Is Alzheimer’s Caused by an Infection?

By Michael A. Smith, MD

Research has shown that some common bacteria are consistently detected in the central nervous system of Alzheimer's patients.1

Doctors from the International Alzheimer Research Center in Switzerland published a study indicating a high probability of a causal relationship, not just an association, between spirochete infections and Alzheimer's disease.

What they discovered was pretty amazing. They found spirochetes in about 90% of Alzheimer's patients, while the bacteria were virtually absent in healthy age-matched controls.1

Could Alzheimer's disease be caused by this infection? Let's explore.

Spirochetes Form Brain Plaques

Much insight about what could happen in the brain during this process comes from studies on a spirochete, Borrelia burgdorferi, which is the cause of Lyme disease. Spirochete infection begins with the bacteria entering the brain. Once within the brain tissue, they cause disease by forming plaques or masses along the cerebral cortex — the surface of the brain.

Agglutination in the center of the plaque results in a homogeneous central core, which attracts brain macrophages, called microglial cells. The macrophages are responsible for recognizing foreign invaders, engulfing them and presenting them to bacteria fighting immune cells.

The macrophages become trapped within the core of the spirochete plaque. Once trapped, they are vulnerable to attack by the spirochetes. This results in their dysfunction and diminished capacity for fighting the infection. The infection spreads and begins to damage and kill brain cells.2

Damaged brain cells produce the characteristic amyloid-beta protein seen in Alzheimer's patients. Now here's where it gets really interesting…

Amyloid-beta Protein has Antibacterial Properties

Scientists have discovered that amyloid-beta protein has anti-bacterial properties, indicating that its production may be an adaptive response to infectious organisms, like invading spirochetes.3,4

The whole process may work something like this:

1.Spirochetes invade and infect the brain.

2.The brain's normal defenses become dysfunctional as the macrophages (microglia) become trapped and then attacked within the core of the spirochete plaque.

3.With immune dysfunction setting in, the spirochete infection intensifies involving more and more brain cells.

4.Damaged brain cells produce amyloid-beta protein as an adaptive response to the infection.

5.Amyloid-beta deposits grow and begin to affect brain cell connections and communication highways.

6.With damaged connections and communication highways, dementia symptoms begin and gradually worsen.

Early Intervention with Antibiotics

These findings have led some researchers to hypothesize that "…early intervention against infection may delay or even prevent the future development of Alzheimer's disease."3

Early intervention might include prophylactic antibiotic therapy in people at high risk of developing Alzheimer's — a person with a strong family history or the presence of the Apo-E4 allele (a lipoprotein used for fat and cholesterol transport).5

Antibiotic therapy could also be used as part of the early treatment regimen in patients diagnosed with Alzheimer's disease.

Reversing Macrophage Dysfunction with Curcumin

Here's something amazing: Curcumin helps enhance the engulfing properties of brain macrophages — the same macrophages that are damaged and dysfunctional by the spirochetes.

As it turns out, curcumin can bind to amyloid-beta plaques, allowing the brain macrophages to "latch on" and engulf the plaques. The clearing of the plaques can help resolve the infection and reestablish normal brain cell connections and communication highways.6

Could antibiotics and curcumin make up an early Alzheimer's prevention and treatment regimen in the future? It sure is looking possible.

References:

1.J Neuroinflammation. 2011 Aug 4;8:90.

2.Neurobiol Aging.2006;27:228–236.

3.Alzheimers Dement. 2009 Jul;5(4):348-60.

4.PLoS One. 2010 Mar 3;5(3):e9505.

5.N Engl J Med. 1995 Nov 9;333(19):1242-7.

6.J Biol Chem. 2005 Feb 18;280(7):5892-901.

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