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Title: | Kajian Histopatologi Otak Mencit Pasca Injeksi Protein Marka Penyakit Alzheimer Amioid Beta-42 (Aβ42) |
Other Titles: | Histopathological Study of Mice Brain Post Alzheimer Protein Marker Amyloid Beta-42 (Aβ42) Injections |
Authors: | Juniantito, Vetnizah Darusman, Huda Shalahudin Alayina, Asyifa Gisya |
Issue Date: | 23-Aug-2021 |
Publisher: | IPB University |
Abstract: | Penyakit Alzheimer merupakan terjadi karena degenerasi progresif dan konis pada sel-sel syaraf pada usia tua, yang ditandai dengan keberadaan senile plaque dan neurofibrillary tangles. Otak merupakan organ vital dengan lesio yang signifikan pada Alzheimer karena retensi protein abnormal amiloid beta-42 (Aβ42) pada sel neuron. Studi ini dilakukan untuk mempelajari adanya perubahan histopatologi otak akibat retensi amiloid beta-42 (Aβ42). Digunakan sebanyak 14 jaringan otak mencit, yang terbagi menjadi dua kelompok, yaitu mencit yang diinjeksi dengan antigen Aβ42 (n=6), dan kontrol (n=8). Pengamatan histopatologi jaringan otak dilakukan pada preparat dengan pewarnaan rutin hematoksilin eosin serta congo red yang spesifik mewarnai amiloid. Temuan lesio dianalisa secara deskriptif dan semikuantitatif menggunakan skoring. Berdasarkan pengamatan yang dilakukan, ditemukan 5 jenis lesio patologis sebagai indikator penyakit Azheimer, yaitu neurofibrillary tangles (NFT), granulovacuolar disease (GVD), hirano bodies, cerebral amyloid angiopathy (CAA) dan senile plaque (SP). Lesio GVD, NFT, dan hirano bodies ditemukan pada dua individu yang sama, dengan lesio NFT dan GVD pada tingkat II dan lesio hirano bodies pada tingkat I, sedangkan SP dan CAA ditemukan di keenam individu dengan kedua lesio pada tingkat I. Hasil studi ini menunjukkan bahwa lesio karakteristik Alzheimer dapat ditemukan pada semua mencit yang diinduksi dengan injeksi protein amiloid beta-42. Hasil studi ini dapat memberikan informasi mengenai patogenesis Alzheimer dan potensi mencit sebagai hewan coba pada penelitian penyakit Alzheimer. Alzheimer's disease is caused by the progressive and chronic degeneration of nerve cells in old age, with senile plaques and neurofibrillary tangles as characteristic lesions. The brain is a vital organ with significant lesions in Alzheimer's due to the abnormal protein amyloid beta-42 (Aβ42) retention within nerve cells. The purpose of this study was to look at the histopathological changes in the brain caused by the retention of amyloid beta-42 (Aβ42). 14 mice’s brain tissue were used and divided into two groups: mice injected with Aβ42 (n=6) and control (n = 8). Histopathological examinations of brain tissue were carried out on preparations stained with routine hematoxylin-eosin and congo red, which mark amyloid deposits. The lesion findings were analyzed descriptively and semi-quantitatively using a scoring method. This study revealed five types of lesions as indicators of Alzheimer's disease: neurofibrillary tangles (NFT), granulovacuolar disease (GVD), Hirano bodies, cerebral amyloid angiopathy (CAA), and senile plaque (SP). GVD, NFT, and Hirano body lesions were found in the same two individuals, with NFT and GVD lesions at grade 2 and Hirano body lesions at grade 1, whereas SP and CAA were found in six mice, with both lesions at grade 1. This study found that all mice induced by injection of amyloid beta-42 protein had typical Alzheimer's lesions. This study could shed light on the pathogenesis of Alzheimer's disease and the utility of mice as animal models in Alzheimer's disease research. |
URI: | http://repository.ipb.ac.id/handle/123456789/108686 |
Appears in Collections: | UT - Veterinary Clinic Reproduction and Pathology |
Files in This Item:
File | Description | Size | Format | |
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Watermark_Fullteks - SKRIPSI - (B04170208) ASYIFA GISYA ALAYINA-2.pdf Restricted Access | Fullteks | 1.01 MB | Adobe PDF | View/Open |
Watermark_Halaman Awal - SKRIPSI - (B04170208) ASYIFA GISYA ALAYINA.pdf Restricted Access | Cover | 526.94 kB | Adobe PDF | View/Open |
Watermark_Lampiran - SKRIPSI - (B04170208) ASYIFA GISYA ALAYINA-3.pdf Restricted Access | Lampiran | 251.62 kB | Adobe PDF | View/Open |
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