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    Home > Biochemistry News > Biotechnology News > Detectable 10 years before Alzheimer's disease symptoms appear!

    Detectable 10 years before Alzheimer's disease symptoms appear!

    • Last Update: 2023-02-01
    • Source: Internet
    • Author: User
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    Alzheimer's
    disease begins decades before any symptoms, such as memory loss, begin to manifest.
    Therefore, early diagnosis increases the chances of slowing the
    disease with medication.
    A new study on the genetic form of the disease suggests that a protein called GFAP may be a biomarker in the early stages of the disease
    .
    The study, conducted by researchers at the Karolinska Institute and published in the journal Brain One Day, may allow us to detect this serious and common disease
    much earlier.

    "Our findings suggest that GFAP, a biomarker thought to activate immune cells in the brain, reflects changes in the brain that occur due to Alzheimer's disease that occur before tau accumulation and measurable neuronal damage," said first author Charlotte Johansson, a doctoral student
    in the Department of Neurobiology, Nursing Science and Sociology at Karolinska Institutet in Sweden 。 "In the future, it could serve as a non-invasive biomarker for early activation of immune cells, such as astrocytes in the central nervous system, which is valuable
    for the development of new drugs and the diagnosis of cognitive diseases.
    "

    According to the Swedish Brain Foundation, Alzheimer's disease causes 60 to 70 percent of dementia cases
    .
    In Alzheimer's disease, nerve cells in the brain degenerate
    due to the abnormal accumulation of β-amyloid and tau proteins.
    As more and more brain neurons are damaged, this manifests itself as impairment
    of cognitive functions such as memory and language.

    The disease develops imperceptibly, and biological changes in the brain begin 20 to 25 years before memory loss and other cognitive symptoms become apparent
    .
    The sooner a patient is correctly diagnosed, the sooner they will receive the right treatment
    .
    This is one of
    the reasons why more research is needed on precise, easy-to-use methods for early diagnosis.

    Researchers at Karolinska Institute and their colleagues at Landspitali University Hospital in Iceland, the University of Gothenburg in the UK and University College London have been studying blood biomarkers for early pathological changes in a rare inherited form of Alzheimer's disease, which accounts for less than 1%
    of all cases.
    If one parent has Alzheimer's disease caused by a genetic mutation, they themselves have a 50% risk of developing the disease
    .

    In their study, the researchers analyzed 164 plasma samples
    from 33 mutation carriers and 42 relatives who did not have a genetic predisposition to disease.
    Data was collected between 1994 and 2018
    .

    Their results revealed clear changes
    in the concentration of several proteins in the blood of the mutation carriers.

    "The first change we observed was an increase in GFAP (glial fibrillary acidic protein) about a decade before the first disease symptoms appeared," said Caroline Graff, the study's last author, a professor
    in the Department of Neurobiology, Nursing Science and Sociology at the Karolinska Institutet.
    "This was followed by an increase in the concentration of P-tau181, followed by NfL (neurofilament photoprotein), which we already know is directly related
    to the extent of neuronal damage in Alzheimer's brain.
    This finding about GFAP raises the chances of
    early diagnosis.

    The research was supported by grants from several institutions, including the Swedish Brain Foundation, the Swedish Alzheimer's Foundation, and the ALF Project (see full list of studies).

    Authors Kaj Blennow and Henrik Zetterberg have been involved in several collaborations
    with private pharmaceutical companies.
    No other conflicts of interest were reported
    .

    Article Plasma biomarker profiles in autosomal dominant Alzheimer's disease


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