scholarly journals Aspartoacylase Supports Oxidative Energy Metabolism during Myelination

2012 ◽  
Vol 32 (9) ◽  
pp. 1725-1736 ◽  
Author(s):  
Jeremy S Francis ◽  
Louise Strande ◽  
Vladamir Markov ◽  
Paola Leone
Keyword(s):  
Energy Metabolism ◽  
Postnatal Development ◽  
Strong Association ◽  
Canavan Disease ◽  
Lipid Synthesis ◽  
Systematic Analysis ◽  
Early Postnatal Development ◽  
Neuronal Viability ◽  
Oxidative Energy Metabolism ◽  
The Brain

The inherited leukodystrophy Canavan disease arises due to a loss of the ability to catabolize N-acetylaspartic acid (NAA) in the brain and constitutes a major point of focus for efforts to define NAA function. Accumulation of noncatabolized NAA is diagnostic for Canavan disease, but contrasts with the abnormally low NAA associated with compromised neuronal integrity in a broad spectrum of other clinical conditions. Experimental evidence for NAA function supports a role in white matter lipid synthesis, but does not explain how both elevated and lowered NAA can be associated with pathology in the brain. We have undertaken a systematic analysis of postnatal development in a mouse model of Canavan disease that delineates development and pathology by identifying markers of oxidative stress preceding oligodendrocyte loss and dysmyelination. These data suggest a role for NAA in the maintenance of metabolic integrity in oligodendrocytes that may be of relevance to the strong association between NAA and neuronal viability. N-acetylaspartic acid is proposed here to support lipid synthesis and energy metabolism via the provision of substrate for both cellular processes during early postnatal development.

scholarly journals Molecular and genetic predictors of endothelial dysfunction and impairment of angioand neurogenesis in the perinatal period (a literature review)

2021 ◽  
Vol 5 ◽  
pp. 14-23
Author(s):  
S.B. Berezhanskaya ◽  
◽  
E.A. Lukyanova ◽  
M.K. Abduragimova ◽  
◽  
...  
Keyword(s):  
Nervous System ◽  
Endothelial Dysfunction ◽  
Literature Review ◽  
Postnatal Development ◽  
Genetic Predisposition ◽  
Fetal Development ◽  
Perinatal Period ◽  
Early Postnatal Development ◽  
Genetic Predictors ◽  
The Brain

Perinatal pathologies serve as the basis for a great variety of diseases in teenagers and adults including the especially frequent and important diseases of the nervous system which is vulnerable during the period of ante- and early postnatal development, especially against the background of genetic predisposition to it. This leads to development of pathology also manifesting at later stages of life. In this connection, the review presents molecular and genetic predictors of endothelial dysfunction and impairment of angio- and neurogenesis during the perinatal period. The article presents facts related to the influence of endothelial dysfunction as a trigger for pregnancy pathology and fetal-programmed diseases. A discussion regarding the contribution made by the congenital and by the acquired into basic mechanisms of fetal development including the brain and its pathologies

Energy Metabolism Impairment in Migraine

2019 ◽  
Vol 26 (34) ◽  
pp. 6253-6260 ◽  
Author(s):  
Sabina Cevoli ◽  
Valentina Favoni ◽  
Pietro Cortelli
Keyword(s):  
Energy Metabolism ◽  
Energy Demand ◽  
Energy Production ◽  
Mitochondrial Respiratory Chain ◽  
Migraine Prophylaxis ◽  
Resonance Spectroscopy ◽  
Oxidative Energy Metabolism ◽  
Spectroscopy Studies ◽  
The Brain ◽  
Brain Energy

Migraine is a common disabling neurological disorder which is characterised by a recurring headache associated with a variety of sensory and autonomic symptoms. The pathophysiology of migraine remains not entirely understood, although many mechanisms involving the central and peripheral nervous system are now becoming clear. In particular, it is widely accepted that migraine is associated with energy metabolic impairment of the brain. The purpose of this review is to present an updated overview of the energy metabolism involvement in the migraine pathophysiology. Several biochemical, morphological and magnetic resonance spectroscopy studies have confirmed the presence of energy production deficiency together with an increment of energy consumption in migraine patients. An increment of energy demand over a certain threshold creates metabolic and biochemical preconditions for the onset of the migraine attack. The defect of oxidative energy metabolism in migraine is generalized. It remains to be determined if the mitochondrial deficit in migraine is primary or secondary. Riboflavin and Co-Enzyme Q10, both physiologically implicated in mitochondrial respiratory chain functioning, are effective in migraine prophylaxis, supporting the hypothesis that improving brain energy metabolism may reduce the susceptibility to migraine.

scholarly journals SARS-CoV-2 infects brain astrocytes of COVID-19 patients and impairs neuronal viability

2020 ◽  
Author(s):  
Fernanda Crunfli ◽  
Victor Corasolla Carregari ◽  
Flavio Protásio Veras ◽  
Pedro Henrique Vendramini ◽  
Aline Gazzola Fragnani Valença ◽  
...  
Keyword(s):  
Stem Cell ◽  
Cognitive Impairment ◽  
Energy Metabolism ◽  
Neural Stem Cell ◽  
Cortical Thickness ◽  
Respiratory Symptoms ◽  
Neuronal Viability ◽  
Secretory Phenotype ◽  
The Brain ◽  
Independent Cohort

Abstract COVID-19 patients may exhibit neuropsychiatric and neurological symptoms. We found that anxiety and cognitive impairment are manifested by 28-56% of SARS-CoV-2-infected individuals with mild respiratory symptoms and are associated with altered cerebral cortical thickness. Using an independent cohort, we found histopathological signs of brain damage in 25% of individuals who died of COVID-19. All of the affected brain tissues exhibited foci of SARS-CoV-2 infection and replication, particularly in astrocytes. Infection of neural stem cell-derived astrocytes changed energy metabolism, altered key proteins and metabolites used to fuel neurons and for biogenesis of neurotransmitters, and elicited a secretory phenotype that reduces neuronal viability. Our data support the model where SARS-CoV-2 reaches the brain, infects astrocytes and triggers neuropathological changes that contribute to the structural and functional alterations in the brain of COVID-19 patients.

scholarly journals Glutamate dehydrogenase is essential to sustain neuronal oxidative energy metabolism during stimulation

2017 ◽  
Vol 38 (10) ◽  
pp. 1754-1768 ◽  
Author(s):  
Michaela C Hohnholt ◽  
Vibe H Andersen ◽  
Jens V Andersen ◽  
Sofie K Christensen ◽  
Melis Karaca ◽  
...  
Keyword(s):  
Energy Metabolism ◽  
Glutamate Dehydrogenase ◽  
Energy Demand ◽  
Glucose Deprivation ◽  
Brain Mitochondria ◽  
Glutamine Metabolism ◽  
Oxidative Deamination ◽  
Oxidative Energy Metabolism ◽  
The Brain

The enzyme glutamate dehydrogenase (GDH; Glud1) catalyzes the (reversible) oxidative deamination of glutamate to α-ketoglutarate accompanied by a reduction of NAD+ to NADH. GDH connects amino acid, carbohydrate, neurotransmitter and oxidative energy metabolism. Glutamine is a neurotransmitter precursor used by neurons to sustain the pool of glutamate, but glutamine is also vividly oxidized for support of energy metabolism. This study investigates the role of GDH in neuronal metabolism by employing the Cns- Glud1−/− mouse, lacking GDH in the brain (GDH KO) and metabolic mapping using 13C-labelled glutamine and glucose. We observed a severely reduced oxidative glutamine metabolism during glucose deprivation in synaptosomes and cultured neurons not expressing GDH. In contrast, in the presence of glucose, glutamine metabolism was not affected by the lack of GDH expression. Respiration fuelled by glutamate was significantly lower in brain mitochondria from GDH KO mice and synaptosomes were not able to increase their respiration upon an elevated energy demand. The role of GDH for metabolism of glutamine and the respiratory capacity underscore the importance of GDH for neurons particularly during an elevated energy demand, and it may reflect the large allosteric activation of GDH by ADP.

Energy Metabolism and Effects of Energy Depletion or Exposure to Glutamate

1992 ◽  
Vol 70 (S1) ◽  
pp. S107-S112 ◽  
Author(s):  
Louis Sokoloff
Keyword(s):  
Energy Metabolism ◽  
Brain Cells ◽  
Cerebral Hypoxia ◽  
Energy Depletion ◽  
Pathological Conditions ◽  
Oxidative Energy Metabolism ◽  
The Subject ◽  
Tissue Acidosis ◽  
The Brain

The entire program of the first day of the IBRO satellite meeting entitled Ions, Water, and Energy in Brain Cells was devoted to the subject of energy. There were three sessions on the topics of energy metabolism, activation, and development and pathological conditions, followed by a final general discussion on the contents of the day's topics. During this general discussion there were spirited exchanges on the role of glycogen in the energy metabolism of the brain, on the metabolic source of the energy consumed by functional activity, e.g., glycolytic or oxidative energy metabolism, and on the sources of the acid-equivalents that are responsible for the tissue acidosis accompanying cerebral hypoxia. Despite the arguments pro and con presented on all of the issues that were discussed, it is doubtful that a consensus was achieved on most of the issues.Key words: glycogen, glycolysis, oxidative metabolism, acidosis, energy metabolism.

scholarly journals SARS-CoV-2 infects brain astrocytes of COVID-19 patients and impairs neuronal viability

2020 ◽  
Author(s):  
Fernanda Crunfli ◽  
Victor Corasolla Carregari ◽  
Flavio Protasio Veras ◽  
Pedro Henrique Vendramini ◽  
Aline Gazzola Fragnani Valença ◽  
...  
Keyword(s):  
Stem Cell ◽  
Cognitive Impairment ◽  
Energy Metabolism ◽  
Neural Stem Cell ◽  
Cortical Thickness ◽  
Respiratory Symptoms ◽  
Neuronal Viability ◽  
Secretory Phenotype ◽  
The Brain ◽  
Independent Cohort

AbstractCOVID-19 patients may exhibit neuropsychiatric and neurological symptoms. We found that anxiety and cognitive impairment are manifested by 28-56% of SARS-CoV-2-infected individuals with mild respiratory symptoms and are associated with altered cerebral cortical thickness. Using an independent cohort, we found histopathological signs of brain damage in 25% of individuals who died of COVID-19. All of the affected brain tissues exhibited foci of SARS-CoV-2 infection and replication, particularly in astrocytes. Infection of neural stem cell-derived astrocytes changed energy metabolism, altered key proteins and metabolites used to fuel neurons and for biogenesis of neurotransmitters, and elicited a secretory phenotype that reduces neuronal viability. Our data support the model where SARS-CoV-2 reaches the brain, infects astrocytes and triggers neuropathological changes that contribute to the structural and functional alterations in the brain of COVID-19 patients.

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