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ALZHEIMER’S DISEASE LINKED TO BACTERIAL INFECTION, CLAIMS REPORT

“A new scientific report claims that Alzheimer’s Disease may be caused by spirochaetal bacteria.

The findings – reported in the July edition of the specialized scientific journal NeuroReport – presents novel data which could redirect current research into the causes of Alzheimer’s Disease.

Alzheimer’s Disease is characterized by a slow, progressive decline of cortical functions particularly cognition and memory. The disease is associated with the formation of plaques in the brain, the main component of which is a peptide called beta-amyloid.

Molecular and biochemical studies have shown that an excess of beta-amyloid is the primary event in Alzheimer’s Disease -  but to date its source has not been established.

This report by Judith Miklossy, from the University Institute of Pathology, Switzerland suggests that spirochaetal bacteria may be the source of this peptide.

Perhaps the most important implication of a spirochaetal cause of Alzheimer’s Disease is that, because of the long latent stage of the spirochaetal diseases (the time between the primary infection and the development of dementia, which may be as long as 43 years), the screening by diagnostic tests and the treatment of the younger population may prevent Alzheimer’s Disease. 

The research has been fully per-reviewed prior to acceptance for publication in this journal.

In an accompanying editorial the significance of the article is discussed. The authors comment that “If the current findings are confirmed in other laboratories, this would certainly rank among the most significant contributions in the history of medicine…”

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http://www.cnrs.fr/cw/fr/pres/compress/diabete.html

Communiqué de presse, Paris, le 2 mars 2000

Le diabète de type 2, une maladie inflammatoire
Un gène " suicide " du pancréas ouvre de nouvelles perspectives thérapeutiques

La découverte d’un nouveau gène et d’un nouveau mécanisme d’action par une équipe franco-suisse relance les perspectives de lutte contre le diabète dit de type 2. Selon l’Organisation mondiale de la santé (OMS), le diabète est la première épidémie non infectieuse qui touche l’humanité. Cette dramatique évolution qui survient dans des populations génétiquement prédisposées au diabète et à l’obésité est liée à la mondialisation du mode de vie occidental. Le diabète est une maladie familiale dont la survenue dépend de facteurs héréditaires et environnementaux étroitement intriqués. Les résultats sont publiés dans la revue Nature Genetics (2 mars 2000).

L’origine du diabète de type 2 est complexe. Jusqu’à présent on avait identifié deux causes principales : l’altération de la sécrétion d’insuline en réponse au glucose, et l’insensibilité des organes à l’insuline produite par le pancréas. Les équipes du Pr Gérard Waeber du CHUV de Lausanne et du Pr Philippe Froguel de l’UPRESA CNRS-Institut de biologie de Lille, Institut Pasteur de Lille et Université Lille 2 ? ont récemment identifié un nouveau gène du diabète, appelé IB-1 (Islet-Brain 1). Et, au-delà, les chercheurs ont découvert un nouveau mécanisme menant au diabète de type 2, l’inflammation des cellules pancréatiques sécrétrices d’insuline entraînant la mort programmée de ces cellules (un phénomène appelé apoptose).

D’après les observations, la cellule qui produit de l’insuline ne se comporte pas normalement en présence d’un gène IB-1 muté. Elle devient plus vulnérable à un stress et meurt plus facilement qu’une cellule non mutée. Cette sensibilité augmentée au stress induit un excès d’apoptose, c’est-à-dire une durée de vie réduite des cellules qui produisent de l’insuline. De plus, cette mutation est responsable d’une diminution de synthèse de l’insuline. La mutation IB-1 pourrait donc mener au diabète de deux manières. D’abord, en contribuant aux troubles de la production d’insuline qui surviennent très tôt dans l’histoire du diabète de type 2. Puis en participant à la destruction progressive des cellules insulino-sécrétrices, un phénomène bien établi chez l’animal diabétique et qui, chez l’homme, conduirait à l’insensibilité progressive aux médicaments antidiabétiques (sauf l’insuline) rencontrée chez la plupart des diabétiques. Même si les mutations d’IB-1 sont rares, ce gène dont l’expression semble bloquée par l’hyperglycémie chronique du diabète, pourrait donc jouer un grand rôle dans le diabète de type 2.

Ces résultats représentent l’aboutissement de trois années de travaux menés grâce à une approche " génomique " associant génétique humaine et génomique fonctionnelle. Gérard Waeber et ses collaborateurs ont initialement travaillé sur des lignées cellulaires produisant de l’insuline et ont identifié un gène, totalement inconnu jusqu’alors, impliqué dans le contrôle de la fonction de la cellule pancréatique. Sur cette base, le gène murin puis humain fut identifié et appelé " Islet-Brain 1 " car son expression maximale fut démontrée dans le cerveau et le pancréas. La localisation d’IB-1 sur le chromosome 11 humain a permis son étude chez l’homme diabétique par l’équipe de Philippe Froguel, et à la découverte d’une mutation du gène IB-1 chez tous les patients diabétiques d’une famille française disposant d’un grand arbre généalogique.

Les approches utilisées par le groupe franco-suisse sont originales pour plusieurs raisons. D’un côté, l’identification d’un gène candidat à la survenue d’un diabète humain s’est faite pour la première fois par une approche expérimentale utilisant des lignées cellulaires et des modèles animaux. De l’autre, ces données permettent de proposer la protéine IB-1 comme cible potentielle d’un traitement radicalement nouveau du diabète. En effet, la démonstration qu’une mutation d’un gène protecteur de la mort cellulaire puisse conduire au diabète modifie nos conceptions des causes du diabète de type 2. Il est possible que des médicaments bloquant le processus inflammatoire conduisant au " suicide " des cellules pancréatiques puissent arrêter l’évolution défavorable de cette maladie. Enfin, le succès de ces travaux confirme l’efficacité et la compétitivité internationale des réseaux européens de recherche médicale, quand les scientifiques sont capables de mettre en commun des compétences complémentaires pour assurer le succès du projet. D’ailleurs, un programme européen sur la génétique du diabète, appelé GIFT (Genomics Integrated Force on Type 2 diabetes), associant 12 équipes de 6 pays dont l’Université de Lausanne et l’Institut de biologie de Lille, vient de débuter, dont l’objectif est de trouver de nouveaux traitements du diabète grâce aux approches génomiques intégrées.

Références : The gene MAPK8IP1, encoding islet-brain-1, is a candidate for type 2 diabetes, G. Waeber, J. Delplanque, C. Bonny, V. Mooser, M. Steinmann, C. Widmann, A. Maillard, J. Miklossy, C. Dina, El Habib Hani, P. Nicod, P. Boutin, P. Froguel. Nature Genetics, 4 mars 2000.

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May 25, 2008

http://www.sciencedaily.com/releases/2008/05/080522155752.htm

The Emerging Role Of Infection In Alzheimer's Disease

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.Share This:14 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 dementia, is a form of amyloidosis. It has been known for a century that dementia, brain atrophy and amyloidosis can be caused by chronic bacterial infections, namely by Treponema pallidum in the atrophic form of general paresis in syphilis. Bacteria and viruses are powerful stimulators of inflammation. 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 apoptosis, 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 å4, 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."


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May 22, 2008, Amsterdam

http://iospress.metapress.com/content/334v885521112263/fulltext.pdf

PRESS RELEASE – FOR IMMEDIATE RELEASE

URL: www.j-alz.com  Researchers Explore the Emerging Role of Infection in Alzheimer’s Disease

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.

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 dementia, is a form of amyloidosis. It has been known for a century that dementia, brain atrophy and amyloidosis can be caused by chronic bacterial infections, namely by Treponema pallidum in the atrophic form of general paresis in syphilis. Bacteria and viruses are powerful stimulators of inflammation. 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 apoptosis, 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 ε4, 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.”

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Role of infections in Alzheimer's put under microscope

Wednesday, May 28, 2008

The emerging role of therapies designed to tackle the latent infections behind chronic diseases such as Alzheimer's is the subject of a special review of historic and new research in the field, according to reports. 

Medical News Today says the review in the Journal of Alzheimer's Disease has been guest edited by Judith Miklossy of the University of British Columbia in Canada and Ralph Martins of Australia's Edith Cowan University. 

It looks at several issues linked to the role of infectious agents in the development of Alzheimer's, as well as evidence on the involvement of spirochetes, Chlamydia pneumoniae and Herpes simplex virus type one in the disease. 

Ms Miklossy and Mr Martins said the independent reviews and observations contained in the journal demonstrate that "high priority" needs to be given to conducting further research into the subject, as there are "major implications" for healthcare and treatment. 

"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," they said. 

According to the World Health Organisation, Alzheimer's disease is estimated to affect around 18 million people worldwide. 
                                                                                      

COULD Alzheimer’s disease (AD) be caused in part by infection

 Evidence has gradually accumulated to suggest that this theory about the etiology of Alzheimer’s disease (AD) should be taken up more seriously. And the serious tone is evidenced now in a series of articles in a special May 2008 issue of the Journal of Alzheimer’s Disease as reported on ScienceDaily and EurekAlert! (Both ScienceDaily and EurekAlert have good summaries of the news, so I'm not attempting a summary here — just passing along the news.) 

 But hasn't public scientific discussion of AD centered primarily on the genetic bases for the disease, for which we have good accumulating evidence? (See e.g. Ertekin-Taner, 2007, below.) And doesn't the apparent genetic basis/susceptibility for AD rather contradict an infection-based theory about the causes of the disease? 
 
Yes … and most definitely No. The approaches are quite compatible. After all, genetics can determine in no small part, for example, one’s susceptibility to certain types of infection. So a disease may have significant genetic and environmental components — essentially a diathesis-stress model of disease. 

 Moreover, roughly 95% of cases of AD are non-familial late-onset Alzheimer’s disease (LOAD), also called “sporadic” AD, which has a number of known genetic risk factors — but risk factors aren't the same as determinants of the disease. Somehow such risk factors interact with environmental factors (in the broad sense of that phrase) to ultimately determine the course (if any) of the disease. 

 The work on AD is exciting and our growing understanding of its causes inspires hope that we'll eventually be able to treat and prevent this horrendous disease. 

 http://www.boehringer-ingelheim.co.uk/news/newsfeed.asp?id=18611792

http://www.boehringer-ingelheim.com/

http://search.eurekalert.org/e3/query.html?col=ev3rel&ht=0&qp=&qt=%2BAlzheimer%2C+infection&qs=&qc=ev3rel&pw=100%25&ws=0&qm=0&st=1&nh=10&lk=1&rf=0&rq=0&si=1

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 Friday May 23, 2008


Infections May Speed Alzheimer’s

By: Rick Nauert, Ph.D. Senior News Editor

Reviewed by: John M. Grohol, Psy.D. 

Emerging evidence suggests a number of chronic diseases are in fact caused by one or more infectious agents. The discovery opens potential lines of prevention by development of anti-viral or anti-bacterial medications.

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.

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 dementia, is a form of amyloidosis. It has been known for a century that dementia, brain atrophy and amyloidosis can be caused by chronic bacterial infections, namely by Treponema pallidum in the atrophic form of general paresis in syphilis.

Bacteria and viruses are powerful stimulators of inflammation. 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 apoptosis, 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 å4, 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.”

Source: 

 http://www.eurekalert.org/pub_releases/2008-05/ip-ret052208.php

http://www.sciencedaily.com/releases/2008/05/080522155752.htm

http://www.iospress.com/pressreleases/jad_infection.pdf

 Article adapted by Medical News Today from original press release. http://www.j-alz.com/press/2008/20080522.html

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