ABSTRAK
PERBAIKAN PLASTISITAS OTAK YANG DITANDAI OLEH
PENIPISAN BETA-AMYLOID DAN PENURUNAN C-REACTIVE PROTEIN SERTA PENINGKATAN BDNF AKIBAT LATIHAN GERAK
PADA TIKUS MODEL DEMENSIA
Plastisitas otak (Neuroplastisitas) adalah istilah yang menggambarkan adanya perubahan interkoneksi saraf berupa perubahan interneural dan reorganisasi sinaptik melalui suatu stimulasi. Brain-derived neurotrophic factor (BDNF) suatu neurotrophin yang merangsang dan mengendalikan plastisitas otak. Demensia adalah sindroma yang ditandai hilangnya memori, disertai gangguan fungsi kognitif lain mengakibatkan gangguan aktivitas sehari-hari dan latihan gerak adalah trigger proses untuk perbaikan plastisitas otak dengan perantara neurotrophin. Penelitian eksperimental laboratorik dengan 33 ekor tikus Wistar jantan usia 3 bulan, sebagai tikus model demensia yang diberikan pelatihan dan tanpa pelatihan.
Hasil penelitian membuktikan bahwa dijumpai perbaikan plastisitas otak akibat latihan gerak yang ditandai oleh penipisan endapan β-Amyloid yang signifikan pada Kelompok latihan gerak 2 rangkai dibandingkan Kelompok satu rangkai latihan dan Kelompok tanpa latihan, dengan uji antar kelompok dijumpai berbeda bermakna (ANOVA, p<0.001). Peningkatan kadar BDNF serum yang jauh lebih tinggi antara Kelompok latihan 2 rangkai dibandingkan tanpa latihan dan juga lebih tinggi dibandingkan Kelompok 1 rangkai, dengan uji antar kelompok dijumpai berbeda bermakna (ANOVA, p=0.022). Penurunan CRP pada Kelompok latihan 2 rangkai dijumpai lebih menurun dibandingkan Kelompok latihan 1 rangkai ataupun tanpa latihan dengan uji antar kelompok dijumpai penurunan yang terjadi tidak berbeda bermakna, penurunan di antara ketiga kelompok (ANOVA, p=0,720). Peningkatan kadar BDNF LCS yang jauh lebih tinggi antara Kelompok latihan 2 rangkai dibandingkan tanpa latihan dan juga lebih tinggi dibandingkan Kelompok 1 rangkai, dengan uji antar kelompok dijumpai berbeda bermakna di antara tiga kelompok (ANOVA, p=0,002). Peningkatan ekspresi BDNF astrosit pada Kelompok latihan 2 rangkaian dibandingkan dengan Kelompok latihan 1 rangkai dan tanpa latihan dengan uji antar kelompok dijumpai perbedaan di antara ketiga Kelompok (ANOVA<0,001). Peningkatan ekspresi BDNF Mikroglia dengan latihan 2 rangkai dibandingkan Kelompok latihan 1 rangkat dan juga Kelompok tanpa latihan, dengan uji antar kelompok tidak dijumpai perbedaan yang bermakna antara ketiga kelompok (ANOVA, p=0,605)
Kesimpulan bahwa perbaikan plastisitas otak ditandai oleh penipisan β-Amyloid, peningkatan BDNF serum/ LCS, penurunan CRP disertai meningkatnya ekspresi BDNF astrosit akibat latihan gerak. Latihan gerak dua rangkai memperbaiki plastisitas dibandingkan Kelompok latihan 1 rangkai ataupun tanpa latihan, Astrosit merupakan sel glia yang aktif pada plastisitas otak. Konsep perbaikan plastisitas otak melalui latihan gerak dapat dipromosikan untuk meningkatkan kualitas hidup dan sumber daya manusia.
Kata Kunci:
ABSTRACT
BRAIN PLASTICITY RECOVERY MARKED BY
DECREASEOF BETA-AMYLOID AND C-REACTIVE PROTEIN ACCOMPANIED BY THE INCREASE OF BDNF AS THE EFFECTS OF
PHYSICAL EXERCISE IN DEMENTIA RAT MODEL
Brain Plasticity (Neuroplasticity) is a term used to describe the changes of neural interconnection in the forms of interneural changes and synaptic reorganisation through simulation. Brain-derived neurotrophic factor (BDNF) a neurotrophin that stimulates and controls brain plasticity. Demensia is a syndrome characterized by memory loss, accompanied by other cognitive impairment, interference of daily life and physical activities is a trigger process to brain plasticity repair through neurotrophin. This Laboratory experimental study examining 33 male wistar rats aged 3 months as dementia rats model by which they were given exercise and no exercise.
The result of the research showed that there was improvement in brain plasticity as the result of physical exercise characterized by significant thinning of Beta Amyloid in 2 series physical exercise group compared to 1 serie of physical exercise group and group non exercise, there was significant difference (ANOVA, p < 0,001) among groups.
The increased serum of BDNF levels was far higher in 2 series exercise group compared to non exercise higher compare to 1 serie exercise group as well by the results test among groups was found significant difference (ANOVA, p = 0,022). It was observed that series of physical exercises in dementia rat model of results in a slightly decrease of serum CRP levels of 1 serie and 2 series exercises compared to non exercise and these effects in 2 series exercises compared to non exercise, but statistically not significant, with test among groups (ANOVA, p=0,720). Increase of CSF BDNF which was far higher among 2 series exercise group compared to non exercise group higher than 1 serie exercise group as well with test among group and statitically significant (ANOVA, p = 0,002). Expression increased of astrocytes BDNF in the 2 series exercise group compared to 1 serie exercise group and non exercise group by test among groups was found having a significantly different result (ANOVA < 0.001). Expression increased of Microglia BDNF with 2 series exercise group compared to 1 serie exercise group as well as group non exercise, by the test between groups, no significant difference was found among the three groups (ANOVA, p = 0.605).
It is concluded that the improvement of brain plasticity is characterized by significant decrease of Amyloid-β, BDNF serum / CSF decrease CRP accompanied with increase of astrocytes BDNF as the result of physical exercise. Two series physical exercises improves brain plasticity compared to 1 serie physical exercise or non exercise. Astrocytes is an active glial cell in brain plasticity. Improvement process of brain plasticity through physical exercise can be promoted to improve the quality of life and human resources.
