Increased MYD88 blood transcript in a mouse model of Alzheimer's disease.

Background: Neuroinflammation plays a prominent role in Alzheimer's disease (AD), both in pathogenesis and disease progression. It has been shown that TLR/MYD88 signaling is involved in the chronic low-grade sterile inflammation associated with AD. Several studies have evidenced high levels of MYD88...

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Published in:BMC Neuroscience Vol. 23; no. 1; pp. 1 - 7
Main Authors: Cucos, Catalina Anca, Dobre, Maria, Dragnea, Elena Mihaela, Manda, Gina, Milanesi, Elena
Format: research Journal Article
Published: BioMed Central 3/11/2022
Online Access:View this record in EBSCOhost
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      jtl: BMC Neuroscience
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      dt: 3/11/2022
      vid: 23
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      pub: BioMed Central
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        NLM35277123
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        10.1186/s12868-022-00699-8
        NLM35277123
        155719562
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        atl: Increased MYD88 blood transcript in a mouse model of Alzheimer's disease.
      aug:
        au:
          Cucos, Catalina Anca
          Dobre, Maria
          Dragnea, Elena Mihaela
          Manda, Gina
          Milanesi, Elena
        affil: Laboratory of Radiobiology, "Victor Babes" National Institute of Pathology, Bucharest, Romania
      sug:
        subj:
          Alzheimer's Disease Metabolism
          Alzheimer's Disease Drug Therapy
          Alzheimer's Disease
          Animal Studies
          Human
          Carrier Proteins
          Models, Biological
          Disease Progression
          Mice
          Protein Precursors Metabolism
          Inflammation Metabolism
          Carrier Proteins Metabolism
          Comparative Studies
          Multicenter Studies
          Evaluation Research
          Validation Studies
      ab: Background: Neuroinflammation plays a prominent role in Alzheimer's disease (AD), both in pathogenesis and disease progression. It has been shown that TLR/MYD88 signaling is involved in the chronic low-grade sterile inflammation associated with AD. Several studies have evidenced high levels of MYD88 in the brain of patients and animal models of AD, but no study has assessed so far its levels in blood.Methods: In this study we evaluated the blood mRNA levels of MYD88 in a mouse model of AD, and also the putative effect of Rivastigmine treatment on MYD88 expression. Twenty-eight transgenic APP/TAU mice (AT) and twenty-two control C57/BL6j mice (WT) were included in this study, out of which five transgenic AT and five WT mice were treated with Rivastigmine.Results: Increased MYD88 transcript in the whole blood from AT mice as compared to WT controls was found, which seems to increase in time due to disease progression and not to aging. This finding suggests that blood leukocytes are primed to develop TLR/MYD-mediated inflammatory processes. Moreover, results indicate that MYD88 blood levels were not modulated by the diseases-specific treatment with Rivastigmine.Conclusions: Our results suggest that MYD88 might be a promising blood biomarker to monitor AD progression.
      pubtype: Academic Journal
      doctype:
        research
        Journal Article
      ougenre: Article
    language: English
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