Protein penting yang bertanggungjawab untuk umur panjang telah dikenal pasti buat kali pertama dalam monyet
Banyak penyelidikan sedang berlaku dalam bidang penuaan kerana adalah penting untuk memahami asas genetik penuaan untuk dapat memahami cara melambatkan penuaan dan merawat penyakit berkaitan usia. Para saintis telah menemui protein yang dipanggil SIRT6 yang dilihat dapat mengawal penuaan pada tikus. Ada kemungkinan bahawa ini juga boleh menjejaskan pembangunan dalam primata bukan manusia. Pada tahun 1999, keluarga gen Sirtuin dan protein homolog mereka termasuk SIRT6 telah dikaitkan dengan panjang umur dalam yis dan kemudiannya pada tahun 2012 protein SIRT6 dilihat terlibat dalam pengawalan penuaan dan umur panjang pada tikus kerana kekurangan protein ini membawa kepada ciri-ciri yang dikaitkan dengan penuaan dipercepatkan seperti kelengkungan tulang belakang, kolitis dll.
Using a model which is evolutionarily similar to manusia, like another primate, can fill the gap and guide us about the relevance of research findings to manusia. A recent study1 diterbitkan dalam Alam ialah kerja pertama untuk memahami peranan SIRT6 dalam mengawal selia pembangunan dan jangka hayat dalam mamalia maju seperti primata1. Para saintis dari China mencipta kejuruteraan biologi kera (monyet) primata pertama di dunia yang kekurangan gen penghasil protein SIRT6 mereka dengan menggunakan teknologi dan eksperimen penyuntingan gen berasaskan CRISPR-Cas9 untuk memerhatikan secara langsung kesan kekurangan SIRT6 dalam primata. Sebanyak 48 embrio 'berkembang' ditanam dalam 12 ibu monyet pengganti di mana empat daripadanya hamil dan tiga melahirkan anak monyet apabila seekor digugurkan. Bayi kera yang kekurangan protein ini mati dalam beberapa jam selepas kelahiran berbanding tikus yang mula menunjukkan penuaan 'pramatang' dalam kira-kira dua-tiga minggu kelahiran. Tidak seperti tikus, protein SIRT6 dilihat memainkan peranan penting dalam perkembangan embrio dalam monyet kerana ketiadaan SIRT6 menyebabkan kelewatan dan kecacatan perkembangan badan penuh yang serius. Tiga bayi yang baru dilahirkan itu menunjukkan kepadatan tulang yang lebih rendah, otak yang lebih kecil, usus yang tidak matang dan otot.
Baby monkeys exhibited serious prenatal development retardation leading to serious birth defects caused by delayed cell growth e.g. in brain, muscle and other organ tissues. If a similar effect would be seen in manusia maka a manusia foetus would not grow more than five months though it will complete the stipulated none months inside mother’s womb. This would be due to loss of function in SIRT6-producing gene in the manusia foetus causing it to grow inadequately or die. Same team of scientists have shown earlier that SIRT6 deficiency in manusia neural stem cells can affect proper transformation into neurons. The new study bolsters that SIRT6 protein is a likely candidate for being a ‘manusia longevity protein’ and could be responsible for regulating manusia development and life span.
Thestudy has opened up new frontiers for understanding manusia longevity proteins in the future. Discovery of crucial proteins can throw light on manusia development and ageing and direct treatment design for developmental delays, age-related disorders and metabolic disease in manusia. This study is already done in monkey, so there is hope that similar studies on manusia can shed light on important longevity proteins.
Penuaan kekal sebagai teka-teki dan misteri bagi manusia. Penyelidikan mengenai penuaan sering dibincangkan lebih banyak daripada bidang lain kerana kepentingan yang diberikan kepada belia dalam masyarakat dan budaya. Kajian lain2 diterbitkan dalam Sains/Ilmu showed that there may not even be a natural limit for longevity in manusia. Scientists from University of Roma Tre in Italy have performed a statistical analysis on the possibilities for survival in around 4000 elderly people who were between 105 years and older and stated that at the age of 105 a ‘mortality plateau’ is reached which means no limit to longevity now exists and after this age the possibility of life and death is at 50:50 i.e. someone could just live much longer hypothetically speaking. It is believed by medical experts that risk of death increases from adulthood till the age of 80 or so. Very less knowledge is available about what happens after 90s and 100s. This study says that manusia lifespan may not have any upper threshold! Interestingly, Italy is one of the countries having highest number of centenarians per capita in the world so it’s a perfect location, however, to generalize the study further work is needed. This is the best evidence for age mortality plateaus in manusia as very interesting patterns emerged. Scientists want to understand the concept of levelling in detail and it seems after one crosses 90s and 100, our body’s cells may reach a point where repair mechanisms in our body can offset the further damage in our cells. Maybe such a mortality plateau could even stall death at any age? There is no immediate answer as the manusia body is designed in such a way that it will have its own limitations and boundaries. Many cells in our body do not replicate or multiple after forming the first time around – example in brain and heart – so these cells will die in the ageing process.
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{Anda boleh membaca kertas penyelidikan asal dengan mengklik pautan DOI yang diberikan di bawah dalam senarai sumber yang dipetik}
Sumber (s)
1. Zhang W et al. 2018. Kekurangan SIRT6 mengakibatkan keterlambatan perkembangan dalam monyet cynomolgus. Alam semula jadi. 560. https://doi.org/10.1038/d41586-018-05970-9
2 Barbi E et al. 2018. The plateau of manusia mortality: Demography of longevity pioneers. Sains. 360 (6396). https://doi.org/10.1126/science.aat3119
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