City scientists to lead pioneering dementia research (From Daily Echo)

It's 'LEAD' not 'LED'!

Whilst it is good to consider all options with research on Alzheimer's it is already generally accepted that stress affects our immune system and thus makes it more difficult to fight of illnesses so stress in any illness has cause and effect.

The research that needs to be replicated is that done by Judith Miklossy
Alzheimer's Disease a Neurospirochetosis Analysis of the evidence following Koch's and Hill's criteria.
Not sure if I can post links but a Google search is worth doing especially also to her website.

Miklossy believes that as in General Paresis from Syphilis another spirochetal infection - treatment by appropriate but simple antibiotics may help patients with Alzheimer's, but taken long term.

Miklossy is not the first to find Borrelia Spirochetes in the brains of people who died of Alzheimer's Dr Alan MacDonald pathologist was the first and found spirochetes in 7 out of 10 brains.

Seek and ye shall find but if the correct methodolgy is not followed such as in the Marques study ( wrong temperature used) then ye may not find.

Alzheimer's disease - a neurospirochetosis. Analysis of the evidence following Koch's and Hill's criteria
Judith Miklossy
http://www.jneuroinf
lammation.com/conten
t/8/1/90/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 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.

http://www.miklossy.
ch/401/index.html
Link to www.preventionalzhei
mer.org

Link to International Alzheimer Research Center


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 various pathogens are associated with atherosclerosis and Alzheimer disease.

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 components 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 already 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. During infection, active oxygen and nitrogen species generated by inflammatory cells can 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 microorganisms can persist in the infected tissues, resulting in chronic, persistent inflammation. 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, including stress and nutrition are critical determinants of disease expression as well.

Pathogens, in addition to strong lymphoplasmocytic infiltrates, can also induce slowly progressive chronic inflammation with poor or absent lymphoplasmocytic infiltrates (e.g. leprosy, syphilis). Activated macrophages and/or microglia are the principal players in this slowly progressive form of infection, which results in slowly progressive parechymal involvement and tissue atrophy.

Highest priority should be given to this emerging field of research. It may have major implications for public health, treatment, and prevention of Alzheimer disease as adequate anti-bacterial drugs are available. Treatment of a bacterial infection may result in regression and, if started early, prevention of the disease. The impact on reducing health-care costs would be substantial.

As it was the case for paretic dementia in syphilis, one may prevent and eradicate dementia in Alzheimer disease.

My note- do not be fooled into the idea that Borrelia (Lyme Disease) is the rare and simple to cure infection the HPA following IDSA guidelines has promulgated for the last 30 years. These spirochetes according to Eva Sapi researcher have a tropism for the head/brain.
The New Forest was recognised as a Lyme Endemic area I think in the 80's although little important research has ever been done here in the UK.
What we do know is that there are a growing number of cases and that about only about 10% ever get recorded. The smallest tick being the size of a poppy seed we are not always aware of being bitten and the infection can lay in a dormant state for many years.
Now we have confirmation by NIH researchers that Borrelia can persist despite long courses of antibiotics - that is if you are lucky to have been diagnosed and treated at all. For information about Lyme Disease here in the UK see http://www.lymedisea
seaction.org.uk/
With reading you will realise this is an important aspect in Alzheimer's disease and as such as Miklossy says we can treat on medications already available - antibiotics.