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Book ; Online ; E-Book: Handbook of infection in Alzheimer's disease

Miklossy, Judith

(Advances in Alzheimer's disease ; 5)

2017

Author's details	edited by Judith Miklossy, MD, Ph.D
Series title	Advances in Alzheimer's disease ; 5
Collection
Language	English
Size	1 Online-Ressourcen (xiii, 406 Seiten), Illustrationen, Diagramme
Publisher	IOS Press
Publishing place	Amsterdam
Publishing country	Netherlands
Document type	Book ; Online ; E-Book
Remark	Zugriff für angemeldete ZB MED-Nutzerinnen und -Nutzer
HBZ-ID	HT019410594
ISBN	978-1-61499-706-1 ; 9781614997054 ; 1-61499-706-3 ; 1614997055
Database	ZB MED Catalogue: Medicine, Health, Nutrition, Environment, Agriculture

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Book ; Online: An Infectious Origin of Alzheimer's Disease: An End for This Devastating Disorder?

Miklossy, Judith / Tanzi, Rudolph / McCully, Kilmer / Perry, George / Cotman, Carl / Crean, StJohn / Richard Chapman, Matthew / Fulop, Tamas / McGeer, Patrick / David Moir, Robert / Allen, Herbert B.

2020

Keywords	Science: general issues ; Neurosciences ; Alzheimer's disease ; Amyloid ; Bacteria ; Infection ; Spirochetes ; Dementia ; Pathogens ; Biofilm ; Senile plaque ; Beta amyloid ; Tau ; Inflammation ; Bacterial amyloid ; HSV1 ; Virus
Size	1 electronic resource (190 pages)
Publisher	Frontiers Media SA
Document type	Book ; Online
Note	English ; Open Access
HBZ-ID	HT021231440
ISBN	9782889639038 ; 2889639037
Database	ZB MED Catalogue: Medicine, Health, Nutrition, Environment, Agriculture

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Article ; Online: Bacterial Amyloid and DNA are Important Constituents of Senile Plaques: Further Evidence of the Spirochetal and Biofilm Nature of Senile Plaques.

Miklossy, Judith

Journal of Alzheimer's disease : JAD

2016 Volume 53, Issue 4, Page(s) 1459–1473

Abstract: It has long been known that spirochetes form clumps or micro colonies in vitro and in vivo. Cortical spirochetal colonies in syphilitic dementia were considered as reproductive centers for spirochetes. Historic and recent data demonstrate that senile ... ...

Abstract	It has long been known that spirochetes form clumps or micro colonies in vitro and in vivo. Cortical spirochetal colonies in syphilitic dementia were considered as reproductive centers for spirochetes. Historic and recent data demonstrate that senile plaques in Alzheimer's disease (AD) are made up by spirochetes. Spirochetes, are able to form biofilm in vitro. Senile plaques are also reported to contain elements of biofilm constituents. We expected that AβPP and Aβ (the main components of senile plaques) also occur in pure spirochetal biofilms, and bacterial DNA (an important component of biofilm) is also present in senile plaques. Histochemical, immunohistochemical, and in situ hybridization techniques and the TUNEL assay were used to answer these questions. The results obtained demonstrate that Aβ and DNA, including spirochete-specific DNA, are key components of both pure spirochetal biofilms and senile plaques in AD and confirm the biofilm nature of senile plaques. These results validate validate previous observations that AβPP and/or an AβPP-like amyloidogenic protein are an integral part of spirochetes, and indicate that bacterial and host derived Aβ are both constituents of senile plaques. DNA fragmentation in senile plaques further confirms their bacterial nature and provides biochemical evidence for spirochetal cell death. Spirochetes evade host defenses, locate intracellularly, form more resistant atypical forms and notably biofilms, which contribute to sustain chronic infection and inflammation and explain the slowly progressive course of dementia in AD. To consider co-infecting microorganisms is equally important, as multi-species biofilms result in a higher resistance to treatments and a more severe dementia.
Language	English
Publishing date	2016-06-13
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	1440127-7
ISSN	1875-8908 ; 1387-2877
ISSN (online)	1875-8908
ISSN	1387-2877
DOI	10.3233/JAD-160451
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Historic evidence to support a causal relationship between spirochetal infections and Alzheimer's disease.

Miklossy, Judith

Frontiers in aging neuroscience

2015 Volume 7, Page(s) 46

Abstract: Following previous observations a statistically significant association between various types of spirochetes and Alzheimer's disease (AD) fulfilled Hill's criteria in favor of a causal relationship. If spirochetal infections can indeed cause AD, the ... ...

Abstract	Following previous observations a statistically significant association between various types of spirochetes and Alzheimer's disease (AD) fulfilled Hill's criteria in favor of a causal relationship. If spirochetal infections can indeed cause AD, the pathological and biological hallmarks of AD should also occur in syphilitic dementia. To answer this question, observations and illustrations on the detection of spirochetes in the atrophic form of general paresis, which is known to be associated with slowly progressive dementia, were reviewed and compared with the characteristic pathology of AD. Historic observations and illustrations published in the first half of the 20th Century indeed confirm that the pathological hallmarks, which define AD, are also present in syphilitic dementia. Cortical spirochetal colonies are made up by innumerable tightly spiraled Treponema pallidum spirochetes, which are morphologically indistinguishable from senile plaques, using conventional light microscopy. Local brain amyloidosis also occurs in general paresis and, as in AD, corresponds to amyloid beta. These historic observations enable us to conclude that chronic spirochetal infections can cause dementia and reproduce the defining hallmarks of AD. They represent further evidence in support a causal relationship between various spirochetal infections and AD. They also indicate that local invasion of the brain by these helically shaped bacteria reproduce the filamentous pathology characteristic of AD. Chronic infection by spirochetes, and co-infection with other bacteria and viruses should be included in our current view on the etiology of AD. Prompt action is needed as AD might be prevented.
Language	English
Publishing date	2015-04-16
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2558898-9
ISSN	1663-4365
ISSN	1663-4365
DOI	10.3389/fnagi.2015.00046
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Chronic or late lyme neuroborreliosis: analysis of evidence compared to chronic or late neurosyphilis.

Miklossy, Judith

The open neurology journal

2012 Volume 6, Page(s) 146–157

Abstract: Whether spirochetes persist in affected host tissues and cause the late/chronic manifestations of neurosyphilis was the subject of long-lasting debate. Detection of Treponema pallidum in the brains of patients with general paresis established a direct ... ...

Abstract	Whether spirochetes persist in affected host tissues and cause the late/chronic manifestations of neurosyphilis was the subject of long-lasting debate. Detection of Treponema pallidum in the brains of patients with general paresis established a direct link between persisting infection and tertiary manifestations of neurosyphilis. Today, the same question is in the center of debate with respect to Lyme disease. The goal of this review was to compare the established pathological features of neurosyphilis with those available for Lyme neuroborreliosis. If the main tertiary forms of neurosyphilis also occur in Lyme neuroborreliosis and Borrelia burgdorferi can be detected in brain lesions would indicate that the spirochete is responsible for the neuropsychiatric manifestations of late/chronic Lyme neuroborreliosis. The substantial amounts of data available in the literature show that the major forms of late/chronic Lyme neuroborreliosis (meningovascular and meningoencephalitis) are clinically and pathologically confirmed. Borrelia burgdorferi was detected in association with tertiary brain lesions and cultivated from the affected brain or cerebrospinal fluid. The accumulated data also indicate that Borrelia burgdorferi is able to evade from destruction by the host immune reactions, persist in host tissues and sustain chronic infection and inflammation. These observations represent evidences that Borrelia burgdorferi in an analogous way to Treponema pallidum is responsible for the chronic/late manifestations of Lyme neuroborreliosis.Late Lyme neuroborreliosis is accepted by all existing guidelines in Europe, US and Canada. The terms chronic and late are synonymous and both define tertiary neurosyphilis or tertiary Lyme neuroborreliosis. The use of chronic and late Lyme neuroborreliosis as different entities is inaccurate and can be confusing. Further pathological investigations and the detection of spirochetes in infected tissues and body fluids are strongly needed.
Language	English
Publishing date	2012-12-28
Publishing country	United Arab Emirates
Document type	Journal Article
ZDB-ID	2395982-4
ISSN	1874-205X ; 1874-205X
ISSN (online)	1874-205X
ISSN	1874-205X
DOI	10.2174/1874205X01206010146
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Emerging roles of pathogens in Alzheimer disease.

Miklossy, Judith

Expert reviews in molecular medicine

2011 Volume 13, Page(s) e30

Abstract: Chronic spirochetal infection can cause slowly progressive dementia, cortical atrophy and amyloid deposition in the atrophic form of general paresis. There is a significant association between Alzheimer disease (AD) and various types of spirochete ( ... ...

Abstract	Chronic spirochetal infection can cause slowly progressive dementia, cortical atrophy and amyloid deposition in the atrophic form of general paresis. There is a significant association between Alzheimer disease (AD) and various types of spirochete (including the periodontal pathogen Treponemas and Borrelia burgdorferi), and other pathogens such as Chlamydophyla pneumoniae and herpes simplex virus type-1 (HSV-1). Exposure of mammalian neuronal and glial cells and organotypic cultures to spirochetes reproduces the biological and pathological hallmarks of AD. Senile-plaque-like beta amyloid (Aβ) deposits are also observed in mice following inhalation of C. pneumoniae in vivo, and Aβ accumulation and phosphorylation of tau is induced in neurons by HSV-1 in vitro and in vivo. Specific bacterial ligands, and bacterial and viral DNA and RNA all increase the expression of proinflammatory molecules, which activates the innate and adaptive immune systems. Evasion of pathogens from destruction by the host immune reactions leads to persistent infection, chronic inflammation, neuronal destruction and Aβ deposition. Aβ has been shown to be a pore-forming antimicrobial peptide, indicating that Aβ accumulation might be a response to infection. Global attention and action is needed to support this emerging field of research because dementia might be prevented by combined antibiotic, antiviral and anti-inflammatory therapy.
MeSH term(s)	Alzheimer Disease/microbiology ; Animals ; Humans ; Mice ; Spirochaetales/physiology ; Spirochaetales Infections/microbiology
Language	English
Publishing date	2011-09-20
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ISSN	1462-3994
ISSN (online)	1462-3994
DOI	10.1017/S1462399411002006
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Alzheimer's disease - a neurospirochetosis. Analysis of the evidence following Koch's and Hill's criteria.

Miklossy, Judith

Journal of neuroinflammation

2011 Volume 8, Page(s) 90

Abstract: It is established that chronic spirochetal infection can cause slowly progressive dementia, brain atrophy and amyloid deposition in late neurosyphilis. Recently it has been suggested that various types of spirochetes, in an analogous way to Treponema ... ...

Abstract	It is established that chronic spirochetal infection can cause slowly progressive dementia, brain atrophy and amyloid deposition in late neurosyphilis. Recently it has been suggested that various types of spirochetes, in an analogous way to Treponema pallidum, could cause dementia and may be involved in the pathogenesis of Alzheimer's disease (AD). Here, we review all data available in the literature on the detection of spirochetes in AD and critically analyze the association and causal relationship between spirochetes and AD following established criteria of Koch and Hill. The results show a statistically significant association between spirochetes and AD (P = 1.5 × 10-17, OR = 20, 95% CI = 8-60, N = 247). When neutral techniques recognizing all types of spirochetes were used, or the highly prevalent periodontal pathogen Treponemas were analyzed, spirochetes were observed in the brain in more than 90% of AD cases. Borrelia burgdorferi was detected in the brain in 25.3% of AD cases analyzed and was 13 times more frequent in AD compared to controls. Periodontal pathogen Treponemas (T. pectinovorum, T. amylovorum, T. lecithinolyticum, T. maltophilum, T. medium, T. socranskii) and Borrelia burgdorferi were detected using species specific PCR and antibodies. Importantly, co-infection with several spirochetes occurs in AD. The pathological and biological hallmarks of AD were reproduced in vitro by exposure of mammalian cells to spirochetes. The analysis of reviewed data following Koch's and Hill's postulates shows a probable causal relationship between neurospirochetosis and AD. Persisting inflammation and amyloid deposition initiated and sustained by chronic spirochetal infection form together with the various hypotheses suggested to play a role in the pathogenesis of AD a comprehensive entity. As suggested by Hill, once the probability of a causal relationship is established prompt action is needed. Support and attention should be given to this field of AD research. Spirochetal infection occurs years or decades before the manifestation of dementia. As adequate antibiotic and anti-inflammatory therapies are available, as in syphilis, one might prevent and eradicate dementia.
MeSH term(s)	Alzheimer Disease/etiology ; Alzheimer Disease/parasitology ; Alzheimer Disease/pathology ; Animals ; Borrelia burgdorferi/pathogenicity ; Central Nervous System Parasitic Infections/complications ; Central Nervous System Parasitic Infections/parasitology ; Central Nervous System Parasitic Infections/pathology ; Dementia/etiology ; Dementia/parasitology ; Dementia/pathology ; Host-Parasite Interactions ; Humans ; Periodontal Diseases/etiology ; Periodontal Diseases/parasitology ; Spirochaetales/pathogenicity ; Spirochaetales Infections/complications ; Treponema/pathogenicity ; Treponemal Infections/complications
Language	English
Publishing date	2011-08-04
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2156455-3
ISSN	1742-2094 ; 1742-2094
ISSN (online)	1742-2094
ISSN	1742-2094
DOI	10.1186/1742-2094-8-90
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Article: Biology and neuropathology of dementia in syphilis and Lyme disease.

Miklossy, Judith

Handbook of clinical neurology

2008 Volume 89, Page(s) 825–844

MeSH term(s)	Borrelia burgdorferi/immunology ; Borrelia burgdorferi/pathogenicity ; Borrelia burgdorferi/ultrastructure ; Brain/microbiology ; Brain/pathology ; Brain/ultrastructure ; Cytokines/metabolism ; Dementia/etiology ; Dementia/microbiology ; Dementia/pathology ; Humans ; Lyme Disease/complications ; Syphilis/complications ; Treponema pallidum/immunology ; Treponema pallidum/pathogenicity ; Treponema pallidum/ultrastructure
Chemical Substances	Cytokines
Language	English
Publishing date	2008
Publishing country	Netherlands
Document type	Journal Article
ISSN	0072-9752
ISSN	0072-9752
DOI	10.1016/S0072-9752(07)01272-9
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Alzheimer's disease - a neurospirochetosis. Analysis of the evidence following Koch's and Hill's criteria

Miklossy Judith

Journal of Neuroinflammation, Vol 8, Iss 1, p

2011 Volume 90

Abstract: Abstract It is established that chronic spirochetal infection can cause slowly progressive dementia, brain atrophy and amyloid deposition in late neurosyphilis. Recently it has been suggested that various types of spirochetes, in an analogous way to ... ...

Abstract	Abstract It is established that chronic spirochetal infection can cause slowly progressive dementia, brain atrophy and amyloid deposition in late neurosyphilis. Recently it has been suggested that various types of spirochetes, in an analogous way to Treponema pallidum, could cause dementia and may be involved in the pathogenesis of Alzheimer's disease (AD). Here, we review all data available in the literature on the detection of spirochetes in AD and critically analyze the association and causal relationship between spirochetes and AD following established criteria of Koch and Hill. The results show a statistically significant association between spirochetes and AD (P = 1.5 × 10 -17 , OR = 20, 95% CI = 8-60, N = 247). When neutral techniques recognizing all types of spirochetes were used, or the highly prevalent periodontal pathogen Treponemas were analyzed, spirochetes were observed in the brain in more than 90% of AD cases. Borrelia burgdorferi was detected in the brain in 25.3% of AD cases analyzed and was 13 times more frequent in AD compared to controls. Periodontal pathogen Treponemas ( T. pectinovorum, T. amylovorum, T. lecithinolyticum, T. maltophilum, T. medium, T. socranskii ) and Borrelia burgdorferi were detected using species specific PCR and antibodies. Importantly, co-infection with several spirochetes occurs in AD. The pathological and biological hallmarks of AD were reproduced in vitro by exposure of mammalian cells to spirochetes. The analysis of reviewed data following Koch's and Hill's postulates shows a probable causal relationship between neurospirochetosis and AD. Persisting inflammation and amyloid deposition initiated and sustained by chronic spirochetal infection form together with the various hypotheses suggested to play a role in the pathogenesis of AD a comprehensive entity. As suggested by Hill, once the probability of a causal relationship is established prompt action is needed. Support and attention should be given to this field of AD research. Spirochetal infection occurs years or decades before the manifestation of dementia. As adequate antibiotic and anti-inflammatory therapies are available, as in syphilis, one might prevent and eradicate dementia.
Keywords	Alzheimer's disease ; bacteria ; Borrelia burgdorferi ; dementia ; infection ; Lyme disease ; periodontal pathogen ; spirochetes ; Treponema ; syphilis ; Medicine (General) ; R5-920 ; Medicine ; R ; DOAJ:Medicine (General) ; DOAJ:Health Sciences ; Neurology. Diseases of the nervous system ; RC346-429 ; Neurosciences. Biological psychiatry. Neuropsychiatry ; RC321-571 ; Internal medicine ; RC31-1245 ; DOAJ:Neurology
Subject code	630
Language	English
Publishing date	2011-08-01T00:00:00Z
Publisher	BioMed Central
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article: Chronic inflammation and amyloidogenesis in Alzheimer's disease -- role of Spirochetes.

Miklossy, Judith

Journal of Alzheimer's disease : JAD

2008 Volume 13, Issue 4, Page(s) 381–391

Abstract: Alzheimer's disease (AD) is associated with dementia, brain atrophy and the aggregation and accumulation of a cortical amyloid-beta peptide (Abeta). Chronic bacterial infections are frequently associated with amyloid deposition. It had been known from a ... ...

Abstract	Alzheimer's disease (AD) is associated with dementia, brain atrophy and the aggregation and accumulation of a cortical amyloid-beta peptide (Abeta). Chronic bacterial infections are frequently associated with amyloid deposition. It had been known from a century that the spirochete Treponema pallidum can cause dementia in the atrophic form of general paresis. It is noteworthy that the pathological hallmarks of this atrophic form are similar to those of AD. Recent observations showed that bacteria, including spirochetes contain amyloidogenic proteins and also that Abeta deposition and tau phosphorylation can be induced in or in vivo following exposure to bacteria or LPS. Bacteria or their poorly degradable debris are powerful inflammatory cytokine inducers, activate complement, affect vascular permeability, generate nitric oxide and free radicals, induce apoptosis and are amyloidogenic. All these processes are involved in the pathogenesis of AD. Old and new observations, reviewed here, indicate that to consider the possibility that bacteria, including several types of spirochetes highly prevalent in the population at large or their persisting debris may initiate cascade of events leading to chronic inflammation and amyloid deposition in AD is important, as appropriate antibacterial and antiinflammatory therapy would be available to prevent dementia.
MeSH term(s)	Alzheimer Disease/epidemiology ; Alzheimer Disease/microbiology ; Alzheimer Disease/pathology ; Amyloid beta-Peptides/metabolism ; Amyloidosis/epidemiology ; Amyloidosis/metabolism ; Amyloidosis/pathology ; Atrophy/epidemiology ; Atrophy/pathology ; Cerebral Cortex/pathology ; Chronic Disease ; Humans ; Inflammation/epidemiology ; Inflammation/microbiology ; Lyme Neuroborreliosis/epidemiology ; Neurofibrillary Tangles/pathology ; Phosphorylation ; Spirochaetales/pathogenicity ; Spirochaetales/physiology ; Syphilis/epidemiology ; Syphilis/microbiology ; Treponema pallidum/pathogenicity
Chemical Substances	Amyloid beta-Peptides
Language	English
Publishing date	2008-05-08
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1440127-7
ISSN	1875-8908 ; 1387-2877
ISSN (online)	1875-8908
ISSN	1387-2877
DOI	10.3233/jad-2008-13404
Database	MEDical Literature Analysis and Retrieval System OnLINE

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