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Google, it's a wonderful thing :-) Many More Links (scientists names) inside :

Posted By: RumorMail
Date: Tuesday, 5-Jul-2016 14:21:17

In Response To: Alzheimer’s – Research Finds Nematode Worms in Alzheimer’s Brains (RumorMail)

Hi CR, there were clickable links on the home webpage and also if you searched out any of the scientists names, you'll find much more information on this. I included one medical journal paper below.



A worldwide team of senior scientists and clinicians have come together to produce an editorial which indicates that certain microbes – a specific virus and two specific types of bacteria – are major causes of Alzheimer’s Disease. Their paper, which has been published online in the highly regarded peer-reviewed journal, Journal of Alzheimer’s Disease, stresses the urgent need for further research – and more importantly, for clinical trials of anti-microbial and related agents to treat the disease.

This major call for action is based on substantial published evidence into Alzheimer’s. The team’s landmark editorial summarises the abundant data implicating these microbes, but until now this work has been largely ignored or dismissed as controversial – despite the absence of evidence to the contrary. Therefore, proposals for the funding of clinical trials have been refused, despite the fact that over 400 unsuccessful clinical trials for Alzheimer’s based on other concepts were carried out over a recent 10-year period.

Microbes and Alzheimer’s Disease” by Itzhaki, Ruth F.; Lathe, Richard; Balin, Brian J.; Ball, Melvyn J.; Bearer, Elaine L.; Bullido, Maria J.; Carter, Chris; Clerici, Mario; Cosby, S. Louise; Field, Hugh; Fulop, Tamas; Grassi, Claudio; Griffin, W. Sue T.; Haas, Jürgen; Hudson, Alan P.; Kamer, Angela R.; Kell, Douglas B.; Licastro, Federico; Letenneur, Luc; Lövheim, Hugo; Mancuso, Roberta; Miklossy, Judith; Lagunas, Carola Otth; Palamara, Anna Teresa; Perry, George; Preston, Christopher; Pretorius, Etheresia; Strandberg, Timo; Tabet, Naji; Taylor-Robinson, Simon D.; and Whittum-Hudson, Judith A. in Journal of Alzheimer’s Disease. Published online March 8 2016 doi:10.3233/JAD-160152


Microbes and Alzheimer’s Disease

Article type: Editorial

Authors: Itzhaki, Ruth F.a; * | Lathe, Richardb; * | Balin, Brian J.c | Ball, Melvyn J.d | Bearer, Elaine L.e | Braak, Heikof | Bullido, Maria J.g | Carter, Chrish | Clerici, Marioi | Cosby, S. Louisej | Del Tredici, Kellyf | Field, Hughk | Fulop, Tamasl | Grassi, Claudiom | Griffin, W. Sue T.n | Haas, Jürgenb | Hudson, Alan P.o | Kamer, Angela R.p | Kell, Douglas B.q | Licastro, Federicor | Letenneur, Lucs | Lövheim, Hugot | Mancuso, Robertau | Miklossy, Judithv | Otth, Carolaw | Palamara, Anna Teresax | Perry, Georgey | Preston, Christopherz | Pretorius, Etheresiaaa | Strandberg, Timobb | Tabet, Najicc | Taylor-Robinson, Simon D.dd | Whittum-Hudson, Judith A.ee

Affiliations: [a] Faculty of Life Sciences, University of Manchester, Oxford Road, Manchester, UK | Division of Infection and Pathway Medicine, University of Edinburgh, Little France, Edinburgh, UK | [c] Center for Chronic Disorders of Aging, Philadelphia College of Osteopathic Medicine, Philadelphia, USA | [d] Department of Pathology (Neuropathology), Oregon Health and Science University, Portland, OR, USA | [e] Department of Pathology, University of New Mexico Health Sciences Center, Albuquerque, NM, USA | [f] Clinical Neuroanatomy Section, Department of Neurology, Center for Biomedical Research, University of Ulm, Ulm, Germany | [g] Centro de Biologia Molecular ‘Severo Ochoa’ (CSIC-UAM), Universidad Autonoma de Madrid, and Centro de Investigacion en Red sobre Enfermedades Neurodegenerativas (CIBERNED), Madrid, Spain | [h] Polygenic Pathways, Hastings, East Sussex, UK | University of Milano and IRCCS SM Nascente, Don C Gnocchi Foundation, Milan, Italy | [j] Centre for Infection and Immunity, Medical Biology Centre, Queen’s University, Belfast, UK | [k] Queens’ College, Cambridge, UK | [l] Department of Medicine, Division of Geriatrics, Université de Sherbrooke, Sherbrooke, PQ, Canada | [m] Institute of Human Physiology, Medical School, Universitá Cattolica, Rome; San Raffaele Pisana Scientific Institute for Research, Hospitalization, and Health Care, Rome, Italy | [n] Department of Geriatrics, University of Arkansas for Medical Sciences, and Geriatric Research, Education, and Clinical Center, Little Rock, AR, USA | [o] Department of Immunology and Microbiology, Wayne State University School of Medicine, Detroit, MI, USA | [p] NYU College of Dentistry, Department of Periodontology and Implant Dentistry, New York, NY, USA | [q] School of Chemistry, Manchester Institute of Biotechnology, University of Manchester, Manchester, UK | [r] Department of Experimental, Diagnostic, and Specialty Medicine, School of Medicine, University of Bologna, Bologna, Italy | [s] INSERM, Université de Bordeaux, Bordeaux, France | [t] Department of Community Medicine and Rehabilitation, Geriatric Medicine, Umeå University, Umeå, Sweden | [u] Don Gnocchi Foundation ONLUS, Milan, Italy | [v] Prevention Alzheimer International Foundation, International Alzheimer Research Center, Martigny-Croix, Switzerland | [w] Institute of Clinical Microbiology, Faculty of Medicine, Austral University of Chile, Valdivia, Chile | [x] Department of Public Health and Infectious Diseases, Institute Pasteur Cenci Bolognetti Foundation, Sapienza University of Rome; San Raffaele Pisana Scientific Institute for Research, Hospitalization, and Health Care, Rome, Italy | [y] College of Sciences, University of Texas at San Antonio, San Antonio, TX, USA | [z] Institute of Virology, Glasgow, UK | [aa] Applied Morphology Research Centre, Department of Physiology, Faculty of Health Sciences, University of Pretoria, Arcadia, South Africa | [bb] Helsinki University Hospital and University of Helsinki; University of Oulu, Centre of Life Course Health Research, Oulu, Finland | [cc] Division of Old Age Psychiatry, Brighton and Sussex Medical School, Brighton, UK | [dd] St Mary’s Hospital, Imperial College London, London, UK | [ee] Departments of Immunology and Microbiology, Internal Medicine (Rheumatology), and Ophthalmology, Wayne State University School of Medicine, Detroit, MI, USA


  • Correspondence to: Current address: Prof. Ruth F. Itzhaki, Nuffield Department of Clinical Neurosciences, University of Oxford, Level 6, West Wing, John Radcliffe Hospital, Oxford, UK. Tel.: +44 01865 250853; E-mail: ruth.itzhaki@manchester.ac.uk.


  • Correspondence to: Richard Lathe, Division of Infection and Pathway Medicine, University of Edinburgh, 49 Little France Crescent, Edinburgh EH16 4SB, UK. E-mail: richardlathe@ed.ac.uk.

    DOI: 10.3233/JAD-160152

    Journal: Journal of Alzheimer's Disease, vol. 51, no. 4, pp. 979-984, 2016
    Accepted 9 February 2016
    | Published 12 April 2016
    Get PDF

    We are researchers and clinicians working on Alzheimer’s disease (AD) or related topics, and we write to express our concern that one particular aspect of the disease has been neglected, even though treatment based on it might slow or arrest AD progression. We refer to the many studies, mainly on humans, implicating specific microbes in the elderly brain, notably herpes simplex virus type 1 (HSV1), Chlamydia pneumoniae, and several types of spirochaete, in the etiology of AD [1–4]. Fungal infection of AD brain [5, 6] has also been described, as well as abnormal microbiota in AD patient blood [7]. The first observations of HSV1 in AD brain were reported almost three decades ago [8]. The ever-increasing number of these studies (now about 100 on HSV1 alone) warrants re-evaluation of the infection and AD concept.

    AD is associated with neuronal loss and progressive synaptic dysfunction, accompanied by the deposition of amyloid-β (Aβ) peptide, a cleavage product of the amyloid-β protein precursor (AβPP), and abnormal forms of tau protein, markers that have been used as diagnostic criteria for the disease [9, 10]. These constitute the hallmarks of AD, but whether they are causes of AD or consequences is unknown. We suggest that these are indicators of an infectious etiology. In the case of AD, it is often not realized that microbes can cause chronic as well as acute diseases; that some microbes can remain latent in the body with the potential for reactivation, the effects of which might occur years after initial infection; and that people can be infected but not necessarily affected, such that ‘controls’, even if infected, are asymptomatic [2].

    (i) Viruses and other microbes are present in the brain of most elderly people [11–13]. Although usually dormant, reactivation can occur after stress and immunosuppression; for example, HSV1 DNA is amplified in the brain of immunosuppressed patients [14].

    (ii) Herpes simplex encephalitis (HSE) produces damage in localized regions of the CNS related to the limbic system, which are associated with memory, cognitive and affective processes [15], as well as personality (the same as those affected in AD).

    (iii) In brain of AD patients, pathogen signatures (e.g., HSV1 DNA) specifically colocalize with AD pathology [13, 16, 17].

    (iv) HSV infection, as revealed by seropositivity, is significantly associated with development of AD [18–21].

    (v) AD has long been known to have a prominent inflammatory component characteristic of infection (reviewed in [22, 23]).

    (vi) Polymorphisms in the apolipoprotein E gene, APOE, that modulate immune function and susceptibility to infectious disease [24], also govern AD risk (reviewed in [25, 26]). Genome-wide association studies reveal that other immune system components, including virus receptor genes, are further AD risk factors [27–32].

    (vii) Features of AD pathology are transmissible by inoculation of AD brain to primates [33, 34] and mice [35, 36].


    (i) In humans, brain infection (e.g., by HIV, herpesvirus, measles) is known to be associated with AD-like pathology [37–42]. Historical evidence shows that the clinical and pathological hallmarks of AD occur also in syphilitic dementia, caused by a spirochaete [4].

    (ii) In mice and in cell culture, Aβ deposition and tau abnormalities typical of AD are observed after infection with HSV1 [43–52] or bacteria [16, 53–55]; a direct interaction between AβPP and HSV1 has been reported [56]. Antivirals, including acyclovir, in vitro block HSV1-induced Aβ and tau pathology [57].

    (iii) Olfactory dysfunction is an early symptom of AD [58]. The olfactory nerve, which leads to the lateral entorhinal cortex, the initial site from where characteristic AD pathology subsequently spreads through the brain [59, 60], is a likely portal of entry of HSV1 [61] and other viruses [62], as well as Chlamydia pneumoniae, into the brain [63], implicating such agents in damage to this region. Further, brainstem areas that harbor latent HSV directly irrigate these brain regions: brainstem virus reactivation would thus disrupt the same tissues as those affected in AD [64].


    (i) The gene encoding cholesterol 25-hydroxylase (CH25H) is selectively upregulated by virus infection, and its enzymatic product (25-hydroxycholesterol, 25OHC) induces innate antiviral immunity [65, 66].

    (ii) Polymorphisms in human CH25H govern both AD susceptibility and Aβ deposition [67], arguing that Aβ induction is likely to be among the targets of 25OHC, providing a potential mechanistic link between infection and Aβ production [68].

    (iii) Aβ is an antimicrobial peptide with potent activity against multiple bacteria and yeast [69]. Aβ also has antiviral activity [70–72].

    (iv) Another antimicrobial peptide (β-defensin 1) is upregulated in AD brain [73].

    Regarding HSV1, about 100 publications by many groups indicate directly or indirectly that this virus is a major factor in the disease. They include studies suggesting that the virus confers risk of the disease when present in brain of carriers of the ɛ4 allele of APOE [74], an established susceptibility factor for AD (APOE ɛ4 determines susceptibility in several disorders of infectious origin [75], including herpes labialis, caused usually by HSV1). The only opposing reports, two not detecting HSV1 DNA in elderly brains and another not finding an HSV1–APOE association, were published over a decade ago [76–78]. However, despite all the supportive evidence, the topic is often dismissed as ‘controversial’. One recalls the widespread opposition initially to data showing that viruses cause some types of cancer, and that a bacterium causes stomach ulcers.

    In summary, we propose that infectious agents, including HSV1, Chlamydia pneumonia, and spirochetes, reach the CNS and remain there in latent form. These agents can undergo reactivation in the brain during aging, as the immune system declines, and during different types of stress (which similarly reactivate HSV1 in the periphery). The consequent neuronal damage— caused by direct viral action and by virus-induced inflammation— occurs recurrently, leading to (or acting as a cofactor for) progressive synaptic dysfunction, neuronal loss, and ultimately AD. Such damage includes the induction of Aβ which, initially, appears to be only a defense mechanism.

    AD causes great emotional and physical harm to sufferers and their carers, as well as having enormously damaging economic consequences. Given the failure of the 413 trials of other types of therapy for AD carried out in the period 2002–2012 [79], antiviral/antimicrobial treatment of AD patients, notably those who are APOE ɛ4 carriers, could rectify the ‘no drug works’ impasse. We propose that further research on the role of infectious agents in AD causation, including prospective trials of antimicrobial therapy, is now justified.

    Authors’ disclosures available online (http://j-alz.com/manuscript-disclosures/16-0152).


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