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    Home > Active Ingredient News > Study of Nervous System > Alzheimer & Dementia: Targeting Aβ to treat Alzheimer's disease?

    Alzheimer & Dementia: Targeting Aβ to treat Alzheimer's disease?

    • Last Update: 2021-11-02
    • Source: Internet
    • Author: User
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    Although the deposition of amyloid fibrin β (Aβ) in the brain is determined to be one of the earliest pathological changes, it has occurred at least ten years before the clinical diagnosis of Alzheimer's disease (AD) , but so far, it has been targeted at Aβ The treatment of is basically ineffective in slowing down cognitive decline.


    Diagnosis of Aβ treatment is basically ineffective in slowing down cognitive decline.


    It is also possible that not all cognitive declines, even if diagnosed as AD, are not due to neurodegeneration caused by Aβ and tau


    The study used partial least squares structural equation pathway model to evaluate imaging biomarkers (global Aβ-PET uptake, regional tau-PET uptake, and MRI-based regional atrophy) among 248 Aβ-positive elderly with cognitive impairment and dementia.


    The results showed that Aβ accounted for 16% of the cross-sectional cognitive impairment variation, tau accounted for 46%-47%, brain atrophy accounted for 25%-29%, but 53%-58% of the total cognitive impairment variation was caused by AD risk factors Intermediary and direct effects explained


    Aβ accounts for 16% of the cross-sectional cognitive impairment variation, tau accounts for 46%-47%, and brain atrophy accounts for 25%-29%.


    The influence of AD risk factors on the overall AD continuity of mPACC and ADAS-Cog measured by baseline cognitive outcome


    To a large extent, the important pathways identified in the cognitive decline model are similar to the pathways in the baseline cognitive impairment model, but men have a significant direct impact on the latent variable (LV) of tau, but they have no effect on any index of cognitive decline.


    Larger WML has a significant direct effect on ΔADAS-Cog, but no effect on ΔmPACC


    In summary, the study suggests that treatments that remove the effects of Aβ and tau on neurodegeneration and downstream effects may not be very effective in slowing down cognitive decline or reversing cognitive impairment in Alzheimer's disease


    references:

    Contribution of Alzheimer's biomarkers and risk factors to cognitive impairment and decline across the Alzheimer's disease continuum.


    Contribution of Alzheimer's biomarkers and risk factors to cognitive impairment and decline across the Alzheimer's disease continuum.


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