An increasing amount of evidence supports the importance of nutritional status in the etiology of neurodegenerative diseases that are associated with cognitive decline and behavioral changes. Poor nutritional status affects the interactions between neurons and astrocytes, and synaptic activity and cerebral metabolism and have been associated with impaired neuronal function, oxidative stress, and, more recently, autophagy in neurons.
The brain is known as a ‘selfish’ organ due to its high level of metabolic activity. It exhibits specificity for glucose as its primary energy substrate. Further, recent research suggests that the metabolic interactions of lactate between astrocytes and neurons are essential for synaptic activity and brain metabolism. Ketone bodies generated in the liver are considered to be an alternative energy source for the brain during the early stages of development, starvation, and ketogenic diet use.
Several studies have demonstrated the role of particular nutrients, such as amino acids and polyunsaturated fatty acids (PUFAs), in changing brain electrical activity and metabolism. High levels of PUFAs, mainly omega-3 eicosapentaenoic acid (20:5, n-3) and docosahexaenoic acid (DHA) (22:6, n-3), are found to be concentrated in synaptic membranes in the brain. Deficiency in linolenic acid, the precursor of omega-3 fatty acids, changes both brain glucose uptake and metabolism, affecting the production of neurotransmitters such as serotonin and dopamine. However, more research is required to fully understand the impact of diet-altered levels of PUFAs and their functional consequences on neuronal activity, metabolism, and behavioral changes such as depression and anxiety. Together, this evidence supports the possibility that nutrients play a main role in brain function and recovery.
This Research Topic aims to provide an update on dietary nutrients and their impact on controlling key mechanisms related to neuronal excitability, brain metabolism, and neurodevelopmental and neurodegenerative disorders. We welcome original research articles and mini or review articles on, but not limited to, the following topics:
1. Dietary manipulations and astrocyte-neuron metabolism changes
2. Nutrient deficiency and brain autophagic activity
3. Polyunsaturated fatty acids and neurogenesis, neurotransmission, and neurodegenerative disorders
4. Nutrition/brain excitability relationships
5. Behavioral and electrophysiological aspects of the nutrition/neuro-glial relationship
6. Nutrition and brain redox imbalance
7. Nutrition and energy-demanding phenomena in the brain
8. Neuro-glial/nutrition interaction on neurotransmitter function
9. Neuro-glial deleterious or toxic food substances
10. Morphological and morphometric consequences of the nutritional/neuro-glial exchange
An increasing amount of evidence supports the importance of nutritional status in the etiology of neurodegenerative diseases that are associated with cognitive decline and behavioral changes. Poor nutritional status affects the interactions between neurons and astrocytes, and synaptic activity and cerebral metabolism and have been associated with impaired neuronal function, oxidative stress, and, more recently, autophagy in neurons.
The brain is known as a ‘selfish’ organ due to its high level of metabolic activity. It exhibits specificity for glucose as its primary energy substrate. Further, recent research suggests that the metabolic interactions of lactate between astrocytes and neurons are essential for synaptic activity and brain metabolism. Ketone bodies generated in the liver are considered to be an alternative energy source for the brain during the early stages of development, starvation, and ketogenic diet use.
Several studies have demonstrated the role of particular nutrients, such as amino acids and polyunsaturated fatty acids (PUFAs), in changing brain electrical activity and metabolism. High levels of PUFAs, mainly omega-3 eicosapentaenoic acid (20:5, n-3) and docosahexaenoic acid (DHA) (22:6, n-3), are found to be concentrated in synaptic membranes in the brain. Deficiency in linolenic acid, the precursor of omega-3 fatty acids, changes both brain glucose uptake and metabolism, affecting the production of neurotransmitters such as serotonin and dopamine. However, more research is required to fully understand the impact of diet-altered levels of PUFAs and their functional consequences on neuronal activity, metabolism, and behavioral changes such as depression and anxiety. Together, this evidence supports the possibility that nutrients play a main role in brain function and recovery.
This Research Topic aims to provide an update on dietary nutrients and their impact on controlling key mechanisms related to neuronal excitability, brain metabolism, and neurodevelopmental and neurodegenerative disorders. We welcome original research articles and mini or review articles on, but not limited to, the following topics:
1. Dietary manipulations and astrocyte-neuron metabolism changes
2. Nutrient deficiency and brain autophagic activity
3. Polyunsaturated fatty acids and neurogenesis, neurotransmission, and neurodegenerative disorders
4. Nutrition/brain excitability relationships
5. Behavioral and electrophysiological aspects of the nutrition/neuro-glial relationship
6. Nutrition and brain redox imbalance
7. Nutrition and energy-demanding phenomena in the brain
8. Neuro-glial/nutrition interaction on neurotransmitter function
9. Neuro-glial deleterious or toxic food substances
10. Morphological and morphometric consequences of the nutritional/neuro-glial exchange
