The brain can also be infected: Viruses and microorganisms as possible causes of Alzheimer’s dementia
The American researcher Dr. Pat McGeer researched whether viruses could possibly cause the alteration of brain cells. He stained brain cells of patients who died with AD using a different staining method. Although he found no evidence of a virus, he found vast amounts of certain brain cells (so-called microglia). These cells only appear in such big amount under certain condition: inflammation! Dr. McGeer researched that microglia had already been discovered in the brain of dementia patients in 1919. However, this theory was not further investigated by that time, but is currently receiving new attention.
In 2004, Dr. Scott Little and his colleagues investigated whether certain bacteria (e.g. chlamydia) might also be possible causes of AD. Dr. Scott and his team had already isolated chlamydia from nine out of ten AD patient brains. In subsequent animal experiments, it was shown that chlamydia can remain in the brain undisturbed by the immune system. Even after three months, the bacteria were still detectable in the animal brains. The researchers were also able to detect certain protein deposits. These deposits were larger and more frequent the more Chlamydia has spread in the brain.
US researcher Herbert Allen has also put forward the hypothesis that bacteria adhere to surfaces as biofilms and are therefore largely resistant to immune attacks or antibiotics. This prompted him to ask whether bacterial biofilms might also play a role in Alzheimer’s disease. When Allen searched for biofilms in the brains of deceased Alzheimer’s patients, he found them at the same sites in the hippocampus as the amyloid plaques. The key factor of innate immunity (the so-called toll-like receptor 2,TLR2) was also present in the same region of the Alzheimer’s brain, but not in the controls. The researcher concluded that TLR2 is activated by the presence of bacteria but is blocked by the bacterial biofilm and instead the surrounding tissue is damaged.
These investigations clearly show that the presence of plaques in the brain is not merely responsible for Alzheimer’s dementia, but infectious processes may also play an essential role. The brain is highly protected by the blood-brain barrier, which controls the passage of molecules into and out of the brain. It is now known that a broad spectrum of pathogens such as viruses, bacteria, fungi and protozoa (animal unicellular organisms) can still gain access to the brain. Bacteria can cross the blood-brain barrier via various mechanisms, including transcellular and paracellular crossing. On the other hand, viruses can directly infect endothelial cells (forming a single layer of cells to line blood vessels) in order to enter the brain via the blood-brain barrier. The table below lists all pathogens that current research suspects are causally linked to the development of Alzheimer’s disease:
|Herpes-simplex-Virus 1 (Human Herpes Virus 1, HHV1)
|Oral Herpes infection
|Herpes-simplex-Virus 2 (HHV2)
|Genital Herpes infection
|Varizella-Zoster Virus (HHV3)
|Human Herpes Virus (HHV5)
|Human Herpes Virus (HHV6)
|Hepatitis-C Virus (HCV)
|Hepatitis C infection
Moreover, the research results further suggest that even if a brain infection with microorganisms is not the triggering event in the neuropathogenesis ending with Alzheimer’s disease, but merely an opportunistic spread of the pathogen to an already damaged organ, such infections may well aggravate or accelerate the course of the disease.
The connections must therefore be multi-causal and it is important not to think in terms of pure repair mechanisms again and now to put all energy and money into the medicinal dissolution of plaques, but to question what is causing and systemically so wrong that more and more people are obviously becoming ill. So the right question is: what is causing our body system to go so wrong that the regeneration of the brain areas is no longer possible?
The answer is largely hidden in our western lifestyle, and this website reports on this in detail.
Akiyama, H., Ikeda, K., Katoh, M., McGeer, E.G, McGeer, P.L. (1992): Expression of MRP14, 27E10, interferon-α and leukocyte common antigen by reactive microglia in postmortem human brain tissue. Journal of Neuroimmunology 50/2, pp 195-201
Little, C.S, Hammond, C.J., MacIntyre, A., Balin, B.J., Appelt, D.M. (2004): Chlamydia pneumoniae induces Alzheimer-like amyloid plaques in brains of BALB/c mice. Neurobiology of Aging 25/4, pp 419-429