People suffering from Alzheimer's and carers of Alzheimer's patients would find the research done by Judith Miklossy very interesting.
'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.
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!