Increased BDNF serum concentration in fibromyalgia with or without depression or antidepressants

Laske, Christoph; Stransky, Elke; Eschweiler, Gerhard W.; Klein, Reinhild; Wittorf, Andreas; Leyhe, Thomas; Richartz, Elke; Köhler, Niklas; Bartels, Matthias; Buchkremer, Gerhard; Schott, Klaus

doi:10.1016/j.jpsychires.2006.02.007

Cited by 105 publications

(109 citation statements)

References 39 publications

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“…Decreased serum BDNF levels in adult patients have been reported in depression, 6,10 bipolar disorder, 11 Huntington disease, 12 late-stage Alzheimer disease, 13 autism, 14 and multiple sclerosis. 15 Increased serum levels have been found in schizophrenia, 16 fibromyalgia, 17 and early-stage Alzheimer disease, 13 and in children with ES. 2 In our study evaluating serum BDNF levels in adult patients with ES, we found decreased levels of serum BDNF in patients with ES, compared to HCs.…”

Section: Subjects Outpatients and Inpatients Were Recruited Frommentioning

confidence: 99%

Decreased serum BDNF levels in patients with epileptic and psychogenic nonepileptic seizures

LaFrance¹,

Leaver²,

Stopa³

et al. 2010

Neurology

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Section: Subjects Outpatients and Inpatients Were Recruited Frommentioning

confidence: 99%

Decreased serum BDNF levels in patients with epileptic and psychogenic nonepileptic seizures

LaFrance¹,

Leaver²,

Stopa³

et al. 2010

Neurology

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“…For example, levels of brain BDNF have been shown to correlate with human learning, memory and cognitive function (205)(206)(207) . Future efforts should focus on whether the ability of flavonoids to induce improvements in cognition is mediated by their ability to induce BDNF and/or other neurotrophin production in either the brain or the periphery (Fig.…”

Section: Present and Future Perspectivesmentioning

confidence: 99%

Beyond antioxidants: the cellular and molecular interactions of flavonoids and how these underpin their actions on the brain

Spencer

2010

Proc. Nutr. Soc.

143

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The consumption of flavonoid-rich foods and beverages has been suggested to limit the neurodegeneration associated with a variety of neurological disorders and to prevent or reverse normal or abnormal deteriorations in cognitive performance. Flavonoids mediate these effects via a number of routes, including a potential to protect neurons against injury induced by neurotoxins, an ability to suppress neuroinflammation and a potential to promote memory, learning and cognitive function. Originally, it was thought that such actions were mediated by the antioxidant capacity of flavonoids. However, their limited absorption and their low bioavailability in the brain suggest that this explanation is unlikely. Instead, this multiplicity of effects appears to be underpinned by three separate processes: first, through their interactions with important neuronal and glial signalling cascades in the brain, most notably the phosphatidylinositol 3-kinase/Akt and mitogen-activated protein kinase pathways that regulate prosurvival transcription factors and gene expression; second, through an ability to improve peripheral and cerebral blood flow and to trigger angiogenesis and neurogenesis in the hippocampus; third, by their capacity to directly react with and scavenge neurotoxic species and pro-inflammatory agents produced in the brain as a result of both normal and abnormal brain ageing. The present review explores the potential inhibitory or stimulatory actions of flavonoids within these three systems and describes how such interactions are likely to underlie neurological effects.

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“…The combination of elevated glutamate and substance P and reduced serotonin supports a role for central amplification in the abnormal pain transmission and perception of patients with FM. Moreover, CSF levels of two neurotrophins, nerve growth factor (NGF) and BDNF, appear to be increased in patients with FM (Giovengo et al, 1999;Laske et al, 2007;Sarchielli et al, 2007). The increased levels of NGF and BDNF correlated with increased glutamate levels in the CSF of patients with FM, and the authors speculated that NGF acted indirectly to increase BDNF expression, which then modulated NMDA receptor activity to increase the excitatory amino acids glutamate and aspartate, supporting the involvement of a central mechanism in the pathophysiology of FM (Sarchielli et al, 2007).…”

Section: Clinical Studies Supporting Centralmentioning

confidence: 99%

Central amplification and fibromyalgia: Disorder of pain processing

Petersel

Dror

Cheung

2010

J of Neuroscience Research

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Fibromyalgia (FM), a complex chronic pain disorder affecting a heterogeneous patient population, is an area of active basic and clinical research. Although diagnostic criteria for FM have been available for 2 decades, there remains no definitive diagnostic and no consensus regarding its etiology. Accumulating evidence suggests the underlying cause of FM pain results from abnormal pain processing particularly in the central nervous system rather than from dysfunction in peripheral tissues where pain is perceived. In this review, we examine recent studies investigating abnormalities in central pain processing as a component of FM in both preclinical models of generalized muscle hypersensitivity and clinical research in patients with FM. We focus our discussion on two areas where strong evidence exists for abnormalities in sensory signaling: the reduction of descending control, including suppression of descending inhibitory pathways and/or enhancement of descending facilitatory pathways, and changes in key neurotransmitters associated with central sensitization. Finally, we discuss currently available pharmacological treatments indicated for the management of pain in FM patients, based on their proposed mechanism of action and efficacy.

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Increased BDNF serum concentration in fibromyalgia with or without depression or antidepressants

Cited by 105 publications

References 39 publications

Decreased serum BDNF levels in patients with epileptic and psychogenic nonepileptic seizures

Decreased serum BDNF levels in patients with epileptic and psychogenic nonepileptic seizures

Beyond antioxidants: the cellular and molecular interactions of flavonoids and how these underpin their actions on the brain

Central amplification and fibromyalgia: Disorder of pain processing

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