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Two new studies point to unexpected ways to understand and treat Alzheimer's disease, a degenerative brain disease that affects more than 30 million people worldwide, particularly the elderly. According to a study published this week, sleep deprivation and the presence of a bacterium at the origin of gum infections are closely correlated with the onset of the disease and, if they were controlled, could reduce their progress.
The two badyzes were coordinated by researchers from American institutions. David Holtzman, of Washington University in St. Louis, led the study on the effects of lack of sleep on the origins of Alzheimer's disease, which just appeared in the journal Science.
Research on the link between bacteria Porphyromonas gingivalis and the disease, in turn, were directed by Stephen Dominy, of the biotechnology company Cortexyme in San Francisco, and are part of the journal Science Advances. The researchers' participation in the study is not a fluke: Dominy and his colleagues, Casey Lynch and Andrei Konradi, have patented drugs that seem to be able to block the action of the microbe.
The roots of Alzheimer's disease, despite the have been the subject of in-depth studies in recent decades and are not yet fully understood. In recent years, the strongest badumption is that the problem starts with changes to the protein called tau (Greek letter name equivalent to our letter T).
Very abundant in healthy neurons, tau protein. can in some contexts undergo changes in its structure, to which several phosphoryl groups (formed by phosphorus and oxygen atoms) are connected. When this occurs, tau molecules can aggregate in fibers and filaments, resulting in loss of neurons and synapses (connections between neurons).
By mechanisms that are not yet completely clear, the process of aggregating tau molecules can propagate from synapse to synapse, progressively killing the neural networks. It is common for this to begin in areas of the brain that are essential for new memories, which explains the recurring forgetfulness of people with Alzheimer's disease. The process can lead the patient to death.
The link with tau is clearer in the first study, which involves sleep deprivation. It turns out that the protein is released more often by neurons when they are excited, with more intense connections in the synapses, which tends to be more common during the waking state. One would expect that an even more potent tau molecule accumulation process would occur when an individual is prevented from sleeping normally
. That's exactly what researchers have discovered, first by badyzing hand-manipulated mice in the laboratory for not sleeping properly: the presence of tau has doubled in normal private sleep rodents.
Already in humans participating in an experiment in which they alternated nights of rest with others where sleep was interrupted periodically, the increase of tau molecules in the so-called cerebrospinal fluid (fluid present in the brain and spinal cord) was 50%. Other experiments on mice injected with human versions of tau in their brain revealed that the protein had spread to other regions of the body during cycles of sleep deprivation.
The presence of the bacterium P. gingivalis which causes chronic periodontitis (essentially a serious inflammation of the gingiva and surrounding areas), constitutes, on the other hand, a known risk factor for the disease. d & # 39; Alzheimer's.
more detailed clues about the cause-and-effect relationship between one thing and another, however. It would be conceivable that people at the beginning of a degenerative disease simply neglect oral hygiene without the bacteria being linked to the problem.
New data, provided by the Dominy team, however, reinforced the idea of a causal link. Mice infected with the oral microbe had also invaded their brain by P. Gingivalis with molecular effects reminiscent of Alzheimer's disease.
The researchers also identified both the proteins and the DNA of the bacterium in virtually every studied Alzheimer's brain (the frequency in healthy human brains). halve.)
A toxin produced by a bacterium is capable of causing the death of neurons and structurally affecting the tau protein, which can trigger the disease. And, finally, the molecules patented by scientists to block this toxin have been able to cope with infections in mice, protecting neurons – something that common antibiotics can not do, as far as we know.
So, if further research confirms these data, regulate sleep, diagnose, and combat the presence of P. gingivalis could be included in the list of promising approaches to disease control. Alzheimer's
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