ایک پیش رفت کی تحقیق میں، سائنسدانوں نے ثابت کیا ہے کہ خاندانی ڈیمنشیا کے علاج کے لیے امینوگلیکوسائیڈز (جینٹامیسن) اینٹی بائیوٹک کا استعمال کیا جا سکتا ہے۔
۔ اینٹی بایوٹک gentamicin, neomycin, streptomycin etc are commonly used to treat bacterial infections. These are broad spectrum اینٹی بایوٹک سے متعلق امینوگلیکوسائڈز کلاس اور خاص طور پر گرام منفی بیکٹیریا کے خلاف سرگرم ہیں۔ وہ بیکٹیریل رائبوزوم کے ساتھ باندھ کر کام کرتے ہیں اور روکتے ہیں۔ پروٹین حساسیت میں ترکیب بیکٹیریا.
But aminoglycosides are also known to induce mutation suppression in eukaryotes to produce full length protein. This is a lesser known function of this اینٹی بائیوٹک which has been used in the past to treat several human diseases such as Duchenne muscular dystrophy (DMD) [2]. Now, there is report that this function may be used in treating منوبرنش اس کے ساتھ ساتھ مستقبل قریب میں.
In a paper published on 08 January 2020 in the journal, Human Molecular Genetics, the researchers of University of Kentucky have provided proof of concept that these اینٹی بایوٹک may be used to treat frontotemporal منوبرنش [1]. This is an exciting breakthrough in science that has potential to improve quality of lives of several people with منوبرنش.
ڈیمنشیا is a group of symptoms involving deterioration in ability to perform usual daily activities and is caused due to deterioration in cognitive function like memory, thinking or behavour. It is a major reason of disability and dependency among elderly people worldwide. It affects carers and families as well. According to an estimate, there are 50 million people with منوبرنش worldwide with 10 million new cases every year. Alzheimer بیماری کی سب سے عام شکل ہے منوبرنش. Frontotemporal منوبرنش is the second-most common form. This is early onset in nature and affects frontal and temporal lobes of the brain.
The patients with frontotemporal منوبرنش have progressive atrophy of frontal and temporal lobes of the brain that leads to gradual deterioration of cognitive functions, language skills and personality and behavioral changes. This is heritable in nature caused by genetic mutations. As a result of these genetic mutations, the brain is unable to form a protein called progranulin. The insufficient production of progranulin in the brain in linked to this form of منوبرنش.
In their study, the University of Kentucky researchers have found that if aminoglycoside اینٹی بایوٹک were added to the neuronal cells with progranulin mutations in an in vitro cell culture, they skip the mutation and form full length protein. The progranulin protein level was recovered up to about 50 to 60%. This finding supports the principle that aminoglycoside (gentamicin and G418) hold the treatment possibility for such patients.
Next step would be to move forward from ”in vitro cell culture model” to ”animal model”. The mutation suppression by aminoglycosides as a therapeutic strategy to treat frontotemporal منوبرنش has come one step closer.
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{آپ اصل تحقیقی مقالے کو ذیل میں دیے گئے DOI لنک پر کلک کر کے پڑھ سکتے ہیں جو حوالہ دیئے گئے ماخذ کی فہرست میں ہے}
ذرائع)
1. Kuang L., et al, 2020. Frontotemporal منوبرنش nonsense mutation of progranulin rescued by aminoglycosides. Human Molecular Genetics, ddz280. DOI: https://doi.org/10.1093/hmg/ddz280
2. ملک V.، et al، 2010. Duchenne Muscular dystrophy کے علاج کی حکمت عملی کے طور پر Aminoglycoside-Induced mutation suppression (کوڈن ریڈ تھرو کو روکیں)۔ اعصابی عوارض میں علاج کی پیشرفت (2010) 3(6) 379389۔ DOI: https://doi.org/10.1177/1756285610388693
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