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    Home > Active Ingredient News > Study of Nervous System > [Two breakthrough new studies] One is a new technology to reduce Alzheimer’s disease β-amyloid protein, and the other is a new link between the subgingival microflora imbalance and Alzheimer’s disease biomarkers

    [Two breakthrough new studies] One is a new technology to reduce Alzheimer’s disease β-amyloid protein, and the other is a new link between the subgingival microflora imbalance and Alzheimer’s disease biomarkers

    • Last Update: 2021-04-23
    • Source: Internet
    • Author: User
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    This article is converted Medicine original, reproduced please indicate the source Author: Yun Introduction: Recently, researchers found that two ground-breaking research on Alzheimer's disease, so that people have the cause of Alzheimer's disease deeper Cognition.

    Alzheimer's disease (Alzheimerpsdisease) is a common neurodegenerative disease in the elderly.

    It is a group of independent degenerative diseases of the central nervous system.
    Its pathological features include decreased number of neurons, senile plaques (SP), neurofibrillary tangles (NFT), vacuolar degeneration of hippocampal pyramidal cells, vascular amyloidosis, etc.
    The most common is that senile plaques increase significantly.

    The exact pathogenesis of Alzheimer's disease is still unclear.
    At present, the formation of amyloid protein and the deposition of β-amyloid peptide are the signs of the pathogenesis of Alzheimer's disease.

    Immunotherapy using anti-amyloid beta antibodies has been emphasized as a promising method to prevent and treat Alzheimer's disease by enhancing the clearance rate of microglia of amyloid beta peptide.

    However, the efficiency of antibody delivery to the brain is limited, so an alternative strategy is needed to promote the clearance of brain amyloid.

    Recently, scientists published a paper entitled "Photo-oxygenation by a biocompatible catalyst reduces amyloid-β levels in Alzheimer's disease mice" in the journal "Brain".

    Studies have proved that the photooxygen catalyst can remove amyloid accumulated in the brain of Alzheimer's disease mice and enhance the microglial degradation of amyloid β peptide.

    This research has developed a new technology for amyloid.

    Researchers have developed a small molecule described as a "photooxygen catalyst.
    "
    Part of the reason for this descriptor is that the molecule contains oxygen atoms, which can change the chemical bonds that hold the molecules together, just like oxidizing bleach can be used to decontaminate washing machines.

    But this catalyst is designed for the folding structure of amyloid and is designed to remove plaque.

    But only when instructed to do so.

    The molecule remains in an inert state until it is activated by near-infrared light.

    Once it is activated, the amyloid is picked up, and the brain's immune cells, also known as microglia, will come to "clean up the mess", remove debris, and leave healthy cells behind.

    This technology was studied in living mice with Alzheimer’s disease.
    Scientists injected its molecules directly into the brains of rodents and used probes to shine light into their brains for 30 minutes a day.
    A week.

    Then they checked their brain tissue by chemical analysis and found that amyloid was significantly reduced.

    As part of a separate experiment on mouse cells, it can be seen that microglia engulf and break down oxygenated amyloid.

    In order to one day transfer their technology to human patients, the scientists also conducted additional experiments on brain samples donated by Alzheimer's patients, and achieved promising results.

    They pointed out that one of the problems that still needs to be overcome is to perfect the design of the catalyst so that it can be triggered by the light outside the skull.

    Coincidentally, recently, researchers at New York University discovered that the increase in "bad" bacteria in the gums and the decrease in "good" bacteria are related to the brain's beta-amyloid protein.

    This study shows that older people who have more harmful bacteria than healthy bacteria in their gums are more likely to find β-amyloid in their brains.

    However, this imbalance of oral bacteria has nothing to do with another Alzheimer's disease biomarker called tau protein.

    The research was published in "Alzheimer's & Dementia: Diagnosis, Assessment & Disease Monitoring", entitled "Periodontal dysbiosis associates with reduced CSF Aβ42 in cognitively normal elderly".

    Alzheimer's disease is characterized by two hallmark proteins in the brain: beta-amyloid and tau protein.

    β-amyloid aggregates together to form plaques.
    It is considered to be the first protein deposited in the brain during the development of Alzheimer's disease.
    Tau protein accumulates in nerve cells and forms tangles.

    The researchers studied 48 healthy, cognitively normal adults 65 years and older.

    Participants undergo oral examinations, collect bacterial samples from under the gums, and obtain cerebrospinal fluid through a lumbar puncture to determine the levels of β-amyloid and tau protein.

    To assess the brain expression of Alzheimer’s disease proteins, researchers looked for low levels of β-amyloid (indicating high levels of β-amyloid in the brain) and high levels of tau (indicating high levels of brain) in the cerebrospinal fluid.
    Tangle accumulation).

    Under the guidance of Dr.
    Deepak Saxena, a microbiologist at the New York University School of Dentistry, he analyzed the bacterial DNA of samples collected from under the gums.
    The researchers analyzed bacteria known to be harmful to oral health (such as Prevotella, Porphyromonas, etc.
    ).
    Freundella) and bacteria that promote oral health (such as coryneform bacteria, actinomycetes, cystosphages).

    The results show that individuals with an imbalance in the number of bacteria, that is, individuals with an imbalance in the ratio of harmful bacteria to healthy bacteria, are more likely to have the characteristics of Alzheimer's disease, that is, the level of β-amyloid in the cerebrospinal fluid is reduced.

    Researchers hypothesized that because high levels of healthy bacteria help maintain bacterial balance and reduce inflammation, they may have a protective effect on Alzheimer's disease.

    This is the first study to show a link between the imbalance of the subgingival flora and the CSF biomarkers of Alzheimer's disease in the elderly with normal cognition.

    Dr.
    Angela Kamer, associate professor of periodontology and implant dentistry at the New York University School of Dentistry, and the lead author of the study, said, “There are both harmful bacteria that promote inflammation and healthy protective bacteria in the mouth.

    We found that there is evidence to prove it.
    Beta-amyloid in the cerebrospinal fluid is related to the increase of harmful bacteria and the decrease of beneficial bacteria.

    " "Our results show the importance of the oral microbiota in regulating the level of beta-amyloid-not only of the'bad' bacteria.
    "There is also the role of'good' bacteria," Kamer said.
    "These findings indicate that a variety of oral bacteria are involved in the expression of β-amyloid lesions.

    " In this study, the researchers did not find gum bacteria and tau protein levels.
    It is still unclear whether the tau protein damage will develop in the future, or whether the subject will develop symptoms of Alzheimer’s disease.

    Researchers plan to conduct a longitudinal study and clinical trial to test whether improving gum health—removing plaque and tartar deposits under the gums through “deep cleaning”—can change the beta-amyloid in the brain and prevent it Alzheimer's disease.

    These two studies have revealed scientists' breakthrough discoveries about Alzheimer's disease.
    In the future, we hope that scientists will have more in-depth research on this.

    Reference materials: [1] https://medicalxpress.
    com/news/2021-04-power-oxygen-alzheimer-disease-protein.
    html [2] https://academic.
    oup.
    com/brain/advance-article- abstract/doi/10.
    1093/brain/awab058/6224831?redirectedFrom=fulltext [3] https://alz-journals.
    onlinelibrary.
    wiley.
    com/doi/10.
    1002/dad2.
    12172 Note: This article aims to introduce the progress of medical research, not As a reference for the treatment plan.

    If you need health guidance, please go to a regular hospital for treatment.

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