Sustained Tau Phosphorylation and Microglial Activation Following Repetitive Traumatic Brain Injury

Authors

  • Andre Marolop Pangihutan Siahaan Department of Neurosurgery, Faculty of Medicine, Universitas Sumatera Utara, Medan, Indonesia http://orcid.org/0000-0003-1107-055X
  • Rr Suzy Indharty Department of Neurosurgery, Faculty of Medicine, Universitas Sumatera Utara, Medan, Indonesia
  • Jessy Chrestella Department of Anatomic Pathology, Faculty of Medicine, Universitas Sumatera Utara, Medan, Indonesia
  • Wismaji Sadewo Department of Neurosurgery, Faculty of Medicine, Universitas Indonesia, Jakarta, Indonesia
  • Steven Tandean Department of Neurosurgery, Faculty of Medicine, Universitas Sumatera Utara, Medan, Indonesia
  • Siti Syarifah Department of Pharmacology and Therapeutic, Faculty of Medicine, Universitas Sumatera Utara, Medan, Indonesia

DOI:

https://doi.org/10.3889/oamjms.2020.5471

Keywords:

Activated microglia, Repetitive traumatic brain injury, Phosphorylated tau

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.

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Author Biography

Andre Marolop Pangihutan Siahaan, Department of Neurosurgery, Faculty of Medicine, Universitas Sumatera Utara, Medan, Indonesia

Department of Neurosurgery

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Published

2020-10-26

How to Cite

1.
Siahaan AMP, Indharty RS, Chrestella J, Sadewo W, Tandean S, Syarifah S. Sustained Tau Phosphorylation and Microglial Activation Following Repetitive Traumatic Brain Injury. Open Access Maced J Med Sci [Internet]. 2020 Oct. 26 [cited 2024 Jun. 17];8(A):837-40. Available from: https://oamjms.eu/index.php/mjms/article/view/5471

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Pathophysiology

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