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    Home > Active Ingredient News > Study of Nervous System > Neurology-C reactive protein, or involved in AD neurodegeneration

    Neurology-C reactive protein, or involved in AD neurodegeneration

    • Last Update: 2021-08-03
    • Source: Internet
    • Author: User
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    The apolipoprotein E4 (APOE ε4) allele is the main genetic risk factor for late-onset Alzheimer's disease (AD)
    .


    However, even among APOE ε4 carriers older than 90 years2, not all APOE ε4 carriers develop dementia


    The increase of CRP in the blood is only related to the increased risk of AD in carriers of APOE ε4 allele, which indicates that CRP may change the role of APOE ε4, leading to AD-related neurodegeneration
    .


    Nevertheless, the interaction of APOE ε4 and CRP on cognitive decline and AD pathology is still unknown


    The interaction of APOE ε4 and CRP on cognitive decline and AD pathology is still unknown


    Immune heart blood vessels

    In this way, Qiushan Tao et al.
    of Boston University School of Medicine used the Alzheimer’s Disease Neuroimaging Initiative (ADNI) cohort to explore the APOE ε4 status (none, one and two APOE ε4 alleles) and peripheral CRP recognition.
    Know the independent and interactive effects of AD biomarkers in vivo, including cerebrospinal fluid (CSF) amyloid β peptide 42 (Aβ42), total tau (t-Tau) and phosphorylated tau (p-Tau)
    .

    They analyzed data from the Alzheimer's Disease Neuroimaging Initiative (ADNI) study, including APOE genotype; plasma CRP concentration; diagnostic status (ie
    .


    dementia due to MCI and AD); mini mental status examination (MMSE) and clinical dementia Scoring (CDR) dementia staging tool; the concentration of amyloid β peptide (Aβ42), total tau (t-tau) and phosphorylated tau (p-tau) in cerebrospinal fluid (CSF); and amyloid (AV45) PET imaging


    diagnosis

     

    Of the 566 ADNI participants, 274 (48.
    4%) did not have one, 222 (39.
    2%) had one, and 70 (12.
    4%) had two APOEε4 alleles
    .

    Only in participants with two APOE ε4 alleles, increased CRP was associated with decreased MMSE at baseline and 12-month follow-up
    .

    The increase in CRP is related to the decrease in MMSE at baseline and 12-month follow-up.
    The increase in CRP is related to the decrease in MMSE at baseline and 12-month follow-up.

    The interaction between the two APOE ε4 alleles and the increase in plasma CRP is associated with t-Tau (β = 11.
    21, SE = 3.
    37, p <0.
    001) and p-Tau (β = +2.
    74, SE = 1.
    14, p < 0.
    01) is related to the increase in the level
    .


    In people without the APOE ε4 allele, an increase in CRP is associated with a decrease in CSF t-Tau and p-Tau


    The important significance of this study is that the CRP released during peripheral inflammation may be a mediator of APOE ε4-related AD neurodegeneration, and can be used as a drug target for AD
    .

    CRP released during peripheral inflammation may be a mediator of APOE ε4-related AD neurodegeneration, and can be used as a drug target for AD
    .


    CRP released during peripheral inflammation may be a mediator of APOE ε4-related AD neurodegeneration, and can be used as a drug target for AD


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