Is Alzheimer’s Caused By a Bacterial Infection of the Brain?

As I noted earlier (, everyone gets chronic bacterial infections; infection rates are nearly 100% in the elderly.  In most people, however, the infection doesn’t progress to overt symptoms until old age. 

The first symptoms, apart from loss of athleticism and energy, often appear in the brain and nerves.  This is because neurons are a uniquely cozy home for bacteria.  Because they cannot burn fats, neurons have high levels of the energy substrates that bacteria rely on – pyruvate, lactate, and other products of glycolysis.

Loss of memory is one of the primary symptoms of bacterial infection of the brain. I myself had a chronic bacterial infection that caused loss of memory, and my memory was recovered with antibiotic treatment. (I now, thankfully, have a 100% functional brain.) The experience persuaded me that Alzheimer’s was very likely due to a bacterial infection of the brain.

Several recent findings support that inference. 

  • Alzheimer’s patients almost invariably have infections of the brain and nerves. C. pneumoniae is the most common agent.  Post-mortem autopsies found that C. pneumoniae infections in 17 of 19 Alzheimer’s brains, but only 1 of 19 non-Alzheimer’s elderly brains. [1]
  • The characteristic physical feature of the Alzheimer’s brain, clumps of amyloid-beta, are plausibly the result of the brain’s antimicrobial defenses.  It turns out that amyloid-beta is an antimicrobial peptide, part of the brain’s defense mechanisms against bacteria. [2]

These findings are consistent with a bacterial origin for Alzheimer’s. In the Alzheimer’s brain, the bacteria are parasites, stealing fuel and nutrients. This may be why the early signs of incipient Alzheimer’s are similar to the cognitive symptoms of hypoglycemia.

If Alzheimer’s is indeed caused by bacterial infection of the brain, then it is a treatable – often, curable – condition.  I’ll discuss in my next post some steps that will treat and help cure Alzheimer’s.

[1] Balin BJ et al. Chlamydophila pneumoniae and the etiology of late-onset Alzheimer’s disease. J Alzheimers Dis. 2008 May;13(4):371-80. Hat tip Stephanie Seneff,

[2] Soscia SJ et al. The Alzheimer’s disease-associated amyloid beta-protein is an antimicrobial peptide. PLoS One. 2010 Mar 3;5(3):e9505.

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    “Evidence that Infection is Associated with Alzheimer’s

    There is substantial evidence that Alzheimer’s is related to an increased likelihood of infective agents appearing in the brain. Some researchers believe that infective agents are the principle cause of Alzheimer’s. There are a number of bacteria that reside in the human digestive system and can co-exist with our own cells without any harm. However, H. pylori, one that is quite common, has been recently shown to be responsible for stomach ulcers. It has been suspected that H. Pylori might be implicated in Alzheimer’s, and, indeed, a recent study showed that Alzheimer’s patients had a significantly higher concentration of an antibody against H. Pylori in both their cerebrospinal fluid and their blood than non-Alzheimer’s controls [26]. H. pylori was detected in 88% of the Alzheimer’s patients but only 47% of the controls. In an effort to treat the Alzheimer’s patients, the researchers administered a potent combination of antibiotics, and assessed the degree of mental decline over the next two years [27]. For 85% of the patients, the infection was successfully routed, and for those patients, cognitive improvement was also detected after two years had elapsed. So this was a nice example of the possibility of treating Alzheimer’s through antibiotics.

    C. pneumoniae is a very common bacterium, estimated to infect 40-70% of adults. But there’s a big difference between a bacterium being in the blood stream and making its way into the inner sanctum of the brain. A study of post-mortem samples from various regions of the brains of Alzheimer’s patients and non-Alzheimer’s controls revealed a remarkably different statistic: 17 out of 19 Alzheimer’s brains tested positive for the bacterium, whereas only 1 out of 19 brains from the control group tested positive [5].

    Many other infective agents, both viruses and bacteria, have been found to be associated with Alzheimer’s, including herpes simplex virus, picornavirus, Borna disease virus, and spirochete [23]. One proposal was that a particular bacteriophage — a virus that infects the bacterium C. pneumoniae — might be responsible for Alzheimer’s [14]. The authors argued that the phages might make their way into the mitochondria of the host cell and subsequently initiate “

  2. Readers of this thread who enjoy going into greater detail may like to spend some time listening to this series of presentations
    Herpes Simplex and Alzheimer’s—Time to Think Again?”
    (I found I had to move the slides forward myself to keep up with the talk) from a selection of expert researchers discussing their work.

    Ruth Itzhaki, University of Manchester, U.K.; Elisa Porcellini, University of Bologna, Italy; Luc Letenneur, INSERM, Bordeaux, France, and Richard Smeyne, St. Jude Children’s Research Hospital, Memphis, Tennessee, shared some of their latest research and field audience questions. Paul Klapper, herpes virologist at Manchester Royal Infirmary, U.K., and Terrence Town, Cedars-Sinai Medical Center, Los Angeles, were on hand for discussion afterward.

    Herpes simplex virus 1 (HSV1) is attracting attention from a growing number of research groups as a possible trigger for Alzheimer’s disease. Recent work has tied the virus to AD biomarkers, and offered some epidemiological and genetic support for the long-proposed connection between HSV reactivation and AD risk.

    There is an interesting question and answer session at the end some of which is online. Although this is a talk for health professionals and other researchers I think the ideas discussed and the research findings are interesting to the layperson and worth consideration.

    During the discussion the question of reactivation of virus is raised and INFLAMMATION may be the trigger setting off a cascade of consequences.

    Those who have read the blog here titled
    “Eleven Steps for Overcoming Alzheimer’s and Other Chronic Infectious Diseases” may like to think of these as different ways of reducing inflammation as is much of the Perfect Health Diet.

  3. Thanks, Ted! Looks like a very interesting panel.

  4. I have HSV-1 (cold sores).
    Get about 4 outbreaks each year.

    I guess there’s no way to kill it, but is there anything I can do to help my body suppress it?

    Better yet, does someone have a top secret way that nobody else knows of to just kill the virus & make it go away forever? 🙂

  5. Hi MacAttack,

    Alas, no way to make it go away forever. But it should be possible to reduce or eliminate your outbreaks.

    Try high vitamin C (, iodine, intermittent fasting, and the other techniques listed in the book and this post (

    Best, Paul

  6. Mac, for what it’s worth, a couple of years ago, the doctor column in our local Daytona Beach paper, mentioned L-Lysine for cold sores and I’ve been taking 500 mg every day since then. Result: absolutely no cold sores.

  7. I’ve heard of people taking that before.
    Is there a downside to taking L-Lysine?

    If not, I think I’ll give it a try.

  8. Hi MacAttack,

    L-lysine is safe, you could take 5 g/day if you want.

    It’s also ketogenic, so good for taking during fasts.

    Here’s some info on dose, from a review (

    It has been known since 1968 that HSV-1 requires arginine for replication,15 and that lysine inhibits HSV-1 replication by competing with arginine.16 These findings led to the use of lysine as a treatment for the common condition known as herpes labialis which, as noted above, is known to be caused by HSV-1. Seven randomized, double-blind, placebo-controlled studies have examined the effectiveness of lysine in preventing outbreaks of herpes labialis and reducing the severity of outbreaks that do occur. Six of these studies found lysine to be effective in preventing or decreasing outbreaks, and only two found that lysine reduced the severity of out-breaks. The first study, conducted in 1978, employed a dosage of 500 mg/day of lysine and found it to be ineffective.17 A 1984 study specified 1,000 mg of lysine, given once a day, and also measured serum lysine levels. Lysine was found to be effective in reducing outbreaks when serum lysine concentration was greater than 165 nmol/mL, but not when it was less than this.18 Another study, also published in 1984, found that a dosage of 1,248 mg/day was effective in reducing outbreak frequency, but that 624 mg/day was ineffective.19 A 1987 study studied lysine 1,000 mg three times a day, and found it to be effective in reducing both the frequency and severity of attacks.20

    So 2 to 3 g/day might be an effective dose.

  9. No experience with it, but I’ve read of using BHT to control herpes.

  10. Alzheimer’s - Page 16 - pingback on March 5, 2012 at 10:58 pm
  11. Hi Paul,
    I thought of your theories when this piece crossed my desk. Sounds like more people are starting to think Alzheimers is the result of infection:

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