Polyunsaturated fatty acids, neuroinflammation and well being.

Posted on March 3, 2012 by Maurice Preter MD

Prostaglandins Leukot Essent Fatty Acids. 2010 Apr-Jun;82(4-6):295-303. Epub 2010 Mar 15.
Polyunsaturated fatty acids, neuroinflammation and well being.
Layé S.
Source

Psychoneuroimmunology, Nutrition and Genetic (PsyNuGen), UMR INRA 1286, CNRS 5226, University Bordeaux 2, Bordeaux, France. sophie.laye@bordeaux.inra.fr
Abstract

The innate immune system of the brain is principally composed of microglial cells and astrocytes, which, once activated, protect neurons against insults (infectious agents, lesions, etc.). Activated glial cells produce inflammatory cytokines that act specifically through receptors expressed by the brain. The functional consequences of brain cytokine action (also called neuroinflammation) are alterations in cognition, mood and behaviour, a hallmark of altered well-being. In addition, proinflammatory cytokines play a key role in depression and neurodegenerative diseases linked to aging. Polyunsaturated fatty acids (PUFA) are essential nutrients and essential components of neuronal and glial cell membranes. PUFA from the diet regulate both prostaglandin and proinflammatory cytokine production. n-3 fatty acids are anti-inflammatory while n-6 fatty acids are precursors of prostaglandins. Inappropriate amounts of dietary n-6 and n-3 fatty acids could lead to neuroinflammation because of their abundance in the brain and reduced well-being. Depending on which PUFA are present in the diet, neuroinflammation will, therefore, be kept at a minimum or exacerbated. This could explain the protective role of n-3 fatty acids in neurodegenerative diseases linked to aging.

Copyright 2010 Elsevier Ltd. All rights reserved.

PMID:
20227866
[PubMed – indexed for MEDLINE]

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Black sheep get the blues: a psychobiological model of social rejection and depression.

Posted on March 3, 2012 by Maurice Preter MD

Black sheep presumably also get less Vitamin D.

Neurosci Biobehav Rev. 2010 Sep;35(1):39-45. Epub 2010 Jan 18.
Black sheep get the blues: a psychobiological model of social rejection and depression.
Slavich GM, O’Donovan A, Epel ES, Kemeny ME.
Source

Department of Psychiatry, University of California, San Francisco, San Francisco, CA 94143-0848, USA. george.slavich@ucsf.edu
Abstract

Major life events involving social rejection are strongly associated with onset of depression. To account for this relation, we propose a psychobiological model in which rejection-related stressors elicit a distinct and integrated set of cognitive, emotional, and biological changes that may evoke depression. In this model, social rejection events activate brain regions involved in processing negative affect and rejection-related distress (e.g., anterior insula, dorsal anterior cingulate cortex). They also elicit negative self-referential cognitions (e.g., “I’m undesirable,” “Other people don’t like me”) and related self-conscious emotions (e.g., shame, humiliation). Downstream biological consequences include upregulation of the hypothalamic-pituitary-adrenal axis, sympathetic-adrenal-medullary axis, and inflammatory response. Pro-inflammatory cytokines play an important role in this process because they induce a constellation of depressotypic behaviors called sickness behaviors. Although these changes can be short-lived, sustained inflammation may occur via glucocorticoid resistance, catecholamines, sympathetic innervation of immune organs, and immune cell aging. This response also may be moderated by several factors, including prior life stress, prior depression, and genes implicated in stress reactivity.

PMID:
20083138
[PubMed – indexed for MEDLINE]
PMCID:
PMC2926175

Free PMC Article

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Inflammation and social experience: an inflammatory challenge induces feelings of social disconnection in addition to depressed mood.

Posted on March 3, 2012 by Maurice Preter MD

As usual, Eisenberger is way ahead of the pack. The relationship between inflammation and social rejection is bi-directional.

Brain Behav Immun. 2010 May;24(4):558-63. Epub 2010 Jan 4.
Inflammation and social experience: an inflammatory challenge induces feelings of social disconnection in addition to depressed mood.
Eisenberger NI, Inagaki TK, Mashal NM, Irwin MR.
Source

Department of Psychology, University of California, Los Angeles, CA 90095-1563, USA. neisenbe@ucla.edu
Abstract

Although research has established links between feelings of social isolation and inflammation, the direction of these effects is unclear. Based on the role that proinflammatory cytokines play in initiating “sickness behavior,” which includes symptoms such as social withdrawal, it is possible that inflammatory processes heighten feelings of ‘social disconnection.’ Here, we examined whether exposure to an inflammatory challenge increased self-reported feelings of social disconnection. In addition, because both inflammatory processes and feelings of social disconnection contribute to depressive symptoms, we also explored whether increases in feelings of social disconnection played a role in the link between inflammation and depressed mood. Participants were randomly assigned to either receive endotoxin, an inflammatory challenge, or placebo. Proinflammatory cytokines (IL-6, TNF-alpha) were collected at baseline and then hourly for 6h. Participants completed self-reports of sickness symptoms (“fatigue”), social disconnection (“I feel disconnected from others”), and depressed mood (“unhappy”) hourly. Results revealed that endotoxin led to significant increases (from baseline) in IL-6 and TNF-alpha levels as well as feelings of social disconnection and depressed mood. Moreover, controlling for increases in social disconnection eliminated the relationship between exposure to inflammatory challenge and depressed mood. This study demonstrates that inflammation can have social psychological consequences, which may play a role in cytokine-related depressive symptoms.

Copyright 2009 Elsevier Inc. All rights reserved.

PMID:
20043983
[PubMed – indexed for MEDLINE]
PMCID:
PMC2856755

Free PMC Article

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Depression and Alzheimer’s disease: neurobiological links and common pharmacological targets.

Posted on March 3, 2012 by Maurice Preter MD

Eur J Pharmacol. 2010 Jan 10;626(1):64-71. Epub 2009 Oct 18.
Depression and Alzheimer’s disease: neurobiological links and common pharmacological targets.
Caraci F, Copani A, Nicoletti F, Drago F.
Source

Department of Pharmaceutical Sciences, University of Catania, 95125, Catania, Italy.
Abstract

Depression is one of the most prevalent and life-threatening forms of mental illnesses, whereas Alzheimer’s disease is a neurodegenerative disorder that affects more than 37 million people worldwide. Recent evidence suggests a strong relationship between depression and Alzheimer’s disease. A lifetime history of major depression has been considered as a risk factor for later development of Alzheimer’s disease. The presence of depressive symptoms can affect the conversion of mild cognitive impairment into Alzheimer’s disease. Neuritic plaques and neurofibrillary tangles, the two major hallmarks of Alzheimer’s disease brain, are more pronounced in the brains of Alzheimer’s disease patients with comorbid depression as compared with Alzheimer’s disease patients without depression. On the other hand, neurodegenerative phenomena have been observed in different brain regions of patients with a history of depression. Recent evidence suggests that molecular mechanisms and cascades that underlie the pathogenesis of major depression, such as chronic inflammation and hyperactivation of hypothalamic-pituitary-adrenal (HPA) axis, are also involved in the pathogenesis of Alzheimer’s disease. In particular, a specific impairment in the signaling of some neurotrophins such as transforming-growth-factor 1 (TGF-1) and brain-derived neurotrophic factor (BDNF) has been observed both in depression and Alzheimer’s disease. In the present review we will examine the evidence on the common molecular pathways between depression and Alzheimer’s disease and we will discuss these pathways as new pharmacological targets for the treatment of both major depression and Alzheimer’s disease.

PMID:
19837057
[PubMed – indexed for MEDLINE]

Posted in Aging | Tagged |

Neurobiology of depression, fibromyalgia and neuropathic pain.

Posted on March 3, 2012 by Maurice Preter MD

Front Biosci. 2009 Jun 1;14:5291-338.
Neurobiology of depression, fibromyalgia and neuropathic pain.
Maletic V, Raison CL.
Source

University of South Carolina, School of Medicine, Department of Neuropsychiatry and Behavioral Sciences, Columbia, SC, USA. vmaletic@bellsouth.net
Abstract

This article synthesizes recent data suggesting that the high rates of comorbidity observed between major depression, fibromyalgia and neuropathic pain likely result from the fact that these disorders share multiple biological and environmental underpinnings. This perspective suggests that these biologically complex conditions result from similar genetic vulnerabilities interacting with environmental adversity. Shared genetic determinants include poorly functional alleles regulating monoaminergic, glutamatergic, neurotrophic, opioid and inflammatory cytokine signaling. Chief among environmental risk factors are psychosocial stress and illness, both of which promote, in vulnerable individuals, relative resistance to glucocorticoids, increased sympathetic/decreased parasympathetic activity and increased production and release of proinflamnmatory mediators. Dysregulation of stress/inflammatory pathways promotes alterations in brain circuitry that modulates mood, pain and the stress response. Over time, these functional changes likely promote disruptions in neurotrophic support and disturbances of glia-neuronal communication. These changes, in turn, have been associated with the related processes of central sensitization in pain disorders and “kindling” in depression, both of which may account for the progressive and self-perpetuating nature of these disorders, especially when inadequately treated.

PMID:
19482616
[PubMed – indexed for MEDLINE]

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