scholarly journals The "selfish brain" hypothesis for metabolic abnormalities in bipolar disorder and schizophrenia

2012 ◽  
Vol 34 (3) ◽  
pp. 121-128 ◽  
Author(s):  
Rodrigo Barbachan Mansur ◽  
Elisa Brietzke
Keyword(s):  
Bipolar Disorder ◽  
Energy Metabolism ◽  
Energy Supply ◽  
Clinical Implications ◽  
Metabolic Abnormalities ◽  
Compensatory Mechanisms ◽  
High Prevalence ◽  
Brain Theory ◽  
The Brain ◽  
Brain Energy

Metabolic abnormalities are frequent in patients with schizophrenia and bipolar disorder (BD), leading to a high prevalence of diabetes and metabolic syndrome in this population. Moreover, mortality rates among patients are higher than in the general population, especially due to cardiovascular diseases. Several neurobiological systems involved in energy metabolism have been shown to be altered in both illnesses; however, the cause of metabolic abnormalities and how they relate to schizophrenia and BD pathophysiology are still largely unknown. The "selfish brain" theory is a recent paradigm postulating that, in order to maintain its own energy supply stable, the brain modulates energy metabolism in the periphery by regulation of both allocation and intake of nutrients. We hypothesize that the metabolic alterations observed in these disorders are a result of an inefficient regulation of the brain energy supply and its compensatory mechanisms. The selfish brain theory can also expand our understanding of stress adaptation and neuroprogression in schizophrenia and BD, and, overall, can have important clinical implications for both illnesses.

scholarly journals Dissociated Expression of Mitochondrial and Cytosolic Creatine Kinases in the Human Brain: A New Perspective on the Role of Creatine in Brain Energy Metabolism

2013 ◽  
Vol 33 (8) ◽  
pp. 1295-1306 ◽  
Author(s):  
Matthew TJ Lowe ◽  
Eric H Kim ◽  
Richard LM Faull ◽  
David L Christie ◽  
Henry J Waldvogel
Keyword(s):  
Energy Metabolism ◽  
Human Brain ◽  
High Energy ◽  
Cellular Energy ◽  
Neuronal Populations ◽  
Neurologic Function ◽  
New Perspective ◽  
The Brain ◽  
Brain Energy

The phosphocreatine/creatine kinase (PCr/CK) system in the brain is defined by the expression of two CK isozymes: the cytosolic brain-type CK (BCK) and the ubiquitous mitochondrial CK (uMtCK). The system plays an important role in supporting cellular energy metabolism by buffering adenosine triphosphate (ATP) consumption and improving the flux of high-energy phosphoryls around the cell. This system is well defined in muscle tissue, but there have been few detailed studies of this system in the brain, especially in humans. Creatine is known to be important for neurologic function, and its loss from the brain during development can lead to mental retardation. This study provides the first detailed immunohistochemical study of the expression pattern of BCK and uMtCK in the human brain. A strikingly dissociated pattern of expression was found: uMtCK was found to be ubiquitously and exclusively expressed in neuronal populations, whereas BCK was dominantly expressed in astrocytes, with a low and selective expression in neurons. This pattern indicates that the two CK isozymes are not widely coexpressed in the human brain, but rather are selectively expressed depending on the cell type. These results suggest that the brain cells may use only certain properties of the PCr/CK system depending on their energetic requirements.

Pharmacological Modulation of Compensatory Mechanisms Energy Metabolism in the Brain of Prenatal Alcoholic Animals

10.12737/5898 ◽  
2014 ◽  
Vol 21 (3) ◽  
pp. 54-58
Author(s):  
Соколик ◽  
E. Sokolik ◽  
Егоров ◽  
A. Egorov
Keyword(s):  
Energy Metabolism ◽  
Fetal Alcohol Spectrum Disorders ◽  
Negative Impact ◽  
Fetal Alcohol ◽  
Compensatory Mechanisms ◽  
Pregnant Rats ◽  
Nootropic Drug ◽  
Neuroprotective Drugs ◽  
Thin Elements ◽  
The Brain

The studies have shown that drinking alcohol by woman during pregnancy can lead not only to a full fetal alcohol syndrome, but also causes less severe dysmorphic, cognitive and behavioral disordersl, i.e. fetal alcohol spectrum disorders, leads to low birth weight, fetal death, and other complications of pregnancy. The purpose of this study was to investigate the influence of neuroprotective drugs tiocetam, cerebrocurin and piracetam on the marks of thin elements of energy metabolism and compensatory shunts in the brain of animals early age undergoing prenatal alcoholism. In pregnant rats with alcoholism were found neuroprotective and nootropic effects of cerebrocurin and tiocetam after parenterally administered to newborn animals for a period of 25 days. The above drugs have a beneficial effect on the main elements of the energy metabolism on the neonatal brain. On the severity of mitoprotective and energotropic mechanisms of neuroprotective action, aimed at reducing the negative impact of alcohol on the progeny, tiocetam and cerebrocurin far exceed basic nootropic drug piracetam.

Photic stimulation-induced alteration of brain energy metabolism in bipolar disorder detected by 31P-MRS

1997 ◽  
Vol 42 (1) ◽  
pp. 208S
Author(s):  
K. Kato ◽  
J. Murashita ◽  
T. Shioiri ◽  
T. Inubushi ◽  
N. Kato
Keyword(s):  
Bipolar Disorder ◽  
Energy Metabolism ◽  
Photic Stimulation ◽  
Brain Energy Metabolism ◽  
31P Mrs ◽  
Brain Energy

scholarly journals Astrocytes as Key Regulators of Brain Energy Metabolism: New Therapeutic Perspectives

2022 ◽  
Vol 12 ◽  
Author(s):  
Elidie Beard ◽  
Sylvain Lengacher ◽  
Sara Dias ◽  
Pierre J. Magistretti ◽  
Charles Finsterwald
Keyword(s):  
Energy Metabolism ◽  
Neurodegenerative Diseases ◽  
Critical Role ◽  
Functional Brain Imaging ◽  
Brain Energy Metabolism ◽  
Lactate Shuttle ◽  
Lactate Release ◽  
Brain Functions ◽  
The Brain ◽  
Brain Energy

Astrocytes play key roles in the regulation of brain energy metabolism, which has a major impact on brain functions, including memory, neuroprotection, resistance to oxidative stress and homeostatic tone. Energy demands of the brain are very large, as they continuously account for 20–25% of the whole body’s energy consumption. Energy supply of the brain is tightly linked to neuronal activity, providing the origin of the signals detected by the widely used functional brain imaging techniques such as functional magnetic resonance imaging and positron emission tomography. In particular, neuroenergetic coupling is regulated by astrocytes through glutamate uptake that triggers astrocytic aerobic glycolysis and leads to glucose uptake and lactate release, a mechanism known as the Astrocyte Neuron Lactate Shuttle. Other neurotransmitters such as noradrenaline and Vasoactive Intestinal Peptide mobilize glycogen, the reserve for glucose exclusively localized in astrocytes, also resulting in lactate release. Lactate is then transferred to neurons where it is used, after conversion to pyruvate, as a rapid energy substrate, and also as a signal that modulates neuronal excitability, homeostasis, and the expression of survival and plasticity genes. Importantly, glycolysis in astrocytes and more generally cerebral glucose metabolism progressively deteriorate in aging and age-associated neurodegenerative diseases such as Alzheimer’s disease. This decreased glycolysis actually represents a common feature of several neurological pathologies. Here, we review the critical role of astrocytes in the regulation of brain energy metabolism, and how dysregulation of astrocyte-mediated metabolic pathways is involved in brain hypometabolism. Further, we summarize recent efforts at preclinical and clinical stages to target brain hypometabolism for the development of new therapeutic interventions in age-related neurodegenerative diseases.

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 Imaging and spectroscopic approaches to probe brain energy metabolism dysregulation in neurodegenerative diseases

2017 ◽  
Vol 37 (6) ◽  
pp. 1927-1943 ◽  
Author(s):  
Gilles Bonvento ◽  
Julien Valette ◽  
Julien Flament ◽  
Fanny Mochel ◽  
Emmanuel Brouillet
Keyword(s):  
Energy Metabolism ◽  
Neurodegenerative Diseases ◽  
Defense Mechanisms ◽  
Cellular Heterogeneity ◽  
Brain Energy Metabolism ◽  
Cellular Processes ◽  
Self Defense ◽  
Health And Disease ◽  
The Brain ◽  
Brain Energy

Changes in energy metabolism are generally considered to play an important role in neurodegenerative diseases such as Alzheimer’s, Parkinson’s, and Huntington’s diseases. Whether these changes are causal or simply a part of self-defense mechanisms is a matter of debate. Furthermore, energy defects have often been discussed solely in the context of their probable neuronal origin without considering the cellular heterogeneity of the brain. Recent data point towards the existence of a tri-cellular compartmentation of brain energy metabolism between neurons, astrocytes, and oligodendrocytes, each cell type having a distinctive metabolic profile. Still, the number of methods to follow energy metabolism in patients is extremely limited and existing clinical techniques are blind to most cellular processes. There is a need to better understand how brain energy metabolism is regulated in health and disease through experiments conducted at different scales in animal models to implement new methods in the clinical setting. The purpose of this review is to offer a brief overview of the broad spectrum of methodological approaches that have emerged in recent years to probe energy metabolism in more detail. We conclude that multi-modal neuroimaging is needed to follow non-cell autonomous energy metabolism dysregulation in neurodegenerative diseases.

Role of lactate in the brain energy metabolism: revealed by Bioradiography

2004 ◽  
Vol 48 (1) ◽  
pp. 13-20 ◽  
Author(s):  
Masaaki Tanaka ◽  
Fusao Nakamura ◽  
Shigekazu Mizokawa ◽  
Akira Matsumura ◽  
Kiyoshi Matsumura ◽  
...  
Keyword(s):  
Energy Metabolism ◽  
Brain Energy Metabolism ◽  
The Brain ◽  
Brain Energy

Regional ketone body utilization by rat brain in starvation and diabetes

1986 ◽  
Vol 250 (2) ◽  
pp. E169-E178 ◽  
Author(s):  
R. A. Hawkins ◽  
A. M. Mans ◽  
D. W. Davis
Keyword(s):  
Energy Metabolism ◽  
Plasma Clearance ◽  
Ketone Body ◽  
Ketone Bodies ◽  
Energy Requirement ◽  
Diabetic Rats ◽  
Beta Hydroxybutyrate ◽  
The Brain ◽  
Brain Energy ◽  
Cerebral Structures

The rate of ketone body (beta-hydroxybutyrate and acetoacetate) metabolism was measured in individual cerebral structures of fed, starved, and diabetic rats. This was done by infusing beta-[3-14C]hydroxybutyrate intravenously and measuring the incorporation of 14C into brain by quantitative autoradiography. The capacity of the brain to use ketone bodies, expressed as plasma clearance, increased in starvation and diabetes by approximately 50-60%. Plasma clearance was near maximal after 2 days starvation and was not significantly increased after 4 days starvation, 6 days of diabetes or 28 days of diabetes. In all situations the ketone bodies provided only a modest amount of fuel for brain energy metabolism; 3.2% after 2 days starvation and 6.5 and 9.9% after 6 and 28 days of diabetes. The fraction of their energy requirement which the various structures could derive from the ketone bodies differed widely. In general the telencephalon made greatest use of ketone bodies, whereas the hindbrain used least. There was no correlation between the energy requirement of structures (estimated from glucose use in fed rats) and the fraction of energy they could derive from ketone bodies.

scholarly journals Ketones, omega-3 fatty acids and the Yin-Yang balance in the brain: insights from infant development and Alzheimer’s disease, and implications for human brain evolution

OCL ◽  
2018 ◽  
Vol 25 (4) ◽  
pp. D409 ◽  
Author(s):  
Stephen C. Cunnane
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Fatty Acids ◽  
Energy Metabolism ◽  
Brain Evolution ◽  
Human Brain Evolution ◽  
Infant Brain ◽  
Infant Brain Development ◽  
The Brain ◽  
Brain Energy

Optimal brain performance is intimately linked to the brain’s Yin and the Yang − the balance between its structure and its energy metabolism. This relationship is clearly exemplified in infant brain development and in Alzheimer’s disease, and probably also applies to human brain evolution. In these examples, redundant pathways help achieve this important balance. For instance, the key structural lipid for the brain, docosahexaenoic acid (DHA), is supplied to the infant brain from at last three overlapping sources: (i) milk; (ii) infant’s own fat stores and (iii) by some endogenous synthesis from α-linolenic acid (ALA) or eicosapentaenoic acid (EPA). On the energy side, glucose is normally the brain’s main fuel but under conditions of prolonged starvation, it can be almost totally replaced by the ketone bodies, acetoacetate and β-hydroxybutyrate. When ketones are present in the blood they spare glucose uptake by the brain because they are actually the brain’s preferred fuel and are essential for normal infant brain development. The redundant sources of ketones are long chain fatty acids (including the relatively ketogenic ALA) in infant stores, and medium chain triglycerides (MCT) in milk. Besides infancy, nowhere is the strain on the brain’s balance between yin and yang more apparent than in Alzheimer’s disease (AD). One of the reasons why attempts to treat AD have largely failed could well be because chronically inadequate glucose supply to some areas of the brain on the order of 10% is present in people at risk of AD long before cognitive decline begins. However, brain ketone uptake is still normal even in moderately advanced AD. Hence, treatments that ignore the brain energy (glucose) deficit in AD would be predicted to fail, but treatments that attempt to rescue brain fuel availability via ketones would be predicted to have a better chance of succeeding. By analogy to ketones sparing glucose for brain energy metabolism, perhaps ALA or EPA entering the brain can help spare (conserve) DHA for its structural role. If so, it would not necessarily be futile to transport ALA and EPA into the brain just to β-oxidize the majority afterwards; DHA sparing as well as ketone production could be important beneficiaries.

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