17 Apr Neural Tube Defects in Infants Share Molecular Processes With Neurodegenerative Diseases
MedicalResearch.com Interview with:
Zhiyong Zhao, Ph.D.
Department of Obstetrics, Gynecology & Reproductive Sciences
University of Maryland School of Medicine
MedicalResearch.com: What is the background for this study? What are the main findings?
Response: Diabetes in early pregnancy can cause neural tube defects in fetus. The defects are a result of failure in neural tube closure, due to excess cell death. The aim of this study was to delineate molecular processes that induce cell death.
The main findings of this study are:
(1) Hyperglycemia disrupts protein folding. The misfolded proteins, including the ones that are associated with neurodegenerative diseases, form aggregates, indicating similar molecular processes in both fetal neural tube defects and adult neurodegenerative diseases.
(2) Protein aggregation leads to formation of a neurodegenerative disease-related cell death inducting mechanism.
MedicalResearch.com: What should readers take away from your report?
Response: First, neural tube defects in infants share similar molecular processes with aging-related neurodegenerative diseases. We need to rethink the strategies in birth defect prevention. Second, hyperglycemia can sufficiently cause protein aggregation. Therefore, diabetes, pre-diabetes, and high carbohydrate intake can be risk factors for neurodegenerative diseases.
MedicalResearch.com: What recommendations do you have for future research as a result of this study?
Response: In birth defect prevention, we need to develop new strategies (1) to disrupt protein aggregation and (2) to clean up protein aggregates in cells. In managing neurodegenerative diseases, glycemic condition should be considered.
MedicalResearch.com: Thank you for your contribution to the MedicalResearch.com community.
Zhiyong Zhao, Lixue Cao, E. Albert Reece. Formation of neurodegenerative aggresome and death-inducing signaling complex in maternal diabetes-induced neural tube defects. Proceedings of the National Academy of Sciences, 2017; 201616119 DOI: 10.1073/pnas.1616119114
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