Chronic traumatic encephalopathy (CTE) is a neurodegenerative disease caused by repetitive brain trauma that cancontinues to be dementia, alzheimer and parkinsonism. Traumatic brain injury increased free radicals in brain thatcaused oxidative stress and induced lipid peroxidation, neuron damage and producing MDA. The purpose is todetermine the correlation between administration of ALA and MDA level in rat’s brain model of traumatic braininjury and its effective dose. Rats are randomLy divided into 7 groups. Normal group without treatment, K(-) wasgiven NaCl 0,9% 1,5 mL, K(+) was given citicoline 6,75 mg, K1 was given ALA 1,0125 mg, K2 was given ALA 2,025mg, K3 was given ALA 4,05 mg, K4 was given ALA 8,1 mg and received 30 days traumatic brain injury treatment bydropped 245 g load on the rat’s head at 35 cm height. MDA level in brain were measured on the 31th day withMDA-TBA method by spectrofotometer. The averages of MDA levels were N 1,64 μg/mL; K(+) 2,09 μg/mL; K(-) 4,87μg/mL; K1 2,73 μg/mL; K2 2,68 μg/mL; K3 2,20 μg/mL and K4 2,02 μg/mL. Pearson’s analysis shows strong andsignificant negative correlation (r= -0,790) between administration of ALA and MDA level in rat’s brain model oftraumatic brain injury (p<0,05). The effective dose of ALA is 8,625 mg/150gBW.Keywords : Alpha lipoic acid, MDA, traumatic brain injury, CTE

THE USE OF ALPHA LIPOIC ACID AS TAU PROTEIN DEGENERATION INHIBITOR ON PREVENCE CHRONIC TRAUMATIC ENCEPHALOPATHYABSTRACTIntroduction: Chronic traumatic encephalopathy (CTE) is progressive neurodegenerative syndrome caused by repeated blunt object injury affects the head. This condition results in degeneration of tau, a protein that can help stabilize and support certain structures in brain’s cells, including internal transport system of the brain’s cell. Repeated injuries cause the degeneration of tau proteins that proteins misfold and change their form and then become free radicals cause neuron death. Alpha lipoic acid (ALA) is one of the antioxidant can bind free radicals and regenerate antioxidant vitamin C, vitamin E, and coenzyme Q10.Aim: To exam the effectiveness of alpha lipoic acid to inhibit the degeneration of tau protein in immunohistochemistry experimental animals’s brain.Methods: Experimental study in vivo of CTE model in rat by dropped 245g load on the head at 35cm height. 28 rats were randomly assigned to 7 groups; normal group without treatment, negative control group is given NaCl 0.9% 1.5mL, positive control group is given citicholine 6.75mg, group A is given ALA 1.0125mg, group B is given ALA 2.025mg, group C is given ALA 4.05mg, group D is given ALA 8.1mg and received 30 days CTE treatment. Experiment was conducted in May 2017 at Medical Faculty University of Jember. Tau protein degeneration were scored immunohistochemically.Results: Group D showed the closest to normal, while group A showed most tau protein degeneration (190.25±26.89) compared to normal group (53.25±43.39). Group D also showed lower tau protein score compared to positive control significantly.Discussion: Alpha lipoic acid is able to inhibit the progression of tau protein degeneration on immunohistochemistry staining of animal’s brains in CTE model.Keyword: Alpha lipoic acid, chronic traumatic encephalopathy, tau proteinABSTRAKPendahuluan: Chronic traumatic encephalopathy (CTE) adalah sindrom neurodegeneratif progresif akibat cedera berulang benda tumpul yang mengenai kepala. Cedera berulang tersebut menyebabkan degenerasi protein tau, yaitu protein yang dapat membantu menstabilkan dan mendukung struktur tertentu dalam sel otak, termasuk sel dari sistem transportasi internal. Akibatnya, protein tau gagal melipat dan mengubah bentuk, sehingga menjadi radikal bebas yang dapat menye- babkan kematian neuron. Alpha lipoic acid (ALA) adalah salah satu senyawa antioksidan yang mampu mengikat radikal bebas dan meregenerasi antioksidan vitamin C, vitamin E, dan koenzim Q 10.Tujuan: Mengetahui efektivitas pemberian alpha lipoic acid dalam menghambat progresivitas degenerasi protein tau pada gambaran imunohistokimia otak hewan coba.Metode: Studi eksperimental in vivo model CTE pada tikus dengan dijatuhi beban 245g di kepala pada ketinggian35cm. Terdapat 28 tikus yang dibagi menjadi 7 kelompok, yaitu: kelompok normal tanpa perlakuan, kelompok kontrol (-) diberikan NaCl 1,5mL, kontrol (+) diberikan sitikolin 6,75mg, kelompok A diberikan ALA 1,0125mg, kelompok B diberi- kan ALA 2,025mg, kelompok C diberikan ALA 4,05mg, serta kelompok D diberikan ALA 8,1mg dan mendapat perlakuan CTE selama 30 hari. Penelitian dilakukan pada bulan Mei 2017 di Fakultas Kedokteran Universitas Jember. Pemeriksaan skor degenerasi protein tau berdasarkan gambaran imunohistokimia.Hasil: Kelompok D dengan dosis tertinggi 8,1mg merupakan gambaran degenerasi protein tau paling sedikit mendekati normal, sedangkan kelompok A dengan dosis terendah 1,0125mg merupakan gambaran degenerasi protein tau paling banyak (190,25±26,89), jauh lebih tinggi dibandingkan kelompok normal (53,25±43,39). Demikian pula kelompok D dengan kontrol positif menunjukkan skor degenerasi protein tau kelompok D lebih rendah dibandingkan dengan kontrol positif secara bermakna.Diskusi: Pemberian ALA dosis tinggi mampu menghambat progresivitas degenerasi protein tau pada gambaran imunohistokimia otak hewan coba yang mengalami cedera kepala berulang.Kata kunci: Alpha lipoic acid, chronic traumatic encephalopathy, protein tau