Alzheimer's disease and dementia

Alzheimers Dement. 2009 Jul;5(4):348-60. Links Alzheimer's disease and infection: do infectious agents contribute to progression of Alzheimer's disease?

Honjo K, van Reekum R, Verhoeff NP. L.C. Campbell Cognitive Neurology Research Unit, Heart and Stroke Foundation Centre for Stroke Recovery, Section of Neurology, Department of Medicine, Sunnybrook Health Science Centre and University of Toronto, Toronto, Ontario, Canada. Infection with several important pathogens could constitute risk factors for cognitive impairment, dementia, and Alzheimer's disease (AD) in particular. This review summarizes the data related to infectious agents that appear to have a relationship with AD. Infections with herpes simplex virus type 1, picornavirus, Borna disease virus, Chlamydia pneumoniae, Helicobacter pylori, and spirochete were reported to contribute to the pathophysiology of AD or to cognitive changes. Based on these reports, it may be hypothesized that central nervous system or systemic infections may contribute to the pathogenesis or pathophysiology of AD, and chronic infection with several pathogens should be considered a risk factor for sporadic AD. If this hypothesis holds true, early intervention against infection may delay or even prevent the future development of AD. PMID: 19560105

http://news.bbc.co.uk/2/hi/health/8051800.stm

Alzheimer's disease is definitively diagnosed by autopsy only. The label of Alzheimer's is used when the clinical picture suggests this disease or sometimes because people understand what that diagnosis means. The general term for a decline in cognitive functioning is dementia.

This study shows Alzheimer's Disease Cases Set to Quadruple Worldwide by 2050

Dementia is a Th1 disease, as is, I suspect, Alzheimers. Did the Vitamin D researchers look at the impact of Vitamin D on the occurrence of Alzhiemers in their cohort? Of course not.

Additionally, they used subsetting in their cohort so as to produce a better result with elderly women. This is about as unethical as you can get, IMO.

~Trevor Marshall, PhD

In a 101-patient Canadian study, Alzheimer's patients treated with antibiotics doxycycline and rifampin for three months had significantly less mental decline than those given dummy pills, said Dr. Mark Loeb, associate professor at McMaster University in Hamilton, Ontario, and the study's lead author. Nevertheless, Loeb suggested that antibiotics may be an option for Alzheimer's patients who are not doing well on standard therapy. “If I had a family member suffering from Alzheimer's, I would show this study to the physician and see what they think,” he said.

http://paktribune.com/news/index.shtml?156669

“A study of identical twins found a strong link between gum disease marked by early tooth loss and (Altzheimer's)….

“Scientists think it is not the gum disease but the accompanying inflammationThe complex biological response of vascular tissues to harmful stimuli such as pathogens or damaged cells. It is a protective attempt by the organism to remove the injurious stimuli as well as initiate the healing process for the tissue. that helps trigger Altzheimer's.

“The study leader is Professor Margaret Gatz from University of Southern California, Los Angeles.

“Early exposure to inflammation quadruples the risk of developing the disease… the research suggests.”

There is a clinic in Germany which is treating dementia with a variation of the MP and has found the patients herx to indicate a Th1 disease. However, by the time the disease becomes advanced, they are no longer able to look after themselves, and the MP requires a lot of self-discipline in order to be effective.

The problem is compliance, as the patients have trouble focusing on avoiding sunlight/Vit-D, and remembering to take their Benicar. They seem to be responding. And, most important, they herx, their disease relapses after a day soaking in the sun, and some show (very) tentative signs of recovery.

There is not much to be gained by varying from the base MP. With the Dementia patients it is tough to get 100% compliance, unless they have an efficient caregiver (in other words, they don't take their meds on time). Additionally, there is little appreciation, at the level of the patient, of avoiding ingested Vitamin D.

There is little chance that a patient having gone through the MP is likely to develop dementia, but at this point it is also unlikely that Alzheimers patients, in an advanced state of disease, would be able to discipline themselves enough for recovery.

~Trevor Marshall, PhD

Dr Alan McDonald is one of the group of colleagues who were brought together by Dr Andy Wright. Like Dr Alan Cantwell, he had been in retirement until I sparked this renaissance in interest in bacterial pathogenesis. He did some wonderful work in the 1970's, particularly. IMO, he is a little too myopic on Borrelia, and we discuss this issue in detail on the (private) professionals' forums.

Most of the German Dementia patients are positive for Rickettsia. (a coccoid, not a spirochete) (as tested by Jardin Labs) and very few have a positive Borrelia titre (as tested by Bowen Labs).

I have had enough of this suggesting that Alzheimers is caused by Borreliosis. It is not. It occurs throughout the world, including areas where there are no Borrelia, nor any spirochetes. Sometimes Rickettsia are found to be coexistent, sometimes other species.

But get rid of this crazy concept that Borrelia causes Alzheimers. It doesn't. As the paper above says “Borrelia burgdorferi persists in the brain in chronic Lyme neuroborreliosis…” The bacteria persist, but they do not cause. Otherwise you would only find Alzheimers where there is Borrelia, and that is not the case.

I have laid out the detailed reasons that Borrelia has to be a co-infection. I have laid out the reasons that what you find in autopsy tissue may have no relevance to the clinical disease that caused the patient's death. And most of all, I have explained that Alzheimers and Dementia occur in regions of the world where there are no ticks carrying Borrelia spirochetes.

Chronic disease is caused by Th1 bacteria, but not by the obvious species (eg, Borrelia, Treponema). Focus on the spirochetes is counter-productive, as it paints the Lyme community into a remote corner of the medical landscape.

Yes, the Th1 pathogens induce production of amyloids, and yes, they also stop the body from dealing effectively with co-infections like Borrelia and Bartonella. But chronic disease (including Alzheimers) will persist after the spirochete has been eliminated. This is the same problem that folks with AIDS find when they get rid of HIV. When the DVDs of my recent conference presentation are available please review very carefully how I explain the problems devising an effective cure for that disease. Modern medicine has not been very good dealing with multifactorial disease.

~Trevor Marshall, PhD

See also:

Duke University researchers connect vitamin D with brain lesions

April 05- I'm wondering if this TH1 factor explains the elevated proteins in my CSF and the high tau protein level with low AB found in the Alzheimer test that was done. It was done because despite mega antibiotics and excellent diet I still continue to loose my brain function slowly bbut noticeably.

July05- the mino has been great at the Alzheimer type symptoms and my spelling has gotten much better.

June 07- Yes my health has improved. Overall the symptoms are less than they were in severity. I am stronger. Still have space outs and forgetfulness. Still have lapses of clarity. It doesn't scare me us much though- I chuckle instead. It's more stress and pressure. Still have physical pain that can make a day hard. BUT I am smiling now more and laughing more. I hear myself singing. I know I must be getting better as people are telling me I am. If they notice then IT MUST BE SO.

~Mkap2nd

Find articles mentioned here: http://bacteriality.com/2008/06/02/alzheimers/

“The majority of community-dwelling older persons have brain pathology. Those with dementia most often have multiple brain pathologies, which greatly increases the odds of dementia.” ¹⁾

52. Balin BJ, Appelt DM. Role of infection in Alzheimer’s disease. J Am Osteopath Assoc. 2001;101:S1-S6.

Beta-amyloid deposition and Alzheimer's type changes induced by Borrelia spirochetes.

Miklossy J, Kis A, Radenovic A, Miller L, Forro L, Martins R, Reiss K, Darbinian N, Darekar P, Mihaly L, Khalili K. Kinsmen Laboratory of Neurological Research, University of British Columbia, 2255 Wesbrook Mall, Vancouver, BC, Canada V6T 1Z3. judmik@telus.net The pathological hallmarks of Alzheimer's disease (AD) consist of beta-amyloid plaques and neurofibrillary tangles in affected brain areas. The processes, which drive this host reaction are unknown. To determine whether an analogous host reaction to that occurring in AD could be induced by infectious agents, we exposed mammalian glial and neuronal cells in vitroA technique of performing a given procedure in a controlled environment outside of a living organism - usually a laboratory. to Borrelia burgdorferi spirochetes and to the inflammatory bacterial lipopolysaccharide (LPS). Morphological changes analogous to the amyloid deposits of AD brain were observed following 2-8 weeks of exposure to the spirochetes. Increased levels of beta-amyloid precursor protein (AbetaPP) and hyperphosphorylated tau were also detected by Western blots of extracts of cultured cells that had been treated with spirochetes or LPS. These observations indicate that, by exposure to bacteria or to their toxic products, host responses similar in nature to those observed in AD may be induced. PMID: 15894409