Alzheimer’s Disease is the most prevalent type of a number of central nervous system conditions broadly known as dementia1.  Most of us know someone who has been afflicted.  Sadly, we all know much more about the devastation of the condition than medicine knows about treating it.  However, there is potential for a cure in the future.

Alzheimer’s falls into two basic categories; Familial Alzheimer’s Disease (FAD) which has been linked to a specific gene mutation2, 3, 4, and Late-onset Alzheimer’s Disease (LOAD) which seems to indiscriminately targets its victims later in life1. For the purposes of this article, we will focus on the latter, late-onset version of this destructive condition.

Current research and therapies have really honed in on targeting something called Amyloid Beta (AB)5.  It is a substance found in the “sick” regions of Alzheimer’s Disease brains on autopsy. Deposition of AB has been correlated to the neurodegeneration and cognitive decline characteristic of LOAD.

However, a dedicated group of physicians and researchers have been literally pounding the pavement (and the keyboard) for decades exploring what happens BEFORE Amyloid Beta starts accumulating. Why do they look beyond Amyloid Beta?  The answer is simple; the current therapeutic options are largely ineffective6.  Ineffective therapies should inherently cause questioning of the dominant hypothesis, but it hasn’t.  A plethora of research studies and review articles strongly point a finger at chronic infection as a catalyst7, 8, 9, 10.

A few bugs in particular continue to stand out, and have the ability to illicit an intense inflammatory response11.  One is Chlamydia pneumoniae, an intracellular organism known to cause respiratory infections12.  Now don’t get all awkward on me, we aren’t talking about the STD Chlamydia (which is called Chlamydia trachomatis).  This is an uptown cousin that enters our bodies when we inhale infected airborne particles (called elementary bodies) shed upon sneezing and coughing.  It presents as a common respiratory infection of the airways or in some cases as pneumonia. Most of us have been exposed before the age of 2013, but for reasons unclear (most likely genetic), some people are excellent hosts.

Another group of bacteria called spirochetes have been linked to LOAD14, 15, 16. Most of us are familiar with Lyme Disease, a condition largely transmitted by tick bite.  It is caused by a specific spirochete called Borrelia burgdorferi.  This family of organisms is also found in the brains of Alzheimer’s patients 17, 18, 19.  In fact, country artist Kris Kristofferson was diagnosed with Dementia only to test positive for Borrelia burgdorferi.  Kris’ symptoms resolved completely with antibiotic therapy. He regained cognitive function, something typically unheard of in the world of Alzheimer’s and dementia.  One doctor pioneering and publishing this body of research on spirochetes like Borrelia and LOAD is Dr. Judith Miklossy of Switzerland.

Despite many published studies and articles, the Alzheimer’s community has turned a blind eye on this body of research.  “Evidence Based Medicine” is a deep-seeded mantra in healthcare, but why is certain credible, peer-reviewed evidence overlooked?  The answer is complex and could be an entire article topic on its own. To boil it down and distill it into simple terms, innovation in healthcare is the progenitor of fear rather than progress.  Let’s chew on a tangible example with a brief story.

I would like to introduce you to two Australian doctors, Dr. Barry Marshall, an Internist and Dr. Robin Warren, a Pathologist.  Their story bears striking resemblance to the landscape in Alzheimer’s Disease and Chlamydia pneumoniae.  Beginning in 1981 Dr.’s Marshall and Warren began compiling evidence that patients with gastrointestinal ulcers and stomach cancer also had a sneaky stealth bacterium present, Helicobacter pylori20.  While causation was far from proven, the hypothesis was formed.

He and Dr. Warren began working to research the organism but ran into ethical concerns while attempting to fund and publish research.  Mouse, pig or rat studies were not an option as the infection would only grow in primates. To give human beings the bacteria and watch them develop gastritis, ulcers and even cancer was out of the question. Attempts to get their early work funded never mind published were thwarted by major pushback in the GI community. The prevailing hypotheses of the time were that stress, smoking, diet and overproduction of acid caused GI ulcers. An American Infectious Disease doctor is even quoted saying “Marshall isn’t a real scientist”.

One day after successfully treating one of many gastritis patients with H. pyloriinfection using a cocktail of antibiotics (after confirming the infection and which antibiotic to use in the lab) Dr. Marshall decided to boldly takes matters into his own hands.  He simply could not tolerate the idea of people dying from a treatable disease and did something historically bold, and even a little bit crazy. He infected himself.

In his own words during an interview with Discover Magazine, “I treated the patient and did an endoscopy to make sure his infection was gone. After that I swizzled the organisms around in a cloudy broth and drank it the next morning. My stomach gurgled, and after five days I started waking up in the morning saying, “Oh, I don’t feel good,” and I’d run in the bathroom and vomit. Once I got it off my stomach, I would be good enough to go to work, although I was feeling tired and not sleeping so well. After 10 days, I had an endoscopy that showed the bacteria were everywhere. There was all this inflammation, and gastritis had developed.”

Now you are probably wondering if the medical community responded to this brazen maneuver.  In 1985, they published their work in the Medical Journal of Australia, but it took another 10 years for the U.S. FDA and NIH to accept this work as fact.  It wasn’t until Reader’s Digest and even the National Enquirer started running stories about the “Guinea Pig Doctor” that everyone was forced to take notice.

Thanks to Barry Marshall we all have a clear diagnostic and treatment path forward when it comes to GI ulcers and stomach cancer.  Ask any doctor, or healthcare provider and they will unanimously agree that H. pylori is the culprit.  A bacterium causes inflammation and cancer21.  Oh, and the guy who wasn’t a “real scientist”, Dr. Barry Marshall, was the recipient of the Nobel Prize for his work in 200522.

Let’s get back to Alzheimer’s Disease.  5.7 Million Americans are currently living with Alzheimer’s or dementia.  It will cost the U.S. 277 Billion dollars in 2018. There is substantial evidence showing that C. pneumoniaeis present and capable of eliciting a deleterious immune response and Amyloid Beta accumulation24-32.  Scientists have shown the organisms path from the nerves in nasal passages for the sense of smell (olfaction) to the common sites of damage first observed in Alzheimer’s brains33, 34.  It has been proven in the case of H. pyloriand GI disease that ignoring evidence leads to costly delays and perhaps more importantly, that chronic infection by certain bacteria is a VERY bad thing.

As you read, history is repeating itself, and not in a good way.  One of the main experts in the field of Chlamydia pneumoniaeand Alzheimer’s Disease, Dr. Brian Balin, just received notice that the Alzheimer’s Association International Conference has refused his proposal for a presentation at their 2018 medical meeting in Chicago. He hoped to present their robust work in a presentation entitled, “Studies Supporting Chlamydia PneumoniaeInfection as a Trigger for Late-Onset Alzheimer Disease”. This work representing a key aspect of the “infection hypothesis” will not be represented at this meeting.

If you or someone you love has Alzheimer’s, you should be concerned.  This denial represents a failure in evidence based medicine. Omitting the research on infection at the biggest Alzheimer’s international medical conference of the year represents a costly delay that people suffering simply cannot afford.  More research is called for, particularly early-intervention, long-term antibiotic trials.  That will be challenging to fund until the Alzheimer’s community acknowledges the work that has already been done.

Philosopher George Santayana said “Those who cannot remember the past are condemned to repeat it.”  If this story sounds like Dr. Marshall and Warrens, it should.  As patients, we need to ask more of the Alzheimer’s community.  We must learn from the past, beware of bias, and when warranted, welcome innovation backed by science.

To read more of the published literature referenced in this article please visit Intracell Research Group.


  1. Terry RD, Davies P. Dementia of the Alzheimer type (1990) Ann Rev Neurosci. 3:77–95.
  2. Gérard HC, Wang GF, Balin BJ, Schumacher HR & Hudson AP (1999) Frequency of apolipoprotein E (APOE) allele types in patients with Chlamydia-associated arthritis and other arthritides. Microb Pathog 26: 35–43.
  3. Gérard HC, Wildt KL, Whittum-Hudson JA, Lai Z, Ager J & Hudson AP (2005) The load of Chlamydia pneumoniae in the Alzheimer’s brain varies with APOE genotype. Microb Pathog 39: 19–26.
  4. Hartman RE, Laurer H, Longhi L, Bales KR, Paul SM, McIntosh TK & Holtzman DM (2002) Apolipoprotein E4 influences amyloid deposition but not cell loss after traumatic brain injury in a mouse model of Alzheimer’s disease. J Neurosci 22: 10083–10087.
  6. David A. Casey, MD, Demetra Antimisiaris, PharmD, and James O’Brien, MD (2010) Drugs for Alzheimer’s Disease: Are They Effective? Pharmacy and Therapeutics 35(4).
  7. Itzhaki et. al. (2016) Microbes and Alzheimer’s Disease. Journal of Alzheimer’s Disease. 51(4):979–984.
  8. Hudson AP (2001) What is the evidence for an infectious causation in late-onset Alzheimer’s disease? Lab Med 32: 680–685.
  9. Miklossy J (2011) Alzheimer’s disease – a neurospirochetosis. Analysis of the evidence following Koch’s and Hill’s criteria. Journal of Neuroinflammation. 8: 90.
  10. Miklossy J (2011) Emerging roles of pathogens in Alzheimer disease. Expert Rev Mol Med 13, e30.
  11. Stratton CW (2000) Association of Chlamydia pneumoniae with Chronic Human Diseases. Antimicrobics and Infectious Diseases Newsletter. Vol. 18 (7) 49-56.
  12. Blasi F, TarsiaP, ArosioC, FagettiL, AllegraL (1998) Epidemiology of Chlamydia pneumoniae. Clinical Microbiology and Infection, 4S1-4S6.
  13. Paldanius M, Bloigu A, Alho M, Leinonen M, Saikku P (2005)Prevalence and Persistence of Chlamydia pneumoniae Antibodies in Healthy Laboratory Personnel in Finland. Clinical Diagnostic and Laboratory Immunology. 12(5): 654–659.
  16. Miklossy J (1993) Alzheimer’s disease – A spirochetosis? Neuroreport 4, 841-848.
  17. MacDonald AB, Miranda JM (1987) Concurrent neocortical borreliosis and Alzheimer’s disease. Hum Pathol 18, 759–761.
  18. MacDonald AB (1988) Concurrent neocortical borreliosis and Alzheimer’s disease: Demonstration of a spirochetal cyst form. Ann N Y Acad Sci 539, 468-470.
  19. Miklossy J, Khalili K, Gern L, Ericson RL, Darekar P, Bolle L, Hurlimann J, Paster BJ (2004) Borrelia burgdorferi persists in the brain in chronic Lyme neuroborreliosis and may be associated with Alzheimer disease. J Alzheimers Dis 6, 639-649.
  20. Marshall BJ, Warren JR (1984) Unidentified curved bacilli in the stomach of patients with gastritis and peptic ulceration. Lancet. 1:1311–1315.
  21. Wroblewski LE, Peek RM, Wilson KT Jr. (2010) Helicobacter pyloriand Gastric Cancer: Factors That Modulate Disease Risk. Clinical Microbiology Reviews. 23(4): 713–739
  22. Van Der Weyden MB, Armstrong RM, Gregory AT (2005) The 2005 Nobel Prize in Physiology or Medicine. Medical Journal of Australia. 183 (11): 612-614.
  23. Alzheimer’ Fact Sheet (2018)
  24. Balin BJ, Gerard HC, Arking EJ, Appelt DM, Branigan PJ, Abrams JT, Whittum-Hudson JA, Hudson AP (1998) Identification and localization of Chlamydia pneumoniae in the Alzheimer’s brain. Med Microbiol Immunol 187, 23-42.
  25. Koskiniemi M, Saarinen A, Klapper PE, Sarna S, Cleator G & Valieri A (1996) Chlamydia pneumoniae associated with central nervous system infections. Eur Neurol 36: 160–163.
  26. Little CS, Hammond CJ, MacIntyre A, Balin BJ & Appelt DM (2004) Chlamydia pneumoniae induces Alzheimer-like amyloid plaques in brains of BALB/c mice. Neurobiol Aging 25: 419–429.
  27. MacIntyre A, Hammond CJ, Little CS, Appelt DM & Balin BJ (2002) Chlamydia pneumoniae infection alters the junctional complex proteins of human brain microvascular endothelial cells. FEMS Microbiol Lett 217: 167–172.
  28. Ossewaarde JM, Gielis-Proper SK, Meijer A & Roholl PJM (2000) Chlamydia pneumoniae antigens are present in the brains of Alzheimer patients but not the brains of patients with other dementias. Chlamydia Research (SaikkuP, ed). Societa Editrice Esculapio, Bologna.
  29. Loeb MB, Molloy DW, Smieja M, Standish T, Goldsmith CH, Mahony J, Smith S, Borrie M, Decoteau E, Davidson W, McDougall A, Gnarpe J, O’DONNell M, Chernesky M (2004) A randomized, controlled trial of doxycycline and rifampin for patients with Alzheimer’s disease. J Am Geriatr Soc. 52:381–387.
  30. Balin BJ, Hudson AP (2014) Etiology and pathogenesis of late-onset Alzheimer’s disease. Curr Allergy Asthma Rep 14, 417.
  31. Little CS, Bowe A, Lin R, Litsky J, Fogel RM, Balin BJ, Fresa-Dillon KL (2005) Age alterations in extent and severity of experimental intranasal infection with Chlamy- dophila pneumoniae in BALB/c mice. Infect Immun 73, 1723-1734.
  32. Balin BJ, Little CS, Hammond CJ, Appelt DM, Whittum-Hudson JA, Gerard HC, Hudson AP (2008) Chlamydophila Pneumoniae and the Etiology of Late-Onset Alzheimer’s Disease. Journal of Alzheimer’s Disease.
  34. Kovács TCairns NJLantos PL. (2001) Olfactory centres in Alzheimer’s disease: olfactory bulb is involved in early Braak’s stages. Neuroreport 12 (2): 285-288.