"Give with a free hand, but give only your own."
 -- J.R.R. Tolkien
The Children of Hurin
- The Role of Infection and Inflammation in Neurodegenerative Diseases -
Where fact and theory are incompatible, it is theory, not fact, that needs to be amended.”

Cat's Claw
Chlamydia pneumoniae
ChitosanBrain Inflammation
Green Tea
Helicobacter pylori

Herpes Simplex Virus
Immune System Reponse
Lyme Disease
Porphyromonas Gingivalis

TNF Alpha


Here’s a wild idea.  Epidemiological studies in India have found that the incidence of AD in that country are quite low [Reference].  We have been thinking that this is due to the curcumin content of curry powder (via turmeric) used in Indian cooking.  However, most of us have been assuming that the objective is to get the curcumin into the blood.  Maybe this shouldn’t be our only objective.  Turmeric has been used for millennia as a food preservative.  Therefore, it is reasonable to assume that it has some bactericidal properties.  Could it be that exposing the spirochete bacteria in the mouth to turmeric kills off a strain that causes AD?  The same goes for green tea.  The incidence of dementia for those who consume green tea regularly is lower. [Reference].  Naturally, I thought that that throwing a few green tea extract supplements into the daily supplement regimen would do the trick.  But again, maybe it is the exposure of harmful bacteria to the tea in the mouth that is responsible for its effectiveness.  Green tea appears to also have bactericidal properties [Reference].  The same could be said for whole cinnamon, red wine, and who knows what else.  I’m sure that pharmaceuticals or chemicals such as lowly old baking soda may be even more effective.  Somewhere I read someone speculating about the “life cycle” of these spirochetes.  Do they multiply only in the mouth and travel to the brain (and other organs), or do they multiply in the other organs once they get there?  The latter seems more likely, but if the former is true, then there seems to be good reason to aggressively pursue ways to killing them off in the mouth.

Spirochetes, at least the Treponema varieties I’ve read about so far, are “anaerobic”:  They don’t do well in oxygen.  This might explain why exercising and activity is linked to reduced or at least delayed dementia.  It may also be why sleep apnea sometimes leads to cognitive impairment.

The spirochete Borellia burgdorferi that causes Lyme disease appears to be incredibly difficult to eradicate.  It may not be possible to rid the body of the periodontal spirochetes either.

Brain Inflammation The Role of Brain Inflammation in Neurodegenerative Diseases

See also    AFA, ALA, Anatabine, Blueberries, Cat's Claw, CCSVI, Chitosan, Cinnamon, Curcumin,
         Enbrel (Etanercept), Herpes simplex virus (HSV-1), Infection and Immune System Response,
                           Journal of Neuroinflammation, Leukine, Porphyromonas Gingivalis, NSAIDs, Nypta, TNF-Alpha,
         Urinary Tract Infection (UTI),

There are so many references in my notes to the suspected role of brain inflammation in neurodegenerative diseases that I thought that a section dedicated to this topic was warranted.

Anyone who had cared for someone with dementia has no doubt witnessed the sudden and alarming decline associated with an infection or immune system response to even a vaccination.  People with dementia seem extremely sensitive to the body's response to infection no matter where it is.  This should be a significant clue to medical researchers.  For us caregivers, the course of action is to find ways to address infections as soon as possible, and to make the dementia patient's medical professional caretakers aware of any possible "smoldering" infections such as a UTI, stomach ulcers, Lyme disease, and especially bad teeth.  The medical profession seems reluctant to pursue this course as a means of preventing or treating dementia.  Sad really, since treating infections is something that they have been doing for over a hundred years. 

Potential Alzheimer's Treatment? Newly Discovered Role for Enzyme in Neurodegenerative Diseases

ScienceDaily (Mar. 11, 2011) — Neurodegenerative diseases like Alzheimer's and Parkinson's are partly attributable to brain inflammation... "The caspases are a group of enzymes known for causing cell death," says Associate Professor Bertrand Joseph, who headed the study. "That they also serve as signal molecules that govern that activity of other cells was an unexpected discovery that gives them an entirely new physiological role."...

Neurospirochetosis (Spirochetes)

The contents of this section have been moved to the Neuorspirochetosis page.

Tetracyclines (Tetracycline, Doxycycline)

The contents of this section have been moved to the Tetracycline page.

***************************************************************************************** ***
Lyme Disease (Borrelia burgdorferi)

The contents of this section have been moved to the Lyme Disease page.

Infection and Immune System Response:

See also Helicobacter pylori

"A number of chronic diseases are in fact caused by one or more infectious agents. For example, stomach ulcers are caused by Helicobacter pylori, chronic lung disease in newborns and chronic asthma in adults are both caused by Mycoplasmas and Chlamydia pneumonia, while some other pathogens have been associated with atherosclerosis. The realization that pathogens can produce slowly progressive chronic diseases has opened new lines of research into Alzheimer's disease."

Here are some excerpts from an article found on ScienceDaily.com:

Cold Sore Virus Linked To Alzheimer's Disease: New Treatment, Or Even Vaccine Possible
ScienceDaily (Dec. 7, 2008)

"Professor Itzhaki explains: "We suggest that HSV1 enters the brain in the elderly as their immune systems decline and then establishes a dormant infection from which it is repeatedly activated by events such as stress, immunosuppression, and various infections."

"The ensuing active HSV1 infection causes severe damage in brain cells, most of which die and then disintegrate, thereby releasing amyloid aggregates which develop into amyloid plaques after other components of dying cells are deposited on them."

"Her colleague Dr Matthew Wozniak adds: "Antiviral agents would inhibit the harmful consequences of HSV1 action; in other words, inhibit a likely major cause of the disease irrespective of the actual damaging processes involved, whereas current treatments at best merely inhibit some of the symptoms of the disease..."

"They believe the herpes simplex virus is a significant factor in developing the debilitating disease and could be treated by antiviral agents such as acyclovir, which is already used to treat cold sores and other diseases caused by the herpes virus."

Another earlier article:

New Evidence Found Linking Herpes And Alzheimer’s
ScienceDaily (May 12, 2000)
"Could Lead to New Treatments Targeting the Herpes Virus"

"Researchers have long suspected a connection between the herpes virus and Alzheimer’s disease. A new study provides a potential explanation that could lead to development of a vaccine to prevent the disease or new drugs to treat it, according to the researchers. The study appears in the May 16 issue of Biochemistry, a peer-reviewed publication of the American Chemical Society, the world’s largest scientific society."

"Researchers at the University of California, Irvine, demonstrated that a synthetic protein that resembles the herpes simplex 1 virus (HSV-1) mimics the structure and function of a protein called beta-amyloid, a toxic agent that accumulates in the brains of Alzheimer’s patients."

"Genetic sequencing revealed that two-thirds of a portion of the viral protein is identical to the beta-amyloid protein. The researchers showed that, like beta-amyloid, it could kill brain neurons, a key feature in the development of Alzheimer’s. Moreover, in laboratory experiments, the viral protein formed abnormal twisted fibers like those found in the brains of Alzheimer’s patients — the definitive hallmark of the disease..."

And, another...

Cold Sore Virus Might Play Role In Alzheimer's
ScienceDaily (Jan. 3, 2007)
"A gene known to be a major risk factor for Alzheimer's disease puts out the welcome mat for the virus that causes cold sores, allowing the virus to be more active in the brain compared to other forms of the gene..."

From these articles (I suggest reading the full articles and others you can find), it seems to be a reasonable theory that this HSV1 virus invades the brain as one's immune system weakens with age, stress or truma. Infected cells then expire, leaving behind amyloid beta (AB). Some people's central nervous system (NS) are probably better than other people's at removing this amyloid beta. So, most people develop the classic characteristics of AD, which are loss of brain mass, clumps of AB, and intracellular tau tangles. Others, whose CNS clears out the AB still suffer the loss of brain mass as the disease ravages the brain, and other proteins accumulate, such as just the tau tangles or clumps of tau.  Could this be behind CBD?

What this theory says to me is that there is a chance that many of what today seem like separate neurodegenerative diseases may actually be manifestations of the same root cause: A virus. But it also says that most of the things we have been trying will ultimately fail. Enbrel addresses inflammatory responses. Methylene blue and cinnamon attack tau and maybe help neurons live longer. MCT's (coconut oil) and cinnamon address sugar metabolism. Lithium fights tau corruption. Curcumin is used in the hopes of reducing the AB load. Likewise with all of the other the pharmaceuticals and supplements we have discussed and had such hopes for.

But, none of these attack what might be the root cause, HSV1; and if they don't, then their positive effects are all doomed to eventually be overwhelmed by the virus' insatiable hunger for brain cells. It is every bit as horrific as the plot from some "B" science fiction movie.

Does anyone have experience with this drug they mention in the first article, acyclovir? What is the likelihood that a physician would prescribe this drug to someone suspected of having AD just to see if it helps?

[NOTE:  Jan. 17, 2009: Recently, some people have mentioned in posts to some discussion forums that curcumin, resveratrol and lauric acid (coconut oil!) may fight the HSV-1 virus. Need to find more info and links to sources.]

I've read before about urinary tract infections causing a sudden worsening of AD symptoms. The question that came to my mind was, why does this happen?

I think I have a possible answer. And with this answer comes the opportunity to do something for someone suffering from AD.

There was a small two-year study done in Greece that was recently published. 50 subjects with AD symptoms were tested for the presence of a Helicobacter pylori (Hp) infection (the bacteria that is said to cause most stomach ulcers). It turned out that nearly 90% of the subjects had H.pylori. So the researchers treated the infection. Eradication of the bacteria was successful in about 85% of the cases. The amazing thing was that in ALL of the 85% where the eradication of the H.pylori was successful, their AD symptoms did not progress over the 2 years of the study, and in fact, their mental abilities improved somewhat. Even though this was a very small study with only 50 participants, to me the results say that there might be something to this that we can use.

How can an H.pylori infection of the stomach affect the brain? The researchers speculated that the body produces substances in its fight against the bacteria that might have deleterious side effects when the blood carries them to the brain. One of these substances is called "tumor necrosis factor alpha", (TNF-alpha).

Last year, there was some excitement over a drug being researched called "Rember". It was theorized that this drug acted directly on the tau protein of the neurons to prevent them from becoming corrupted, or to even dissolve clumps and tangles of currupted tau that had already formed. The researchers were disappointed to discover that the highest dose pill they used was not effective because, unlike its smaller dose cousins, the 100mg pill dissolved in the intestines rather than the stomach. What is "Rember"? Well, it is essentially methylene blue. And methylene blue happens to be an antibiotic known to kill off H.pylori.

Let's go to the other side of the Earth for another piece of the puzzle. In California there is this controversial physician, Dr. Tobinick, who discovered by accident that when he injected the arthritis drug Enbrel into the spines of his patients suffering from spinal arthritis, sometimes their AD symptoms would suddenly improve in a matter of minutes. How could this happen? Well, Enbrel blocks the effects of TNF!

What does this have to do with urinary tract infections? Could a UTI cause the body to produce TNF? A quick search of the Internet with Google using the two phrases "tumor necrosis factor" "urinary tract infection" makes me think that, yes indeed, we may have the connection. The body produces TNF in its fight against the UTI bacteria, which is then circulated by the blood to the brain.

What can you do with this? Find out if your loved one with AD symptoms has a chronic infection. Look for H.pylori, a UTI, maybe even pockets of infection in the jaw left over from a tooth problem. Periodontal (gum) disease may increase the risk of cognitive dysfunction associated with Alzheimer's disease in healthy individuals as well as in those who already are cognitively impaired. Another possibility is the presence of Lyme disease. If they have one of these infections, get it treated.

The Pathogen Hypothesis (Live Discussion on www.alzforum.org)
Moderator’s summary: Pathogens as a cause of Alzheimer’s disease
By June Kinoshita

The notion that microbes such as herpes simplex virus 1 (HSV1) and Chlamydophila pneumoniae (Cp) could be a causal factor in Alzheimer’s diseases would probably be viewed by the main stream of AD researchers as being beyond the pale. Although a small body of recent findings has reported strikingly strong associations between these pathogens and AD [1,7], subsequent attempts to replicate the findings have met with mixed results (discussed in [10]). At this juncture, it might be convenient to dismiss the hypothesis, but as both sides of this debate session agreed, there are plausible reasons for these discrepancies that deserve to be resolved through further research. While opinions diverged on the strength of evidence for and against the hypothesis, there was a consensus that the possibility of common infectious agents causing such a widespread scourge of old age is one that is too important to ignore.

Among Older Patients, Severe Sepsis Associated With Development of Cognitive and Functional Disability
ScienceDaily (Oct. 27, 2010)
Older adults who survived severe sepsis were more likely to develop substantial cognitive impairment and functional disability, according to a study in the October 27 issue of JAMA... The researchers found that the prevalence of moderate to severe cognitive impairment increased 10.6 percentage points among patients who survived severe sepsis, and their odds of acquiring moderate to severe cognitive impairment were 3.3 times higher. Also, a high rate of new functional limitations was seen following sepsis, with an additional average increase of 1.5 new functional limitations per person among those with no or mild to moderate pre-existing functional limitations.

Nonsepsis general hospitalizations were associated with no change in moderate to severe cognitive impairment and with the development of fewer new limitations.

"Cognitive and functional declines of the magnitude seen after severe sepsis are associated with significant increases in caregiver time, nursing home admission, depression, and mortality. These data argue that the burden of sepsis survivorship is a substantial, underrecognized public health problem with major implications for patients, families, and the health care system."...


The contents of this section have been moved to the TNF-Alpha page.


(Water-soluble Chitosan, chitosan oligosaccharide)The contents of this section have been moved to the Chitosan page.

Cat's Claw  (Uncaria tomentosa, Una de Gato)

The contents of this section were moved to the Cat's Claw page.

Helicobacter pylori (the stomach ulcer bacteria):

The contents of this section have been moved to the Helicobacter pylori page.

Green Tea (EGCG, epigallocatechin gallate)

The contents of this section have been moved to the Green Tea page.

Tooth/Gum Health

The contents of this section have been moved to the Gum Health page.

Herpes Simplex Virus

The contents of this section have been moved to the Herpes Simplex Virus page.


Common Bacteria May Trigger or Accelerate the Disease
WebMD Health News

Oct. 11, 2002 -- Evidence is growing that there may be a link between a common bacterial infection and Alzheimer's disease. New research shows mice exposed to the bacteria developed Alzheimer's-like deposits in their brains.

The study found that when the bacteria were sprayed into the noses of healthy laboratory mice, it caused the growth of amyloid plaques in their brains, which are the same type of brain-clogging deposits found in people with Alzheimer's disease.

Previous research by the same group revealed that the bacterium, known as chlamydia pneumoniae or C. pneumoniae, was present in the brains of 90% of people who had died of Alzheimer's disease...


Immunohistological detection of Chlamydia pneumoniae in the Alzheimer's disease brain.
BMC Neurosci. 2010 Sep 23;11:121. doi: 10.1186/1471-2202-11-121.
Hammond CJ, Hallock LR, Howanski RJ, Appelt DM, Little CS, Balin BJ.
Source: Pathology/Microbiology/Immunology and Forensic Medicine Department, Philadelphia College of Osteopathic Medicine, 4170 City Ave, Philadelphia, Pennsylvania, USA.
PMID:20863379 [PubMed] PMCID:PMC2949767

Chlamydophila pneumoniae and the etiology of late-onset Alzheimer's disease.
J Alzheimers Dis. 2008 May;13(4):371-80.
Balin BJ, Little CS, Hammond CJ, Appelt DM, Whittum-Hudson JA, Gérard HC, Hudson AP.
Source: Department of Pathology, Microbiology, Immunology and Forensic Medicine, Philadelphia PA 19131, USA.
PMID:18487846 [PubMed]

Inhibition of apoptosis in neuronal cells infected with Chlamydophila (Chlamydia) pneumoniae.
BMC Neurosci. 2008 Jan 24;9:13. doi: 10.1186/1471-2202-9-13.
Appelt DM, Roupas MR, Way DS, Bell MG, Albert EV, Hammond CJ, Balin BJ.
Source: Department of Neuroscience, Physiology & Pharmacology, Philadelphia College of Osteopathic Medicine, Philadelphia, USA.
PMID: 18218130 [PubMed]
PMCID: PMC2266938

Chlamydophila (Chlamydia) pneumoniae in the Alzheimer's brain.
FEMS Immunol Med Microbiol. 2006 Dec;48(3):355-66. Epub 2006 Oct 18.
Gérard HC, Dreses-Werringloer U, Wildt KS, Deka S, Oszust C, Balin BJ, Frey WH 2nd, Bordayo EZ, Whittum-Hudson JA, Hudson AP.
Source: Department of Immunology and Microbiology, Wayne State University School of Medicine, Detroit, MI 48201, USA.
PMID: 17052268 [PubMed]

Infiltration of the brain by pathogens causes Alzheimer's disease.
Neurobiol Aging. 2004 May-Jun;25(5):619-27.
Itzhaki RF, Wozniak MA, Appelt DM, Balin BJ.
Source: Department of Optometry and Neuroscience, University of Manchester Institute of Science and Technology (UMIST), Manchester M60 1QD, UK.
PMID: 15172740 [PubMed]

Chlamydia pneumoniae induces Alzheimer-like amyloid plaques in brains of BALB/c mice.
Neurobiol Aging. 2004 Apr;25(4):419-29.
Little CS, Hammond CJ, MacIntyre A, Balin BJ, Appelt DM.
Source: Department of Pathology, Microbiology, and Immunology, Philadelphia College of Osteopathic Medicine, 4170 City Avenue, Philadelphia, PA 19131, USA.
PMID: 15013562 [PubMed]

Chlamydia pneumoniae infection promotes the transmigration of monocytes through human brain endothelial cells.
J Neurosci Res. 2003 Mar 1;71(5):740-50.
MacIntyre A, Abramov R, Hammond CJ, Hudson AP, Arking EJ, Little CS, Appelt DM, Balin BJ.
Source: Department of Biomedical Sciences, Philadelphia College of Osteopathic Medicine, Philadelphia, Pennsylvania, USA.
PMID: 12584732 [PubMed]

Role of infection in Alzheimer's disease.
J Am Osteopath Assoc. 2001 Dec;101(12 Suppl Pt 1):S1-6.
Balin BJ, Appelt DM.
Source: Department of Pathology/Microbiology, Philadelphia College of Osteopathic Medicine, Pennsylvania 19131, USA.
PMID: 11794745 [PubMed]

Identification and localization of Chlamydia pneumoniae in the Alzheimer's brain.
Med Microbiol Immunol. 1998 Jun;187(1):23-42.
Balin BJ, Gérard HC, Arking EJ, Appelt DM, Branigan PJ, Abrams JT, Whittum-Hudson JA, Hudson AP.
Source: Department of Pathology and Laboratory Medicine, MCP-Hahnemann School of Medicine, Allegheny University of the Health Sciences, Philadelphia, PA 19102, USA.
PMID: 9749980 [PubMed]

1. Chronic Inflammation in the Brain Leads the Way to Alzheimer's Disease
ScienceDaily (July 2, 2012) — Research published July 2 in Biomed Central's open access journal Journal of Neuroinflammation suggests that chronic inflammation can predispose the brain to develop Alzheimer's disease...

Systemic immune challenges trigger and drive Alzheimer-like neuropathology in mice.
Dimitrije Krstic, Amrita Madhusudan, Jana Doehner, Prisca Vogel, Tina Notter, Claudine Imhof, Abigail Manalastas, Martina Hilfiker, Sandra Pfister, Cornelia Schwerdel, Carsten Riether, Urs Meyer and Irene Knuesel.
Journal of Neuroinflammation, 2012 DOI: 10.1186/1742-2094-9-151

Systemic immune challenges trigger and drive Alzheimer-like neuropathology in mice.
Krstic D, Madhusudan A, Doehner J, Vogel P, Notter T, Imhof C, Manalastas A, Hilfiker M, Pfister S, Schwerdel C, J Neuroinflammation. 2012 Jul 2;9(1):151. [Epub ahead of print]Riether C, Meyer U, Knuesel I.
Alzheimer's disease (AD) is the most prevalent form of age-related dementia, and its effect on society increases exponentially as the population ages. Accumulating evidence suggests that neuroinflammation, mediated by the brain's innate immune system, contributes to AD neuropathology and exacerbates the course of the disease. However, there is no experimental evidence for a causal link between systemic infection or neuroinflammation and the onset of the disease.

The viral mimic, polyriboinosinic-polyribocytidilic acid (PolyI:C) was used to stimulate the immune system of experimental animals. Wild-type (WT) and transgenic mice were exposed to this cytokine inducer prenatally (gestation day (GD)17) and/or in adulthood. Behavioral, immunological, immunohistochemical, and biochemical analyses of AD-associated neuropathologic changes were performed during aging.

We found that a systemic immune challenge during late gestation predisposes WT mice to develop AD-like neuropathology during the course of aging. They display chronic elevation of inflammatory cytokines, an increase in the levels of hippocampal amyloid precursor protein (APP) and its proteolytic fragments, altered Tau phosphorylation, its mis-sorting to somatodendritic compartments, and significant impairments in working memory in old age. If this prenatal infection is followed by a second immune challenge in adulthood, the phenotype is strongly exacerbated, and mimics AD-like neuropathologic changes. These include deposition of APP and its proteolytic fragments, along with Tau aggregation, microglia activation and reactive gliosis. Whereas Abeta peptides were not significantly enriched in extracellular deposits of double immune-challenged WT mice at 15 months, they dramatically increased in age-matched immune-challenged transgenic AD mice, precisely around the inflammation-induced accumulations of APP and its proteolytic fragments, in striking similarity to the post-mortem findings in human patients with AD.

Chronic inflammatory conditions induce age-associated development of an AD-like phenotype in WT mice, including the induction of APP accumulations, which represent a seed for deposition of aggregation-prone peptides. The PolyI:C mouse model therefore provides a unique tool to investigate the molecular mechanisms underlying the earliest pathophysiological changes preceding fibrillary Abeta plaque deposition and neurofibrillary tangle formations in a physiological context of aging. Based on the similarity between the changes in immune-challenged mice and the development of AD in humans, we suggest that systemic infections represent a major risk factor for the development of AD.
PMID: 22747753 [PubMed]
Full Text: http://www.jneuroinflammation.com/content/9/1/151/abstract
Chronic Inflammation in the Brain Leads the Way to Alzheimer's Disease
ScienceDaily (July 2, 2012) — Research published July 2 in Biomed Central's open access journal Journal of Neuroinflammation suggests that chronic inflammation can predispose the brain to develop Alzheimer's disease…

Systemic immune challenges trigger and drive Alzheimer-like neuropathology in mice.
Dimitrije Krstic, Amrita Madhusudan, Jana Doehner, Prisca Vogel, Tina Notter, Claudine Imhof, Abigail Manalastas, Martina Hilfiker, Sandra Pfister, Cornelia Schwerdel, Carsten Riether, Urs Meyer and Irene Knuesel.
Journal of Neuroinflammation, 2012 DOI: 10.1186/1742-2094-9-151

Gabe Mirkin, M.D.

"Dr. Mark Loeb, associate professor at McMaster University in Hamilton, Ontario, presented a study in San Diego at the meeting of the Infectious Diseases Society of America (10/9/03) to show that antibiotics may slow brain damage caused by Alzheimer's disease. Patients on two antibiotics, doxycycline and rifampin, for three months had significantly less loss of mental function than those given placebos."

Infection and Immune System Response:

The Emerging Role Of Infection In Alzheimer's Disease
ScienceDaily (May 25, 2008) — A number of chronic diseases are in fact caused by one or more infectious agents. For example, stomach ulcers are caused by Helicobacter pylori, chronic lung disease in newborns and chronic asthma in adults are both caused by Mycoplasmas and Chlamydia pneumonia, while some other pathogens have been associated with atherosclerosis. The realization that pathogens can produce slowly progressive chronic diseases has opened new lines of research into Alzheimer's disease.

Tooth Loss, Dementia May Be Linked, Study Suggests
ScienceDaily (Oct. 11, 2007) — Tooth loss may predict the development of dementia late in life, according to research published in the October issue of The Journal of the American Dental Association.

Yahoo Group:  Dental Cleanse
"Dental Cleanup- removing one of the main causes of "incurable diseases" and curing "incurable" diseases. Amalgam, Root Canals, Cavitations Surgery (Curettment), Nickel / Gold Crowns, fluoride, dental risk. We are people sharing information on health hazard of Amalgam dental fillings,mercury, Root canal fillings, Gold and Nickel crowns, and other dental metal. We have been learning from:-Dr.Hulda Clark, Dr.Hall Higgins, Veston Price, Tom Warren and many other. "What is it about the mouth that makes this hazardous waste non-toxic?" - Sandra Denton, M.D. Dentists have the highest suicide and divorce rates among professional. Female dental personnel have a higher spontaneous abortion rate, a raised incidence of premature labour, and an elevated perinatal mortality. - --Research has demonstrated that 100% of all root canals result in residual infection due to the imperfect seal that allows bacteria to penetrate. The toxins given off by these bacteria are more toxic than mercury. These toxins can cause systemic diseases of the heart, kidney, uterus, and nervous and endocrine systems. --This list is for healthy people and for people suffering of degenerative diseases: Cancer,Leukemia,Colitis/Colitus,ALZHEIMER,MS,Irritable Bowel Syndrom,Chron's disease, Diverticolitis, Ulcerative Colitis,Constipation, Parasite Infections, Aids, Allergies, Asthma, Food intollerance, mercury - nickel-thalium - heavy metal poisoning ... "

Profiling the culprit in Alzheimer's disease (AD): bacterial toxic proteins - Will they be significant for the aetio-pathogenesis of AD and the transmissible spongiform encephalopathies?
Schmitt HP.
Institute of Pathology, Department for Neuropathology, University of Heidelberg, Germany.
Med Hypotheses. 2007;69(3):596-609. Epub 2007 Mar 6.

The aetiology of Alzheimer's disease (AD) and the transmissible spongiform encephalopathies (tSEs) is still elusive. The concept that prion protein (PrP(Sc)) is the aetiological agent (infectious protein) in the tSEs has recently been questioned. In AD, the cause of the aberrant cleavage of the beta-amyloid precursor protein (APP), resulting in the production of amyloidogenic Abeta fragments, has yet remained obscure. Moreover, the amyloid hypothesis of AD has been seriously challenged. In both AD and the tSEs, pathogens of various nature, including bacteria, have been discussed as possible causal factors. However, aetiological considerations have completely neglected microbial products such as the bacterial toxic proteins (BTPs). The present paper is aimed at drawing a "culprit profile" of these toxic molecules that can exert, at low-dosage, neuro-degeneration through various effects. Clearly, BTPs may affect cell-surface receptors including modulatory amine transmitter receptor expression, block neuro-transmitter release, increase intra-cellular Ca(2+) levels, affect intra-cellular signal transduction, change cyto-skeletal processing, alter synaptic transmission, influence APP proteolysis, interact with cell surface proteins like PrP(C) or their GPI anchors, act as chaperones inducing conformational change in proteins (e.g., PrP(C) to PrP(Sc)), alter lipid membrane integrity by affecting phospholipases or forming pores and channels, induce vacuolar (spongiform) change and elicit inflammatory reactions with cytokine production including cytokines that were demonstrated in the AD brain. Like PrP(Sc), BTPs can be heat-stable and acid-resistant. BTPs can meet the key-proteins of AD and tSEs in the lipid-rich domains of the plasma membrane called rafts. Basically, this might enable them to initiate a large variety of unfavourable molecular events, eventually resulting in pathogenetic cascades as in AD and the tSEs. All in all, their profile lends support to the hypothesis that BTPs might represent relevant culprits capable to cue and/or promote neuro-degeneration in both AD and the tSEs.
PMID: 17337124

Jean McCann
NeurologyReviews.com December 1999
Prions—proteinaceous infectious particles that lack nucleic acid—are most familiar as the pathogenic agents in Creutzfeld-Jakob disease in humans and scrapie in sheep. However, Dr. Prusiner suggested that they may also play a role in more common neurodegenerative diseases, including Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, and frontotemporal dementia. If the new compounds prove successful in treating Creutzfeld-Jakob disease and related conditions, they may provide a blueprint for intervention in these other diseases as well.

Eradication of Helicobacter pylori may be beneficial in the management of Alzheimer’s disease
Journal of Neurology Volume 256, Number 5 / May, 2009

"...At the 2-year clinical endpoint, cognitive and functional status parameters improved in the subgroup of patients where Hp eradication was successful..."

Abstract  Infectious agents have been proposed as potential causes of Alzheimer’s disease (AD). Recently, we documented a high prevalence of Helicobacter pylori (Hp) infection in patients with AD. We aim to access the effect of Hp eradication on the AD cognitive (MMSE: Mini Mental State Examination and CAMCOG: Cambridge Cognitive Examination for the Elderly) and functional (FRSSD: Functional Rating Scale for Symptoms of Dementia) status parameters. In the first part of the study, a total of 50 consecutive patients with AD and 30 age-matched anaemic controls underwent an upper gastrointestinal endoscopy, and gastric mucosal biopsies were obtained to detect the presence of Hp infection by histologic analysis and rapid urease test. Serum anti-Hp-specific IgG level was analysed by enzyme-linked immunosorbent assay. In the second part, Hp-positive AD patients received a triple eradication regimen (omeprazole, clarithromycin and amoxicillin), and all patients were followed up for 2 years, while under the same treatment with cholinesterase inhibitors. Hp was detected in 88% of AD patients and in 46.7% of controls (P < 0.001). Hp eradication was successful in 84.8% of treated patients. At the 2-year clinical endpoint, cognitive and functional status parameters improved in the subgroup of patients where Hp eradication was successful (P < 0.001 and P = 0.049 for MMSE and CAMCOG, respectively; P < 0.001 for FRSSD), but not in the other patients. Hp eradication may positively influence AD manifestations, suggesting a possible common link between Hp and AD.

Infections May Lead To Faster Memory Loss In Alzheimer's Disease
ScienceDaily (Sep. 8, 2009)
Getting a cold, stomach bug or other infection may lead to increased memory loss in people with Alzheimer's disease, according to research published in the September 8, 2009, print issue of Neurology®, the medical journal of the American Academy of Neurology.

The study found that people who had respiratory, gastrointestinal or other infections or even bumps and bruises from a fall were more likely to have high blood levels of tumor necrosis factor-α, a protein involved in the inflammatory process, and were also more likely to experience memory loss or other types of cognitive decline than people who did not have infections and who had low levels of the protein...

Gum Inflammation Linked to Alzheimer's Disease
ScienceDaily (Aug. 4, 2010) — NYU dental researchers have found the first long-term evidence that periodontal (gum) disease may increase the risk of cognitive dysfunction associated with Alzheimer's disease in healthy individuals as well as in those who already are cognitively impaired...

Immune System Linked With Accumulation of Toxic Tau Protein
ScienceDaily (Oct. 7, 2010)
Cells that help to protect the central nervous system may also contribute to pathological changes in the brain. New research, published by Cell Press in the October 7th issue of the journal Neuron, provides mechanistic insight into a link between the immune system and neurodegenerative disorders like Alzheimer's disease that are associated with abnormal accumulation of tau protein... "While some research has suggested a correlative link between neuroinflammation and tauopathies, there is little mechanistic evidence that altered microglial activation plays a pathogenic role in the formation of MAPT pathologies,"... In addition to documenting the effects of a specific microglial receptor on MAPT pathology, the researchers also gained new insight into specific signaling molecules downstream of the CX3CL1/CX3CR1 interaction. Taken together, the findings reveal a direct link between the activation of microglia and the abnormal phosphorylation and aggregation of MAPT in neurons and suggest potential novel therapeutic strategies for tauopathies...

Systemic immune challenges trigger and drive Alzheimer-like neuropathology in mice
Dimitrije Krstic, Amrita Madhusudan, Jana Doehner, Prisca Vogel, Tina Notter, Claudine Imhof, Abigail Manalastas, Martina Hilfiker, Sandra Pfister, Cornelia Schwerdel, Carsten Riether, Urs Meyer and Irene Knuesel
Journal of Neuroinflammation 2012, 9:151 doi:10.1186/1742-2094-9-151
Published: 2 July 2012

[The tobacco plant extract anatabine is also thought to be a strong anti-inflammatory.  It has also been shown in mouse studies to reverse AD.  But, mice are not men.  Still… might it be inhibiting the same processes?]

New Drug Could Treat Alzheimer's, Multiple Sclerosis and Brain Injury
ScienceDaily (July 24, 2012) — A new class of drug developed at Northwestern University Feinberg School of Medicine shows early promise of being a one-size-fits-all therapy for Alzheimer's disease, Parkinson's disease, multiple sclerosis and traumatic brain injury by reducing inflammation in the brain… By addressing brain inflammation, the new class of drugs -- represented by MW151 and MW189 -- offers an entirely different therapeutic approach to Alzheimer's than current ones being tested… MW151 and MW189 work by preventing the damaging overproduction of brain proteins called proinflammatory cytokines…
[No PubMed citation yet]


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Updated: August 27, 2011
Inception: August 27, 2011