Sustained tau phosphorylation and microglial activation following repetitive traumatic brain injury

Andre Marolop Pangihutan Siahaan, Rr Suzy Indharty, Jessy Chrestella, Wismaji Sadewo, Steven Tandean, Siti Syarifah

Research output: Contribution to journalArticlepeer-review

Abstract

BACKGROUND: Repetitive traumatic brain injury (TBI), even without acute sequela, can induce a delayed neurodegenerative with overexpression of phosphorylated tau (p-tau) as hallmark, caused by chronic inflammation mediated in part by microglial activation. AIM: The aim of this study was to examine the dynamics of p-tau accumulation and microglial activation following repetitive TBI. MATERIALS AND METHODS: Thirty Sprague–Dawley rats were randomized into a sham control group and two treatment groups receiving three successive closed-skull impacts (TBI model) from a 40-g mass dropped from a 1-m height on alternating days (days 0, 1, 3, and 7). The first treatment group was sacrificed on the last day of trauma and the second treatment group after 7 days of no trauma. The expression level of p-tau was evaluated by AT-8 antibody immunostaining and microglial activation by anti-CD-68 immunostaining. RESULTS: Immunoexpression of AT-8 was significantly elevated 7 days after TBI compared to the last day of trauma and compared to the sham control group, while CD-68 expression was significantly higher than sham controls on the last day of trauma and remained elevated for 7 days without trauma. CONCLUSION: The study showed that brain trauma can induce p-tau overexpression and microglial activation that is sustained during the non-trauma period.

Original languageEnglish
Pages (from-to)837-840
Number of pages4
JournalOpen Access Macedonian Journal of Medical Sciences
Volume8
Issue numberA
DOIs
Publication statusPublished - 2 Jan 2020

Keywords

  • Activated microglia
  • Phosphorylated tau
  • Repetitive traumatic brain injury

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