ENO۱/PI۳K/STAT۳ promoting PKM۲ nuclear translocation to drive neuronal metabolic reprogramming in Alzheimer Disease patients" >ENO۱/PI۳K/STAT۳ promoting PKM۲ nuclear translocation to drive neuronal metabolic reprogramming in Alzheimer Disease patients" >STAT۳ Transcription Factor, Tau Proteins" >ENO۱/PI۳K/STAT۳ promoting PKM۲ nuclear translocation to drive neuronal metabolic reprogramming in Alzheimer Disease patients" >STAT۳ Transcription Factor, Tau Proteins" >

Research on the mechanism of <em style="mso-bidi-font-style: normal;">ENO۱/<em style="mso-bidi-font-style: normal;">PI۳K/<em style="mso-bidi-font-style: normal;">STAT۳ promoting <em style="mso-bidi-font-style: normal;">PKM۲ nuclear translocation to drive neuronal metabolic reprogramming in Alzheimer Disease patients

سال انتشار: 1405
نوع سند: مقاله ژورنالی
زبان: انگلیسی
مشاهده: 69

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شناسه ملی سند علمی:

JR_CMBR-6-1_001

تاریخ نمایه سازی: 14 مرداد 1405

چکیده مقاله:

Alzheimer's is an incurable, degenerative neurological disease that ultimately causes death. For this reason, it has been aim to discuss the molecular and bioinformatic mechanisms related to ENO۱/PI۳K/STAT۳/PKM۲ factors in Alzheimer's in this study. The results of this study showed that ENO۱ and PI۳K genes modulate PKM۲ nuclear translocation through direct molecular processes, while the STAT۳ gene affects PKM۲ nuclear translocation through indirect processes. In general, modulating the nuclear translocation of PKM۲ and reducing the expression of this gene is an effective step in the treatment of Alzheimer's disease. In addition, these mechanisms improve the effective neuronal metabolisms in the synaptic space and specifically stimulate neural stimuli. In other words, these mechanisms are effective in the regeneration of nerve cells in a planned manner and play an effective role in the activation of neurons. The results of this study also showed that the STAT۳ factor, in addition to its indirect effect on the nuclear translocation of PKM۲, aggravates the disease by affecting various signaling pathways. On the other hand, the ENO۱ and PI۳K factors prevent the loss of neurons and the synaptic space in the brain through other molecules and various transcriptional pathways. Also, the ENO۱ and PI۳K genes prevent abnormal phosphorylation of this protein by blocking the phosphorylation pathway of the tau factor. On the other hand, these genes limit the production of amyloid beta and facilitate glucose synthesis in the brain. The results of gene expression analysis also showed that the ENO۱ and PI۳K genes are highly expressed in the cerebellum and hippocampus, which emphasizes the importance of these organs in stimulating neurons. High STAT۳ gene expression in the medulla oblongata indicates significant beta-amyloid in acute Alzheimer's stages. The results of this study also showed that the ENO۱ and PI۳K genes have a direct effect on improving learning disorders and increasing the volume of the hippocampus, which ultimately leads to the regulation of synaptic space activity. In general, these findings highlight the role of ENO۱, PI۳K, and STAT۳ factors. Research into Alzheimer's mechanisms offers a promising perspective for treatment development.

نویسندگان

Mohammad Hasan Mohammadi

Department of Pediatrics, School of Medicine, Amir al momenin Hospital, Zabol University of Medical Sciences, Zabol, Iran

Alireza Mirzaei

Department of Biotechnology, Faculty of Biological Sciences, Alzahra University, Tehran, Iran

Bahman Fazeli-Nasab

Department of Agronomy and Plant Breeding, Agriculture Institute, Research Institute of Zabol, Zabol, Iran

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