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All Journal Qanun Medika - Medical Journal Faculty of Medicine Muhammadiyah Surabaya
Pradana Zaky Romadhon
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Health Professions Medicine & Pharmacology

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CRISPR-Cas9 through AAV delivery system as a gene therapy in Parkinson’s disease Maulana Bagus Adi Cahyono; Ilham Rahmanto; Zahras Azimuth Doman; Galuh Senjani Yulfani Putri; Christopher Surya Lodianto; Pradana Zaky Romadhon
Qanun Medika - Jurnal Kedokteran FK UMSurabaya Vol 7 No 2 (2023): Journal Qanun Medika Vol 07 No 02
Publisher : Universitas Muhammadiyah Surabaya

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.30651/jqm.v7i2.16117

Abstract

The global population living with Parkinson’s disease is estimated to reach 9.4 million people, which has increased significantly since 2016, with a total of 6 million people. Parkinson's is a neurodegenerative disease of the substantia nigra that causes a decrease in dopamine production and is characterized by the appearance of cytoplasmic misfold proteins called Lewy bodies. The study found that abnormalities or mutations in the SNCA and LRRK2 genes correlated with the overproduction of the ɑ-synuclein protein, which forms Lewy bodies that cause Parkinson's. Current Parkinson's medications only temporarily replace lost dopamine but do not treat the direct cause of Parkinson's; this research used qualitative literature study with content analysis, observation, and development; the use of CRISPR-Cas9 through AAV genetic engineering in repairing SNCA and LRRK2 mutant gene. This genetic therapy works by cutting the mutant DNA base sequences in the SNCA and LRRK2 genes and then replacing them with normal sequences through a homology-direct repair mechanism. As a result, the abnormalities or mutations that cause Parkinson's in these two genes can be corrected, so that dopaminergic levels in the brain can return to normal and excessive accumulation of α-synuclein protein can be suppressed.
Tandem peptide lipid CRISPR-Cas9 complex combating APP and APOE4 gene abnormality in Alzheimer's disease Ilham Rahmanto; Maulana Bagus Adi Cahyono; Husnul Khatimah; Rahmi Nugraningrum; Pionera Seconda Giyanti Putri; Nurul Zulfa Sahiruddin; Nabila Rahmaniah; Pradana Zaky Romadhon
Qanun Medika - Jurnal Kedokteran FK UMSurabaya Vol 8 No 01 (2024): Qanun Medika Vol 08 No 01 January 2024
Publisher : Universitas Muhammadiyah Surabaya

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.30651/jqm.v8i01.16054

Abstract

Alzheimer's attacks 24 million global population and dominates 60-80% of existing cases of dementia. It causes the accumulation of beta-amyloid (Aβ) plaques in the hippocampus and entorhinal cortex, resulting in decreased mass from the brain. Recent studies have shown that the manifestation of this disease is due to an overaccumulation of abnormal Aβ protein due to abnormalities in the APP and APOE4 genes. Point mutations in the APP gene will create the toxic form of Aβ protein, namely Aβ42, and the toxic APOE4 gene will accelerate the onset of Aβ42 deposition and pro-inflammatory activity that exacerbates the degenerative process of the brain. Gene editing as a potential definitive therapy was recently a concern by researchers. CRISPR-Cas9 repairs the APP gene and substitutes the APOE4 gene with APOE3 by modifying the gene's DNA sequence. Nano complex CRISPR-Cas9 tandem peptide lipid is a model for clinicians to target brain nerve cells. In vivo research on an Alzheimer's mouse model proved the potential of nano-complex-based peptides as carriers of CRISPR-Cas9 in brain nerve cells. This engineering technology offers satisfactory results with high precision, minimal side effects, and a relatively low price for long-term therapeutic effects and even a lifetime.
Co-Authors Christopher Surya Lodianto Galuh Senjani Yulfani Putri Husnul Khatimah Ilham Rahmanto Maulana Bagus Adi Cahyono Nabila Rahmaniah Nurul Zulfa Sahiruddin Pionera Seconda Giyanti Putri Rahmi Nugraningrum Zahras Azimuth Doman