On the track of Alzheimer's disease
Alzheimer's disease - a forgetful disease. This yet untreatable disease, which disrupts the proper functioning of the brain, is currently the most common cause of dementia. In a recent study, Czech scientists have tried to uncover the possible cause of this disease. Tomáš Macháček from the Department of Parasitology at the Faculty of Science, Charles University has also contributed to the search for the mechanism of this disease, especially with his knowledge of infectious biology and immunology.
This progressive disease of the nervous system, first described in 1907 by the German scientist Alois Alzheimer, currently affects around 100,000 seniors in the Czech Republic. In addition to memory disorders, the so-called "Alzheimer's" is manifested mainly by confusion, loss of orientation in space-time, but also by impaired motor coordination, speech disorders or personality changes. In the late stages, patients are completely dependent on the care of others.
Source: Wikipedia, Author: Jeff Brender
However, the complete mechanism of Alzheimer's disease has not yet been described. The cause is thought to be the pathological accumulation of amyloid beta (Aβ) peptide and hyperphosphorylated Tau protein. However, this hypothesis has not yet led to a resolution of the origins of Alzheimer's disease or to its successful treatment.
Aβ in the brain of an Alzheimer's patient forms so-called senile plaques. Tau proteins are also found in nervous tissue and functionally bind to microtubules. If they are hyperphosphorylated, they unbind from microtubules, aggregate into neurofibrillary tangles, and cause nerve cell breakdown. Neuroinflammation, an inflammation of nervous tissue, is also an important pathological manifestation of this disease. These pathological processes then lead to a visible loss of nerve tissue, which can be detected by imaging methods such as magnetic resonance imaging.
Aβ is produced in the human body by cleavage of amyloid precursor protein, which is further degraded under normal conditions. In Alzheimer's disease, however, there is an imbalance between the production and degradation of Aβ, which then accumulates in the brain and forms the aforementioned plaques that prevent proper communication between neurons. In the ageing body, it thus becomes a trigger for neurodegenerative changes.
Source: Wikipedia.org
Tomáš Macháček joined a team of scientists from the National Institute of Mental Health and the Laboratory of Neurophysiology of Memory of the Institute of Physiology of the Czech Academy of Sciences - Iveta Vojtěchová, Zdena Krištofiková, Aleš Stuchlík, and Tomáš Petrásek, and together they made a detailed research on what may cause the pathological changes leading to the development of Alzheimer's disease. They focused in particular on the so-called infectious hypothesis.
Research to date suggests that Aβ, commonly perceived as the causative agent of pathology, may actually behave antimicrobially, even protecting the brain from pathogens. The infectious hypothesis proposes that Aβ is naturally produced in response to neuroinfections and only when its production or clearance is poorly regulated does it accumulate and become pathogenic. But for what reason does Aβ accumulation occur in some people and not in others? Unfortunately, what triggers such changes is not yet known. Scientists report that, unfortunately, it is impossible to identify something like a universal "Alzheimer's germ" that is behind the clear origin of the disease. However, the study compared different pathogens and their ability to cause neuroinfections and increased Aβ production.
One potential pathogen could be the Lyme disease bacterium Borrelia burgdorferi. This spirochete has been found several times in the brains of Alzheimer's patients. It commonly causes inflammation of the central nervous system and, according to recent research, Borrelia can induce Aβ production and Tau hyperphosphorylation when in contact with human neurons.
Other bacterial pathogens that can cause inflammation of the central nervous system include bacteria of the genus Treponema, specifically the species found in the oral cavity that cause periodontitis, or the lung bacteria Chlamydia pneumoniae. Viruses include Herpes simplex virus (HSV1), which has been shown to increase Aβ levels in in vitro experiments, and anti-herpetic treatment has been observed to reduce the risk of later development of dementia. The role of microscopic fungi/yeasts (Candida albicans) in the development of neuroinfections (and thus potentially Alzheimer's disease) is still questionable. The parasites mentioned in the review - Toxoplasma gondii and Toxocara canis - could be of great help in future research on neuroinfections and the infection hypothesis - but there is not yet enough experimental or epidemiological data to draw a clear conclusion.
The infectious hypothesis has been re-emerging in the minds of scientists in the last few years. Previously, theories of infectious origins of Alzheimer's disease tended to be dismissed or shelved due to insufficient evidence. Now we can say with certainty – neuroinfections are not to be taken lightly even in the longer term. Scientists are calling for future research on immunity in the context of Alzheimer's disease. We can hope that this comprehensive study will also contribute to the mosaic of possible causes of Alzheimer's disease and offer an alternative view of it as an infectious (though not contagious) disease.
Tereza Žirovnická
Published:
Feb 20, 2024 10:00 AM
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