Scientific Evidences of Calorie Restriction and Intermittent Fasting for Neuroprotection in Traumatic Brain Injury Animal Models: A Review of the Literature

• Published in: Nutrients 2022-03, Vol.14 (7), p.1431
• Main Authors: Xu, Yang, Liu, Zejie, Xu, Shuting, Li, Chengxian, Li, Manrui, Cao, Shuqiang, Sun, Yuwen, Dai, Hao, Guo, Yadong, Chen, Xiameng, Liang, Weibo
• Format: Article
• Language: English
• Subjects: Alzheimer's disease; Animal cognition; Animal models; Animals; Apoptosis; Autophagy; Brain Injuries, Traumatic; Brain research; Caloric Restriction; calorie restriction; Calories; Cell growth; Cognitive ability; Disease Models, Animal; Fasting; Fasting - physiology; Food availability; glial cell responses; Glial cells; Glial plasticity; hippocampal neurogenesis; Hippocampus; intermittent fasting; Literature reviews; Malnutrition; Mitochondria; mitochondrial dysfunction; Neurogenesis; Neuronal-glial interactions; Neuroplasticity; Neuroprotection; Neuroprotective Agents - pharmacology; Nutrient deficiency; Pathogenesis; Review; Traumatic brain injury
• ISSN: 2072-6643; 2072-6643
• DOI: 10.3390/nu14071431

It has widely been accepted that food restriction (FR) without malnutrition has multiple health benefits. Various calorie restriction (CR) and intermittent fasting (IF) regimens have recently been reported to exert neuroprotective effects in traumatic brain injury (TBI) through variable mechanisms. However, the evidence connecting CR or IF to neuroprotection in TBI as well as current issues remaining in this research field have yet to be reviewed in literature. The objective of our review was therefore to weigh the evidence that suggests the connection between CR/IF with recovery promotion following TBI. Medline, Google Scholar and Web of Science were searched from inception to 25 February 2022. An overwhelming number of results generated suggest that several types of CR/IF play a promising role in promoting post-TBI recovery. This recovery is believed to be achieved by alleviating mitochondrial dysfunction, promoting hippocampal neurogenesis, inhibiting glial cell responses, shaping neural cell plasticity, as well as targeting apoptosis and autophagy. Further, we represent our views on the current issues and provide thoughts on the future direction of this research field.