Recently, transcriptional and metabolic reprogramming has been raised as a novel molecular mechanism that mediates the development of a large variety of diseases. It is speculated that metabolic dysfunction results in the accumulation of metabolic intermediates, which affect the function and expression of some genes by posttranslational modification. For instance, a recently published work reveals that microglial glucose metabolism is disturbed in the development of Alzheimer's disease (AD), which leads to the accumulation of lactate and upregulation of histone lactylation, altering the transcription of many genes. Further research focused on the role and mechanism of metabolic dysfunction in the development of brain disease may help us find some novel pharmaceutical targets and biomarkers.
This topic intends to highlight the recent advances in metabolic reprogramming-induced chromatin remodeling in the development of neurodegenerative diseases. Therefore, we would like to address the dysfunction in cellular glucose and lipid metabolism during the progress of brain disease from early to late stages, and to reveal the mechanism of metabolic dysfunction and its role in the development of brain diseases, such as AD, Parkinson’s diseases (PD) and stroke. In recent years, the application of some new technologies, such as single-cell RNA sequencing, single-cell metabolome, cut&Tag assay, and imaging mass spectrometry, provides new opportunities to study mechanism of metabolic dysfunction in neurodegenerative diseases at the molecular and cellular level. Secondly, we want to collect the clinical evidence of metabolic dysfunction for brain disease, which may help us find novel biomarkers for disease diagnosis (e.g., metabolic intermediates from brain-derived exosomes). Lastly, we want to address whether some metabolic intermediates or enzyme that regulates glucose and lipid metabolism could be targeted for brain disease therapy. Targeting drug delivery systems, Cre/loxP system mediated conditional knockout and virus-mediated interference technologies now have been widely used, which may help us achieve the above goals.
Research articles and reviews are welcomed on this topic. For revealing the cellular and molecular mechanism of brain disease, this topic appreciates articles that address the phenomena, mechanism and role of glucose and lipid metabolism dysfunction in the progress of brain disease from early to late stages. Contributions on the following themes will be particularly encouraged, but are not limited to:
- Evidence that proves that the glucose or lipid metabolism is disturbed in brain disease.
- Study on the mechanism of metabolic dysfunction in the development of brain disease, especially neurodegenerative disease.
- Methods for analysis of the levels of metabolic intermediates in brain tissue or brain-derived exosomes.
- Study on the effects of reprogramming the glucose or lipid metabolism on the development of brain disease.
- Review or systematic reviews and meta-analyses on this topic.
Dr. Henderson is the Chief Scientific Officer of Cerecin. This should not pose any conflict for this project, as he is also an academic and will maintain objectivity.
Recently, transcriptional and metabolic reprogramming has been raised as a novel molecular mechanism that mediates the development of a large variety of diseases. It is speculated that metabolic dysfunction results in the accumulation of metabolic intermediates, which affect the function and expression of some genes by posttranslational modification. For instance, a recently published work reveals that microglial glucose metabolism is disturbed in the development of Alzheimer's disease (AD), which leads to the accumulation of lactate and upregulation of histone lactylation, altering the transcription of many genes. Further research focused on the role and mechanism of metabolic dysfunction in the development of brain disease may help us find some novel pharmaceutical targets and biomarkers.
This topic intends to highlight the recent advances in metabolic reprogramming-induced chromatin remodeling in the development of neurodegenerative diseases. Therefore, we would like to address the dysfunction in cellular glucose and lipid metabolism during the progress of brain disease from early to late stages, and to reveal the mechanism of metabolic dysfunction and its role in the development of brain diseases, such as AD, Parkinson’s diseases (PD) and stroke. In recent years, the application of some new technologies, such as single-cell RNA sequencing, single-cell metabolome, cut&Tag assay, and imaging mass spectrometry, provides new opportunities to study mechanism of metabolic dysfunction in neurodegenerative diseases at the molecular and cellular level. Secondly, we want to collect the clinical evidence of metabolic dysfunction for brain disease, which may help us find novel biomarkers for disease diagnosis (e.g., metabolic intermediates from brain-derived exosomes). Lastly, we want to address whether some metabolic intermediates or enzyme that regulates glucose and lipid metabolism could be targeted for brain disease therapy. Targeting drug delivery systems, Cre/loxP system mediated conditional knockout and virus-mediated interference technologies now have been widely used, which may help us achieve the above goals.
Research articles and reviews are welcomed on this topic. For revealing the cellular and molecular mechanism of brain disease, this topic appreciates articles that address the phenomena, mechanism and role of glucose and lipid metabolism dysfunction in the progress of brain disease from early to late stages. Contributions on the following themes will be particularly encouraged, but are not limited to:
- Evidence that proves that the glucose or lipid metabolism is disturbed in brain disease.
- Study on the mechanism of metabolic dysfunction in the development of brain disease, especially neurodegenerative disease.
- Methods for analysis of the levels of metabolic intermediates in brain tissue or brain-derived exosomes.
- Study on the effects of reprogramming the glucose or lipid metabolism on the development of brain disease.
- Review or systematic reviews and meta-analyses on this topic.
Dr. Henderson is the Chief Scientific Officer of Cerecin. This should not pose any conflict for this project, as he is also an academic and will maintain objectivity.