joke on my sister, pretending to be dead and then jump up laughing because she scared her.


She has not been this responsive in close to a year! I attribute it to the antibiotic drip. In the past when she took antibiotics orally she significantly improved but the drip seemed to really make a huge difference. I hope something can be done to research this. I am trying to tell everyone I can. Please let me know if this has been researched.

Reply from Brian Balin, Ph.D., Philadelphia College of Osteopathic Medicine—Posted 20 July 2004

Remarkably, this is something that has been recognized by clinicians for many, many years. I have innumerable accounts from individuals who have reported on exactly the same response. There have been reports back to me of individuals who have not spoken for years that have "recovered" this ability following antibiotic therapy. Is the response specific to treating an infection systemically or in the brain, or does it have to do with an anti-inflammatory action of the antibiotics? We just don't have the answers to these questions at this time. In my estimation, there has to be a mandate in this for performing clinical trials based on the antibiotic approach. Hopefully, we can convince the NIH or big pharma that these trials would be worthwhile.


Q. by Allen Cox—Posted 30 July 2004

Several Alzheimer's patients have had postmortem studies done and the Lyme spirochete has been found in the brain embedded in neurons. The following web site lists an article by Thomas Grier on Lyme spirochetes in Alzheimer patients. (Here's another link—ARF)

Q. by Donna Walraven, MSW—Posted 23 January 2009

When my father was alive there was an occasion where he had a serious bladder infection that was finally treated by a urologist outside of the nursing home where he stayed in Port Lavaca, Texas. The urologist gave him powerful antibiotics. After a few days on these antibiotics my father became lucid for over a week. He did not know my name before; now he was calling me by name again, and not just responding to questions, but actually carrying on a conversation with me.

It was a gift because soon after this episode he was overfed again and had to be resuscitated for the third time, but this time something happened to his throat and he was unable to eat again. He died about 10 days later.

I just thought that someone should know because it did seem to help him for a time.

__________________________________________


Comment by Stephen R. Robinson, Monash University, Australia—Posted 1 July 2004

When will the pathogen hypothesis catch on?

The idea that Alzheimer's disease is caused by a pathogen which invades the brain has been around for decades, but this notion has never attracted serious attention from mainstream researchers. It is often dismissed because "if AD was really caused by a virus or bacteria, they would have found it by now, and in any case everyone knows that AD is not contagious—it only affects the aged".

This reasoning overlooks the fact that the vast majority of diseases known to humanity are caused by pathogens, including quite a few that affect cognitive function, either directly (eg. HIV-1) or indirectly (eg. hepatitis). That the pathogen has not yet been identified is hardly surprising. After all, it took thousands of researchers, two decades and many billions of dollars to reach the conclusion that amyloid deposition does not cause AD.

The marginalization of the pathogen hypothesis has stymied research in this area, and much of the supporting data which exists was generated on a pauper's budget, doing credit to the tenacity of proponents such as Ruth Itzhaki, Brain Balin and Mel Ball.

Since the leading proponents of the amyloid deposition hypothesis capitulated (Hardy and Selkoe, 2002), the Alzheimer's field has been left in a vacuum. Sure we still have the 'oligomeric amyloid hypothesis' the 'inflammation hypothesis' and the 'oxidative stress hypothesis' but when one looks beyond the hype it is clear that they merely describe a facet of AD, not its cause.

They cannot explain for example, the spatiotemporal spread of plaques and tangles, why certain neurotransmitter types are preferentially affected, or why particular pathways in the brain are selectively targeted. They cannot account for the non-cognitive behavioural disturbances (eg sundowning), or the predilection for old age, and they struggle to explain why ApoE4 is the major genetic risk factor.

The pathogen hypothesis by contrast, offers explanations for all facets of AD, and for this reason it deserves serious consideration. The pathogen hypothesis was showcased in a debate at the second Challenging Views of Alzheimer's Disease conference in July, 2003.

As an 'outsider' I was astounded to discover that despite three decades of publications by its proponents, not a single skeptic had taken the pathogen hypothesis seriously enough to write a critique. With colleagues Curtis Dobson and Joseph Lyons, we have now written that critique (Robinson et al., 2004).

It is clear to us that much research remains to be done before a strong case can be established, yet it is equally evident that many important questions and issues are ripe for investigation. Certainly there are enough indirect observations to pique the interest of any objective researcher, including reports in the past few months of HSV-1 in the brain tissue of AD patients (Denaro et al., 2003; Mori et al., 2004).

Who knows, perhaps one day we will be able to immunize against AD!

References

Denaro, F.J., Staub, P., Colmer, J. and Freed, D.M. (2003) Coexistence of Alzheimer disease neuropathology with herpes simplex encephalitis. Cell Mol Biol (Noisy-le-grand). 49: 1233-40.

Hardy, J., and Selkoe, D.J. (2002) The amyloid hypothesis of Alzheimer's disease: progress and problems on the road to therapeutics. Science. 297: 353-6.

Mori, I., Kimura, Y., Naiki, H., Matsubara, R., Takeuchi, T., Yokochi, T. and Nishiyama, Y. (2004) Reactivation of HSV-1 in the brain of patients with familial Alzheimer's disease. J. Med. Virol., 73: 605-11.

Robinson, S.R., Dobson, C. and Lyons, J. (2004) Challenges and directions for the pathogen hypothesis of Alzheimer's disease. Neurobiol. Aging, 25: 629-637.

_____________________________

More here:

http://www.alzforum.org/res/fo...al/balin/default.asp
Anonymous
Posted: Saturday, January 7, 2012 7:55 AM
Originally posted by: amelia99

One of the reasons that doctors and scientists may not prescribe antibiotics for extended periods of time is that prolonged use may make them non effective for general use against bacterial infections. Even though some people may have reported that they saw improvements in cognition, they may have thought this wasn't a good reason to keep using the antibiotic and run the risk of making it impotent. This is just a thought I had as to why they would ignore any good reports.
Anonymous
Posted: Saturday, January 7, 2012 7:55 AM
Originally posted by: JAB

Like any other drug, they can cause adverse effects. Many of our loved ones take a nose dive from the antibiotics, although they usually return to baseline after the med has had a chance to clear out of their system.

More importantly, widespread and improper use of these meds has resulted in numerous strains of resistant pathogens springing up, some of which are highly virulent and easily spread. Indiscriminant use of antibiotics and antivirals is therefore strongly recommended against nowadays.

We've had a number of caregivers whose loved ones had an infection and were prescribed an antibiotic for it, developed adverse reactions, stopped the antibiotic too soon, and developed resistant infections that caused a lot of suffering. See, e.g.:
http://alzheimers.infopop.cc/e...=799103051#799103051
Anonymous
Posted: Saturday, January 7, 2012 7:55 AM
Originally posted by: onward

Swarfmaker, like you, lately I'm trying using pure baking soda instead of toothpaste about once a day (but using, at another time of day, another toothpaste followed by Listerine). Btw, I've read to be sure to brush only very gently when using baking soda since it's mildly abrasive.

What seems to work well for me is to pour a little baking soda into a very small cup, add a few drops of water, wet my toothbrush, then keep dipping the brush into the baking soda as I brush, to keep getting fresh baking soda onto the brush. (I hold the brush in one hand and the cup in the other.) Then before rinsing my mouth, I floss, hoping to get the baking soda up under the gum line. Then I rinse with water. Not sure if this is the best way to do it but I find it easy, fwiw.

And thanks very much for the green tea info.

Swarfmaker (or anyone), does green tea have to be caffeinated to be healthful, or is decaf green tea just as good?
Anonymous
Posted: Saturday, January 7, 2012 7:55 AM
Originally posted by: john1943

Swarfmaker, in the version of cinnamon tea that you make do you believe you are capturing the oily part as well as the aqueous part?
Anonymous
Posted: Saturday, January 7, 2012 7:55 AM
Originally posted by: onward

Quoting from a paper cited in my post above, re the potential of Vitamin D to suppress TNF-a:

quote:
"... we showed for the first time that a daily supplement of 50 µg vitamin D for 9 mo is able to increase serum concentrations of the antiinflammatory cytokine IL-10 and to prevent an increase in serum concentrations of the proinflammatory cytokine TNF-α in CHF [congestive heart failure] patients... Our results agree with experimental data showing that vitamin D is able to suppress the release of TNF-α..."


For the nonscientific types like me, here's a translation:

1 microgram (μg or mcg or mug) equals 40 International Units (IU).

1000 IU equals 0.025 mg or 25 microgram (μg or mcg or mug).

So...

A daily dose of 50 µg of vitamin D (to suppress TNF-a) = 2000 IU per day.

Ok, so that was the dosage that suppressed TNF-a in congestive heart failure patients. Whether a greater dose might be needed to suppress TNF-a in AD, I don't know. Wonder if any studies have been done on this.

(I keep remembering those tantalizing anecdotal reports from the Vitamin D Council - posted on the Vit. D thread - about some amazing improvements in AD that were attributed to Vit. D.) See: http://alzheimers.infopop.cc/e...62104261/m/274308273

and specfically:

http://alzheimers.infopop.cc/e...=474300673#474300673

and

http://alzheimers.infopop.cc/e...=546300673#546300673
Anonymous
Posted: Saturday, January 7, 2012 7:55 AM
Originally posted by: onward

Swarf, thanks. My guess (only a guess, obviously) is that the claim about baking soda killing spirochetes in 5 seconds is based on what seem to be extensive observations (of oral spirochete activity) made by that particular dental office (some of whose spirochete videos are posted at youtube, as linked in one of my posts above). I'm also speculating that the degree and speed of effectiveness of baking soda on spirochetes depends on at least 3 things:

- how concentrated the baking soda is (full strength, as recommended by that dental office quoted above, cf. more diluted as in baking soda toothpastes) (and I'm wondering what "1.0 M NaHCO3" means in the article you cited; is that a designation of concentration?),

- the type of spirochete (maybe some are killed rapidly while others take much longer?),

- and other oral factors such as how regularly baking soda has been used in the past,

- and probably other criteria as well. (Again, obviously I'm just speculating.)

In any case, here's more info, focusing mainly on just one type of oral spirochete:

Sodium bicarbonate and hydrogen peroxide: the effect on the growth of streptococcus mutans
http://findarticles.com/p/arti...s_4_79/ai_n29239237/



quote:
... some studies have shown that the sodium bicarbonate must be allowed to interact at least 30 minutes with the bacteria cell to be fully effective. Fletcher et al. showed that sodium bicarbonate had no effect on the viability of S. mutans when exposed only for a short time. (7) A study by Pihlstrom et al. also showed no benefit of using sodium bicarbonate. (

In many cases, sodium bicarbonate was found to be effective against periodontal microorganisms. In a study by Rams et al., a five-minute exposure to sodium bicarbonate quickly immobilized spirochetes and motile rods. (9) Gram-positive cocci bacteria, such as S. mutans, were also shown to be susceptible against 4% sodium bicarbonate in a study by Drake. (5) Additionally, in a four-week study by Legier-Vargas et al., it was found that regular use of Arm & Hammer Dental Care dentifrice (Church & Dwight, Inc., Princeton, NJ), containing 65% sodium bicarbonate, lowered the level of S. mutans in saliva. (10) It has also been demonstrated that brushing with a dentifrice that contains high concentrations of sodium bicarbonate may not only suppress harmful bacteria in the mouth, but may also lead to increases in healthy bacteria. (11)

As well as affecting microbial populations, sodium bicarbonate may also neutralize the acidic environment in the oral cavity produced by the bacteria present. (10) The critical pH level in human dental biofilm is from 4.5 to 5.5. (12) When the pH is at the critical level, enamel is more susceptible to decalcification, which can lead to dental caries. The ideal pH of dental biofilm is a neutral 7.0. Acting as a buffering agent, sodium bicarbonate can raise the pH from the critical pH to a safer pH closer to neutrality. Thus, in addition to the ability of sodium bicarbonate to reduce the effects of harmful bacteria in the mouth, it also increases pH levels to a safe, neutral level.


The above quote is from a lengthy article I haven't had time to read in full yet.

The key thing, though, is whether this spirochete research and theorizing will lead us to treatments that will really help our loved ones. If indeed spirochetes truly are a central factor in AD, suppressing them in the mouth seems an important idea, and finding a way to safely suppress them in the blood seems even better.
Anonymous
Posted: Saturday, January 7, 2012 7:55 AM
Originally posted by: swarfmaker

Perhaps it is not the bacteria or infection itself, but rather some substance the body manufactures to fight the infection. One intriguing possibility is TNF-alpha. It might be possible to test this idea by blocking the action of TNF-alpha. The arthritis drug Enbrel, I think, is said to block TNF-alpha.

Of course, I think it would be better to remove the infection than to use Enbrel long-term to block the effect.

Isn't "Borrelia burgdorferi" Lyme Disease?
Anonymous
Posted: Saturday, January 7, 2012 7:55 AM
Originally posted by: swarfmaker

The purpose of the "cinnamon tea" is to remove the solids and the oils since these were not thought to contribute. The method I used was based on one used by Type II diabetics.

However, we started out using whole cinnamon, and I often wondered if we didn't see better results. Of course, I thought it was the tau-untangling property, but maybe it was the antibiotic quality... or maybe both.

I think that Ceylon cinnamon (Cinnamomum zeylanicum a.k.a. Cinnamomum verum, "true cinnamon", or Sri Lanka cinnamon) is the best choice since you don't have to worry about ingesting too much coumarin. However, the beneficial properties my be present in all species of the cinnamon since the plants are related.

Another interesting "antibiotic" to investigate is silver, especially what is known as "colloidal sliver". Health food stores charge a fortune for the stuff. But, it can be easily produced using two silver electrodes, mineral water and a couple of 9V batteries. (Where does one find "pure" silver without contaminants like lead?)
Anonymous
Posted: Saturday, January 7, 2012 7:55 AM
Originally posted by: onward

That's great news, swarfmaker. Very interesting. Thanks for posting.
Anonymous
Posted: Saturday, January 7, 2012 7:55 AM
Originally posted by: JAB

The idea that an infectious agent can cause Alzheimer's and/or other neurodegenerative disorders has been around for a very long time, and has been studied in quite a few labs. Results from different studies have been conflicting and confusing. Sink your teeth into:
http://www.medscape.com/viewarticle/574944
http://roczes.ovh.org/borelioz...urodegenerative1.pdf
http://www.jacemedical.com/art...%20and%20Disease.pdf
http://www.ncbi.nlm.nih.gov/pubmed/21446901

The idea that an antibiotic or antiviral can help treat Alzheimer's has been around for an equally long time ... and the results from clinical trials on using antibiotics or antivirals to treat Alzheimer's have been conflicting and confusing.
Anonymous
Posted: Saturday, January 7, 2012 7:55 AM
Originally posted by: swarfmaker

The idea of using baking soda to kill of spirochetes is appealing. But, if this is true, there should be some sort of research to back it up. I found some saying that it does work, but not in 5 seconds. It takes more like a half hour to two hours of direct contact...

Bactericidal action of bicarbonate ion on selected periodontal pathogenic microorganisms.

Newbrun E, Hoover CI, Ryder MI.

J Periodontol. 1984 Nov;55(11):658-67.



Abstract

Organisms representative of soil, skin and fecal flora and of supragingival and subgingival flora were tested for inhibition of growth and killing by various salts (NaHCO3, NaCl, MgSO4). The antimicrobial activities of KHCO3, NaF, sodium lauryl sulfate (SLS) and chloramine T were also compared with that of NaHCO3, and the rate at which NaHCO3 exerts its bactericidal effect was studied. Suspected periodontal pathogens were more susceptible to salts than were control non-oral bacteria. Supragingival plaque organisms showed intermediate susceptibility. Periodontal pathogens were more susceptible to NaHCO3 than to NaCl; NaHCO3 and KHCO3 showed similar activity against all strains tested. Accordingly, the antibacterial activity of NaHCO3 is not simply an osmotic effect and is due to the bicarbonate ion. NaF, SLS and chloramine T had greater antimicrobial activity than NaHCO3. Supragingival bacteria required at least 6-hour exposure to 1.0 M NaHCO3 to produce 99% lethality (decrease colony-forming units by 2 log10), whereas selected periodontal pathogens were killed more rapidly (30-120 minutes). The higher the concentration of bicarbonate, the faster the lethality. Morphologic examination by transmission electron microscopy of organisms exposed to bactericidal salt concentrations revealed marked fibrillar condensations within the cytoplasm and shrinkage of the cytoplasm from the outer membrane. For NaHCO3 to be clinically effective, a high concentration must be introduced into the periodontal pocket and maintained there long enough to kill periodontal pathogens. Furthermore, NaHCO3 must be reapplied often enough to prevent recolonization by these pathogens. An advantage of NaHCO3 over NaF, SLS and other antimicrobial agents is its safety, availability and low cost.



PMID:6094783[PubMed

http://www.ncbi.nlm.nih.gov/pubmed/6094783
Anonymous
Posted: Saturday, January 7, 2012 7:55 AM
Originally posted by: swarfmaker

There was this book written by a guy named "Tom Warren" (I think) who claimed to have cured his "brain fog" by ridding himself of as many sources of inflammation as he could. One in particular I remember was pockets of infection left behind in the jawbone because the dentist did not clean out the sockets after extracting bad teeth. If I remember correctly, he wrote they used some sort of ultrasonic imaging device to find the pockets.

While this is an interesting idea to pursue for someone with mild cognitive impairment, or someone without any noticeable signs but bad teeth, I have to wonder if correcting tooth/gum problems would help someone with symptoms or not? I mean, has anyone ever heard of slowing or stopping dementia by addressing tooth/gum disease? Or, is it too late, and the bacteria has already spread to the brain? It sounds to me like the latter is the case. I don't mean "too late" as in nothing can be done, but rather, after fixing the tooth/gum disease problems, an aggressive regimen of antibiotics would have to be used to kill off the bacteria that have already infected the brain.

So, what about the herpes virus being found at the core of amyloid beta plaques?

What about the study done in Greece that seemed to link an infection of the stomach with H.pylori with AD?

Why does a urinary tract infection or other infection make a person with dementia so much worse?

The only theory I can come up with is that infections cause the body to produce TNF-alpha to fight the invasion and the brain becomes sensitive to this, so even a remote infection in the stomach or bladder makes things worse. Also, as I noted before in another post, maybe in the Greek study, the antibiotics used to fight the H.pylori killed off the spirochetes in the brain.
Anonymous
Posted: Saturday, January 7, 2012 7:55 AM
Originally posted by: swarfmaker

This was posted to "Antibiotics and AD" on October 01, 2009 10:11 PM:

"Antibiotics May Slow Alzheimer's-Related Cognitive Decline"
By Megan Rauscher
NEW YORK (Reuters Health) Oct 09 - Treatment with two antibiotics, doxycycline and rifampin, may curb cognitive decline in patients with symptoms of Alzheimer's disease, suggest results of a study presented Thursday at the 41st Annual Meeting of the Infectious Disease Society of America (IDSA) in San Diego.
The findings fuel the belief that infection is involved in the development of Alzheimer's disease. "These two antibiotics have high activity against Chlamydia pneumonia, which is theorized to play a role in Alzheimer's disease," Dr. Mark B. Loeb from McMaster University in Hamilton, Ontario, who led the study, told Reuters Health.
Previous research has shown that C. pneumoniae-infected cells are often and selectively present in areas of neuropathology in the AD brain (See Reuters Health report August 13, 199. This finding, coupled with in vitro findings suggesting that doxycycline and rifampin interfere with the build-up of amyloid beta, led to the current trial, Dr. Loeb said.
Conducted at five centers throughout Canada, the randomized triple-blinded study included 101 patients with symptoms consistent with mild-to-moderate Alzheimer's disease. Fifty-one were randomly assigned to 200 milligrams doxycycline plus 300 milligrams rifampin, and 50 to matching placebo daily for 3 months. The primary outcome was a change in Standardized Alzheimer's Disease Assessment Scale cognitive subscale at 6 months. Forty-three patients in the antibiotic arm and 39 in the placebo arm completed the study.
The rate of cognitive decline was lower among those taking antibiotics than among those taking placebo. "The difference in scores between the two groups was significant at 6 months, with a p value of 0.034," Dr. Loeb told Reuters Health.
He also noted that the "magnitude of the effect is actually in the ballpark range of the magnitude of the effect seen with cholinesterase inhibitors," the only medications approved by the U.S. Food and Drug Administration and Canadian Health Protection Branch to treat Alzheimer's disease. Patients in this study were on stable doses of cholinesterase inhibitors but were not responding well to them.
At 12 months, the apparent protective effects of antibiotic therapy on cognitive decline "was actually larger, but the difference between the two groups was not statistically significant," Dr. Loeb said. Patients treated with antibiotics also showed a "significantly reduced decline in Standardized Mini-Mental Status Exam Scores at 12 months and significantly less deterioration in functional status, depression, and dysfunctional behavior at 3 months," according to the meeting abstract.
There were no between-group differences in C. pneumoniae detection by polymerase chain reaction or antibodies (IgG or IgA).
These findings, Dr. Loeb said, clearly warrant additional studies. "We need more data. This is very interesting information but other groups should be conducting similar or larger controlled trials to see if these findings can be replicated," the researcher said.

http://alzheimers.infopop.cc/e...62104261/m/808107612
Anonymous
Posted: Saturday, January 7, 2012 7:55 AM
Originally posted by: swarfmaker

With observations like this, why has the idea taken so long to catch on? Why didn't the physicians follow through when they see someone respond so well to a course of antibiotics, why not continue them?

I saw the same thing with my father. Even though he was officially diagnosed with "multi-infarct demenentia", I think there is more going on. He responds to using MCT oils. And, every time he gets an infection, he gets much worse, and while on the antibiotics, he's more with it. And, he has bad teeth. For years I've tried to get him to do something about them, but he was so afraid of the dentist that he never did. (I have to think that once the bacteria reaches the brain, even fixing teeth/gum problems won't be enough, but might prevent a re-infection or exacerbation of symptoms.)

I don't know if I will be successful, but I'm going to see if I can get his PCP to put him on low dose Doxycycline or tetracycline.

Tetracycline is a "naturally occurring" substance. I read somewhere that archeologists think that the ancient Egyptians were skilled at culturing the mold that produces it. I guess it would produce a gold-colored mass floating on the top of beer, if they did things right.
 
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