Friday 12 March 2010

ALZHEIMER'S RESEARCH

People suffering from Alzheimer's and carers of Alzheimer's patients would find the research done by Judith Miklossy very interesting.
http://www.miklossy.ch/401/index.html
'The realization that pathogens can produce slowly progressive chronic diseases has resulted in a new concept of infectious diseases. A number of chronic diseases are caused by one or more infectious agents: e.g., stomach ulcer is caused by Helicobacter pylorii; chronic lung disease in newborns and chronic asthma in adults are caused by Mycoplasmas; and, Chlamydia pneumoniae and some other pathogens have been associated with atherosclerosis.
It has been known from a century that chronic bacterial infections are frequently associated with amyloid deposition and that experimental models of inflammation and amyloidosis can be produced by injecting living or killed bacteria or their toxic products to animals.
It has also been known from a century that chronic bacterial infection can cause dementia. Treponema pallidum, the causative agent of syphilis, causes slowly progressive dementia, cortical atrophy, chronic inflammation and amyloid deposition in the affected brain. Alzheimer’s disease (AD), the most frequent cause of dementia, is a form of amyloidosis. The pathological mechanisms driving the accumulation of amyloid remain unclear. Bacteria, including spirochetes, are powerful stimulators of inflammation and are amyloidogenic. They were suggested to be contributors in generating and sustaining chronic inflammation and amyloid deposition in Alzheimer’s disease. The concept is not new. Fischer, Alzheimer and their colleagues have discussed the possibility that microorganisms may play a role in senile plaque formation a century ago.
The fact that pathogens may suppress, subvert or evade host defenses and establish chronic or latent infection has received little attention in the past'

I think Judith Miklossy's work is ground breaking and I had the privilege to here her present last year at Lyme Disease Action 2009 conference.
Judith Miklossy has also done much research on Borrelia, Lyme disease. She like Alan MacDonald before her, found the DNA for Borrelia in the brain of Alzheimer's patients.

I see there is now further research in this field done by Rudolph E. Tanzi, Robert D. Moir et al

The Alzheimer's Disease-Associated Amyloid β-Protein Is an Antimicrobial Peptide
The amyloid β-protein (Aβ) is believed to be the key mediator of Alzheimer's disease (AD) pathology. Aβ is most often characterized as an incidental catabolic byproduct that lacks a normal physiological role. However, Aβ has been shown to be a specific ligand for a number of different receptors and other molecules, transported by complex trafficking pathways, modulated in response to a variety of environmental stressors, and able to induce pro-inflammatory activities.
Here, we provide data supporting an in vivo function for Aβ as an antimicrobial peptide (AMP). Experiments used established in vitro assays to compare antimicrobial activities of Aβ and LL-37, an archetypical human AMP. Findings reveal that Aβ exerts antimicrobial activity against eight common and clinically relevant microorganisms with a potency equivalent to, and in some cases greater than, LL-37. Furthermore, we show that AD whole brain homogenates have significantly higher antimicrobial activity than aged matched non-AD samples and that AMP action correlates with tissue Aβ levels. Consistent with Aβ-mediated activity, the increased antimicrobial action was ablated by immunodepletion of AD brain homogenates with anti-Aβ antibodies.
Our findings suggest Aβ is a hitherto unrecognized AMP that may normally function in the innate immune system. This finding stands in stark contrast to current models of Aβ-mediated pathology and has important implications for ongoing and future AD treatment strategies.

http://www.plosone.org/article/info:doi/10.1371/journal.pone.0009505

Judith Miklossy goes on to say
'Highest priority should be given to this emerging field of research. 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 the disease. The impact on reducing health-care costs would be substantial.'

I look forward to hearing more research of similar ilk, rather than how many cups of coffee should or shouldn't be drunk!

2 comments:

  1. Several recent articles indicate Alzheimer's Disease (AD) is a prion disease.

    " http://www.santacruzsentinel.com:80/localnews/ci_12180851
    UCSC researchers find key to prion diseases
    By Alia Wilson

    Posted: 04/20/2009 01:30:05 AM PDT



    "“Human prion diseases include classic and variant types of Creutzfeldt-Jakob disease, mad cow disease, Alzheimer's and Parkinson's."

    http://sludgevictims.com/pathogens/ALZHEIMERS-CJD-samepriondisease.doc

    http://sludgevictims.com/alzheimer.html

    Researchers have found prions in blood, urine, saliva and feces of human and animal victims of Transmissible Spongiform Encephalopathies (TSEs - prion diseases).

    "OPKO Health Announces Development of Blood Test for Alzheimer’s Disease
    February 11, 2010 10:47 AM Eastern Time
    MIAMI--(EON: Enhanced Online News)--OPKO Health, Inc. (NYSE Amex:OPK) today announced the development of a
    simple diagnostic blood test for Alzheimer’s disease. The test, designed to detect elevated levels of antibodies unique
    to Alzheimer’s disease, was approximately 95% accurate in initial testing. "

    http://eon.businesswire.com/portal/site/eon/permalink/?ndmViewId=news_view&newsId=20100211006100&newsLang=en
    **************************************************************************************************************

    http://www.ncbi.nlm.nih.gov/pubmed/16127436
    Nat Med. 2005 Sep;11(9):982-5. Epub 2005 Aug 28.

    Detection of prions in blood.
    Castilla J, Saá P, Soto C.

    Department of Neurology, University of Texas Medical Branch, 301 University Boulevard, Galveston, Texas, 77555-0646, USA.


    "These findings represent the first time that PrP(Sc) has been detected biochemically in blood, offering promise for developing a noninvasive method for early diagnosis of prion diseases."

    ***************************************************************************************************************

    http://www.sciencealert.com.au/news/20091310-19987-2.html

    Tuesday, 13 October 2009




    "The human prion is resistant to both heat and chemicals and is reported to be up to a hundred thousand times more difficult to deactivate than the animal form of infective agent which causes well known diseases in cattle, such as mad cow disease, and scrapie in sheep. "

    Any error in identifying a CJD-carrier can be fatal and costly - many hospitals around the world have been forced to destroy millions of dollars worth of instruments when patients were diagnosed with CJD some time after undergoing routine eye and neurosurgical procedures.

    A further factor limiting decontamination from prions is that existing cleaning protocols are damaging to medical instruments such as flexible endoscopes and some instruments used in neurosurgical, dental and opthalmological procedures."

    *********************************************************************

    There are 5.3 million AD victims in the United States, with a new case every 70 seconds - an epidemic of almost a half million new cases of a transmissible prion disease each year. The CDC and medical community must promptly deal with the issue of potential iatrogenic transmission of Alzheimer's Disease.

    Helane Shields, PO Box 1133, Alton, NH 03809 603-875-3842 hshields@worldpath.net

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  2. Helane
    Many thanks for your comments and links which I will have a good look at.
    Clearly my interest is from a Lyme Disease perspective but I do recognise that there are likely to be a multitude of factors and co founders to this disease.

    ReplyDelete