Neuronal–immune interactions in mediating stress effects in the etiology and course of schizophrenia: Role of the amygdala in developmental co-ordination

Anderson, Geoffrey M.

doi:10.1016/j.mehy.2010.08.029

Cited by 34 publications

(20 citation statements)

References 106 publications

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“…As such, the results described above have significant implications and will be important to replicate and extend. The importance of the TRYCAT pathways in immune cells, both centrally and peripherally, suggests a powerful role for immune-mediated control of neuronal activity, driving variation over development, out of which psychiatric presentations emerge (151). It could be argued that cytokines are associated with depressive symptoms (152,153), for example, typhoid vaccination in people elicits an inflammatory response, increasing IL-6, and after 3 h decreasing mood.…”

Section: Oxidative and Nitrosative Stress And Autoimmunitymentioning

confidence: 99%

Biological phenotypes underpin the physio‐somatic symptoms of somatization, depression, and chronic fatigue syndrome

Anderson¹,

Berk

Maes

2013

Acta Psychiatr Scand

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Section: Oxidative and Nitrosative Stress And Autoimmunitymentioning

confidence: 99%

Biological phenotypes underpin the physio‐somatic symptoms of somatization, depression, and chronic fatigue syndrome

Anderson¹,

Berk

Maes

2013

Acta Psychiatr Scand

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“…Sixty percent of central kyn is peripherally derived, being readily transported over the blood–brain barrier, where it is converted to KYNA by astrocytes and to wider kyn pathway products, including the excitotoxic quinolinic acid (QUIN), by microglia. KYNA inhibits the alpha 7 nicotinic acetylcholine receptor (á7nAChr), decreasing glutamate, acetylcholine, and dopamine levels in the cortex, contributing to decreased cortex activity, cognition, and cortex influence in refining affectively driven behaviors 31. In rodents, prenatal and postnatal exposure to kyn results in cognitive deficits in adulthood 32.…”

Section: Immunological Conceptualizations Of Depressionmentioning

confidence: 99%

“…Repeat stress is known to decrease allopregnanolone,42 an important regulator of IL-1â modulation of oxytocin in pregnancy 43. This is a perspective that emphasizes the importance of the TRYCAT pathways in driving immunological influences on patterned neuronal activity, both centrally and peripherally 31,44…”

Section: Immunological Conceptualizations Of Depressionmentioning

confidence: 99%

Postpartum depression: psychoneuroimmunological underpinnings and treatment

Anderson¹,

Maes²

2013

NDT

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Postpartum depression (PPD) is common, occurring in 10%–15% of women. Due to concerns about teratogenicity of medications in the suckling infant, the treatment of PPD has often been restricted to psychotherapy. We review here the biological underpinnings to PPD, suggesting a powerful role for the tryptophan catabolites, indoleamine 2,3-dixoygenase, serotonin, and autoimmunity in mediating the consequences of immuno-inflammation and oxidative and nitrosative stress. It is suggested that the increased inflammatory potential, the decreases in endogenous anti-inflammatory compounds together with decreased omega-3 poly-unsaturated fatty acids, in the postnatal period cause an inflammatory environment. The latter may result in the utilization of peripheral inflammatory products, especially kynurenine, in driving the central processes producing postnatal depression. The pharmacological treatment of PPD is placed in this context, and recommendations for more refined and safer treatments are made, including the better utilization of the antidepressant, and the anti-inflammatory and antioxidant effects of melatonin.

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“…If indeed astrocytes have a co-ordinating and perhaps controlling role in their interactions with neurons and other CNS cells (Anderson, 2011) …”

Section: Mitochondria Melatonin and Msmentioning

confidence: 99%

Multiple sclerosis: The role of melatonin and N-acetylserotonin

Anderson¹,

Rodriguez

2015

Multiple Sclerosis and Related Disorders

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Multiple sclerosis (MS) is an immune mediated disorder that is under intensive investigation in an attempt to improve on available treatments. Many of the changes occurring in MS, including increased mitochondrial dysfunction, pain reporting and depression may be partly mediated by increased indoleamine 2,3-dioxygenase, which drives tryptophan to the production of neuroregulatory tryptophan catabolites and away from serotonin, N-acetylserotonin and melatonin production. The consequences of decreased melatonin have classically been attributed to circadian changes following its release from the pineal gland. However, recent data shows that melatonin may be produced by all mitochondria containing cells to some degree, including astrocytes and immune cells, thereby providing another important MS treatment target. As well as being a powerful antioxidant, anti-inflammatory and antinociceptive, melatonin improves mitochondrial functioning, partly via increased oxidative phosphorylation. Melatonin also inhibits demyelination and increases remyelination, suggesting that its local regulation in white matter astrocytes by serotonin availability and apolipoprotein E4, among other potential factors, will be important in the etiology, course and treatment of MS. Here we review the role of local melatonin and its precursors, N-acetylserotonin and serotonin, in MS.

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Neuronal–immune interactions in mediating stress effects in the etiology and course of schizophrenia: Role of the amygdala in developmental co-ordination

Cited by 34 publications

References 106 publications

Biological phenotypes underpin the physio‐somatic symptoms of somatization, depression, and chronic fatigue syndrome

Biological phenotypes underpin the physio‐somatic symptoms of somatization, depression, and chronic fatigue syndrome

Postpartum depression: psychoneuroimmunological underpinnings and treatment

Multiple sclerosis: The role of melatonin and N-acetylserotonin

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