Pathomechanisms and Neuroprotective Strategies in Traumatic Brain Injury

Authors

  • Mufidah Radwah Ja'faruddin Universitas Mataram
  • Anis Wulan Prabajati Universitas Mataram
  • Ni Luh Putu Faniacetta Dahayu Wedantari Universitas Mataram
  • Nurussifa' Innuffus Universitas Mataram

DOI:

https://doi.org/10.58258/wj4xqr67

Abstract

Cedera otak traumatik (traumatic brain injury/TBI) merupakan penyebab penting kematian dan disabilitas neurologis akibat cedera primer serta kaskade cedera sekunder yang melibatkan eksitotoksisitas, disfungsi mitokondria, neuroinflamasi, gangguan blood–brain barrier (BBB), edema, degenerasi akson, dan kematian sel. Tinjauan ini membahas patomekanisme cedera primer dan sekunder, mekanisme neuroprotektif endogen, strategi terapi neuroprotektif, serta peran biomarker pada TBI. Tinjauan naratif ini disusun melalui sintesis literatur ilmiah mengenai TBI, neuroproteksi, biomarker, dan terapi inovatif, terutama publikasi tahun 2016–2026. Cedera sekunder merupakan proses multifaktorial yang saling berhubungan; eksitotoksisitas glutamat memicu influx Ca²⁺, disfungsi mitokondria, produksi reactive oxygen species (ROS), dan apoptosis, sedangkan neuroinflamasi, gangguan BBB, edema, serta degenerasi akson memperburuk kerusakan neurologis. Strategi neuroprotektif meliputi modulasi eksitotoksisitas, perlindungan antioksidan dan mitokondria, modulasi inflamasi, faktor neurotrofik, terapi sel punca, dan vesikel ekstraseluler. GFAP dan UCH-L1 berpotensi mendeteksi cedera intrakranial akut, sedangkan NF-L mencerminkan cedera aksonal persisten. Neuroproteksi TBI memerlukan pendekatan multipel target berbasis waktu, heterogenitas pasien, dan profil biomarker. 
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Published

2026-09-21

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Vol. 7 No. 3 (2026): Research of Service Administration Health and Sains Healthys (September)

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How to Cite

Pathomechanisms and Neuroprotective Strategies in Traumatic Brain Injury. (2026). Research of Service Administration Health and Sains Healthys, 7(3), 205-212. https://doi.org/10.58258/wj4xqr67