The Emerging Role Of Infection In Alzheimer's Disease

23 May 2008

A number of chronic diseasesi 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 asthmai 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.

In a special issue of the Journal of Alzheimer's Disease published May 2008, guest editors Judith Miklossy, from The University of British Columbia, and Ralph N. Martins, from Edith Cowan University and Hollywood Private Hospital, Perth, Western Australia, and a group of experts explore this exciting topic.

Alzheimer's disease (AD), the most frequent cause of dementiai, is a form of amyloidosis. It has been known for a century that dementia, brain atrophy and amyloidosis can be caused by chronic bacterial infectionsi, namely by Treponema pallidum in the atrophic form of general paresis in syphilis. Bacteria and viruses are powerful stimulators of inflammationi. It was suggested by Alois Alzheimer and his colleagues a century ago that microorganisms may be contributors in the generation of senile plaques in AD.

The fact that pathogens may suppress, subvert or evade host defenses and establish chronic or latent infection has received little attention in the past. During infection, active oxygen and nitrogen species generated by inflammatory cells may cause DNA damage, induce apoptosisi, and modulate enzyme activities and gene expression. Depending upon the biology of the pathogen and the host defense mechanisms the organism can persist in the infected tissues and cause chronic inflammation and amyloid deposition. The outcome of infection is as much determined by the genetic predisposition of the patient as by the virulence and biology of the infecting agent. Environmental factors and nutrition are critical determinants of disease expression as well.

In this special issue a series of reviews draws attention to both historic and recent observations related to this emerging field of AD research. The first review shows the importance of chronic inflammation in AD, followed by three articles presenting evidence on the involvement of spirochetes, Chlamydia pneumoniae and Herpes simplex virus type 1 in AD. These are followed by a review of amyloid proteins, which occur in many cellular forms in Eukaryotes and Prokaryotes.

The link between several viral and bacterial infections and the most significant genetic factor for AD, APOE a4, is discussed in the next review. The link between excessive or misplaced iron and a variety of neurodegenerative diseases and infection is reviewed in the final article.

According to Miklossy and Martins, "The historic and new observations reviewed in this special issue clearly show that high priority should be given for further research in this field as it may have major implications for public health, treatment, and prevention as adequate anti-bacterial and anti-viral drugs are available. Treatment of a bacterial infection and associated viral infection may result in regression and, if started early, prevention of disease. The impact on reducing healthcare costs would be substantial."

----------------------------
Article adapted by Medical News Today from original press release.
----------------------------

Source: Astrid Engelen
IOS Press <

Article URL: http://www.medicalnewstoday.com/articles/108565.php<

 

Another indicator that doctors and scientist were on the right track a long time ago, and we seem to have lost our way in between times.   Maybe the weight of evidence will eventually reach the awareness of todays 'experts'.

Michèle (UK) GFAi: Wheldon CAPi 1st May 2006. Daily Doxyi, Azi MWF, metroi pulse. Zoo keeper for Ella, RRMSi, At worse EDSSi 9, 3 months later 7 now 5.5 Wheldon CAP 16th March 2006

Michèle (UK) GFAi: Wheldon CAPi 1st May 2006. Daily Doxyi, Azi MWF, metroi pulse.

Will add this to the thread.

Have given the research papers in the link below by Alan MacDonald, MD, a  credible medical center/research pathologist to several caregivers of Alzheimer patients.

Dr. MacDonald's work reminds me a lot of Barry Marshall's work on H. Pylorii

Hmmm... Pathologist consistently finds bacteria where they are not suppose to be...causing what they are not known to cause...  same could be said of microbiologist consistently finding bacteria...

Here< is the link to his research page.

All four of the links at the bottom of the page are worthy of reading (IMHOi).

Daisy - Husband on CAPi 5/07.   Roxyi, Diflucan, Rifampin, Bactrim DS, Mepron 4-6, Prednisone, Novantrone, Doxyi, Azithromycin, Flagyli, Minoi<

Daisy - Husband on CAPi 5/07.  Husband died from Acute Myelogenous Leukemia Secondary to the Infusion of Novantrone.  Ie - the treatment with the conventional MSi drugs killed him.

Daisy on her own CAP 11/2012. 

Here's one of my favorite excerpts from one Dr. MacDonald's papers,

Substitute CPNi where it says spirochete, substitute Reticular body where it says corkscrew, etc, etc...... and the quote is applicable to CPN too,

"Stereotypes of what a spirochete "should" look like, have actually produced a state of "perseveration" in spirochetal pathobiology.  We have been "stuck" like a broken record on the corkscrew form, and have failed to see the rest of the life cycle. 

Cystic, granular, and cell wall deficient spirochetal profiles, which were well known in the 19th and 20th centuries in such titans as Schaudin, Hoffman, Noguchi, Delamater, Steiner and Mattman, hae been repudiated by professional microbiologists, and by pathologists who practice and who confer the status of 21st century truths in microbiology matters. 

Proper microscopic study as required by Dr. Robert Koch's second postulate, for establishing links between microbes and disease, presupposes that the microscopist be aware of the complete array of morphologic repertoires of the alledged pathogen."

This physician express his indignation at the medical communities refusal to look at the microscopic evidence of the pathogen as well as any I have read.

His writings definitely remind me of Barry Marshall's. 

DUH ???? - Dr. MacDonald clearly seems to be saying - How can you treat a pathogen if you don't know and address all of it's life forms ?

  Daisy - Husband on CAPi 5/07.   Roxyi, Diflucan, Rifampin, Bactrim DS, Mepron 4-6, Prednisone, Novantrone, Doxyi, Azithromycin, Flagyli, Minoi<

Daisy - Husband on CAPi 5/07.  Husband died from Acute Myelogenous Leukemia Secondary to the Infusion of Novantrone.  Ie - the treatment with the conventional MSi drugs killed him.

Daisy on her own CAP 11/2012. 

Also - while I am on a roll today, Laughing, the title of the article Jim first referenced should perhaps be "Revitalizing Ignored Knowledge of the Role of Infection..." .    The role of microbes in "autoimmune" diseasesi has been known for well over 100 years. 

Thought of this bit about who really first discovered HPylori in ulcers (clue - it wasn't Barry Marshall).

From Paul Ewald: In 1874, Arthur Boettcher, a microbe hunter, published a paper on a small, curved bacterium that he found repeatedly in stomach ulcers. Over the next fifty years, others confirmed the findings, even experimentally transmitting the bacterium to lab animals. In the late 1940s peptic ulcers were being successfully treated with antibioticsi, Aureomycin (chlortetracycline), in New York hospitals. Then, around 1950, discussion of infectious causation of ulcers disappeared from the literature and the treatment regimen. Medical texts from 1950 through early 1990s attributed peptic ulcers to gastric acidity, smoking, acohol consumption, and genetic preidspositions--anything but infection.

Around 1980, after three decades of medical impotence against ulcers, a young internist in Perth, Australia named Barry Marshall noticed the curved bacteria in tissue samples of ulcer patients. Microbiologists found the bacilli in all their duodenal ulcer patients and 80% of peptic ulcers. In 1982 they cultured Helicobacter pylori

"It is not clear why almost all medical experts ignored for four decades the evidence that ulcers could be caused by infection." (page 100).

Paul Ewald< is a professor of biology at Amherst College.

LeGac, Steiner, Brorsons, Stratton, etc... the clues are all there...

Daisy - Husband on CAPi 5/07.   Roxyi, Diflucan, Rifampin, Bactrim DS, Mepron 4-6, Prednisone, Novantrone, Doxyi, Azithromycin, Flagyli, Minoi<

Daisy - Husband on CAPi 5/07.  Husband died from Acute Myelogenous Leukemia Secondary to the Infusion of Novantrone.  Ie - the treatment with the conventional MSi drugs killed him.

Daisy on her own CAP 11/2012. 

From NeuroReport Vol. 4 No. 7 July 1993 [pages 841-848]

Alzheimer's disease--a spirochetosis?

Judit Miklossy

University Institute of Pathology, Division of Neuropathology,
University of Lausanne, Rue du Bugnon 27, 1005 Lausanne, Switzerland

The aetiology of Alzheimer's disease (AD), which affects a large proportion of the aged population is unknown and the treatment unresolved. The role of beta amyloid protein (ßA4), derived from a larger amyloid precursor protein (APP) in AD is the subject of intense research.

Here I report observations that in 14 autopsy cases, with histopathologically confirmed AD, spirochetes were found in blood and cerebrospinal fluid and, moreover, could be isolated from brain tissue. Thirteen age-matched control cases were without spirochetes.

Reference strains of spirochetes and those isolated from brains of AD patients, showed positive immunoreaction with monoclonal antibody against the ß amyloid precursor protein. These observations suggest that spirochetes may be one of the causes of AD and that they may be the source of the ß amyloid deposited in the AD brain

 Daisy - Husband on CAPi 5/07.   Roxyi, Diflucan, Rifampin, Bactrim DS, Mepron 4-6, Prednisone, Novantrone, Doxyi, Azithromycin, Flagyli, Minoi<

Daisy - Husband on CAPi 5/07.  Husband died from Acute Myelogenous Leukemia Secondary to the Infusion of Novantrone.  Ie - the treatment with the conventional MSi drugs killed him.

Daisy on her own CAP 11/2012. 

 Daisy- this odd split between what microbiologists know and find and what medicine thinks it knows is indeed an old story. I'm stunned when I read medical studies concluding that 6 months of azithromycin didn't cure heart diseasei, therefore Cpni is not a causal factor. They clearly know nothing of the organism they are treating. Nothing about the persistant state even, quite common knowledge to microbiologists who understand it as a hallmark characteristic of Cpn. I'm sure the cardiologists included an ID doctor in the study thinking that this would cover the expertise needed, but we all know how ignorant that group is about Cpn. They may be more resistant than neurologists to considering infectious sources to "autoimmune" problems. 

It seems to me that the difficulty is that microbiologists are doing basic science and medicine thinks it is scientific, but it's science is derivative of the basic science. Medical science tends to circulate somewhat stagnantly within it's own pond and only changes when the basic science reaches a point of flood stage that slops into the medical pond. Basic science work accumulates very slowly, so the floods don't happen often. And the money put into microbiology is tiny compared to pharmaceutical and surgical technology, because microbes are not seen to be the problem they once were. After all, they don't cause heart disease, or MS, or cancer do they? (Tongue firmly in cheek here!)

To grossly extend an already overwrought metaphor: who has the motivation to break the boundaries between these waters? The patients who are sinking beneath the stagnant waters of Medical practice, hoping for an incoming wave t push us to the banks! Thank God for the internet, by which means we can bypass such stagnant ignorance and inform ourselves.

CAPi for Cpn 11/04. Dxi: 25yrs CFSi & FMSi. Protocol: 200mg Doxyi, 300mg Roxithromycin, Tinii 1000mg/day pulses; Vit D1000 units, Iodoral 50mg, T4 & T3

 

CAPi for Cpni 11/04. Dxi: 25+yrs CFSi & FMSi. Currently: 250 aithromycin mwf, doxycycline 100mg BIDi, restarted Tinii pulses; Vit D2000 units, T4 & T3, 6mg Iodoral

Here, Here!

Jim K & Daisy, thanks so much for posting the history & the latest & greatest research.  It is truly sad that medicine has turned over to the pharmaceutical industry.  A better balance would be great for us patients!  Not so good in the pocket books of big pharma though.

I have passed this link on to my spouse & my father, Mum having stomach problems.

CFIDSi/ME 26yrs, FMSi, IBSi<, EBVi, CMV, Cpni, chronic insomnia, Lymes, HME, Natural HRT peri-M, NACi 2.5 gm, 6-07 Doxy 200 mg day pm, Azith 375 mg M/W/Fday, Pulse#10 1000 mg 3 days & 750mg 2 days, 5-17-8

CFIDSi/ME, FMSi, MCS, IBSi, EBVi, CMV, Cpni, H1, chronic insomnia, Chronic Lyme, HME, Babesia, Natural HRT-menopause, NAC 2.4 gm,Full CAP 6-2-07, all supplementsi+Iodorol, Inositol-depression, ultra Chitosan, L lysine Pulse#27 04-19-10 1gm Flagyli/day-5 days<

Thanks, Daisy and Jim.  Excellent roll and commentaries so well stated and supported.  I certainly want to hold onto this thread and it's continued conversation. 

Louise, CFSi. CPnPositive. BbPositive. WheldonCAP began6/24/07. NACi,Doxyi, Roxi,FullTiniPulses. Intermittent Cholestyramine,1-2packets, at bedtime,most often with pulses,and as needed, for Phorphoria & liposacaride Endotoxini Die-OffExperiences.

  • CAPi(TiniOnly): 06/07-02/09 for CFSi<
  • MethylationProtocolSupplements: Started08/08
  • Intermtnt CAP: 02/09-02/10
  • Full MethylProtocol & LDNi 02/09
  • Off CAP: 02/10, cont LDN & MethlyProtocol support
  • <

Comment viewing options

Select your preferred way to display the comments and click "Save settings" to activate your changes.