Blood BDNF concentrations reflect brain-tissue BDNF levels across species

Klein, Anders Bue; Williamson, Rebecca; Santini, Martin A.; Clemmensen, Christoffer; Ettrup, Anders; Rios, Maribel; Knudsen, Gitte M.; Aznar, Susana

doi:10.1017/s1461145710000738

Cited by 588 publications

(400 citation statements)

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“…Although the source of serum BDNF relevant to depressive symptoms appears to be concentrated in the platelets (Karege et al, 2005a;Lee and Kim, 2009), its functional significance with regard to central BDNF levels remains unclear. In rats, a positive correlation between serum and central BDNF levels is generally observed at baseline, particularly in young animals (Karege et al, 2002;Klein et al, 2011;Sartorius et al, 2009). Following stress or antidepressant treatment, however, such correlation is inconsistent, probably because of conflicting factors such as age or strain of the animals, or the time of analysis (Béjot et al., 2011; Elfving et al, 2010;Kyeremanteng et al, 2012;Luo et al, 2010).…”

Section: Florian Duclot and Mohamed Kabbaj*mentioning

confidence: 99%

Epigenetic mechanisms underlying the role of brain-derived neurotrophic factor in depression and response to antidepressants

Duclot

Kabbaj

2015

Journal of Experimental Biology

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Major depressive disorder (MDD) is a devastating neuropsychiatric disorder encompassing a wide range of cognitive and emotional dysfunctions. The prevalence of MDD is expected to continue its growth to become the second leading cause of disease burden (after HIV) by 2030. Despite an extensive research effort, the exact etiology of MDD remains elusive and the diagnostics uncertain. Moreover, a marked inter-individual variability is observed in the vulnerability to develop depression, as well as in response to antidepressant treatment, for nearly 50% of patients. Although a genetic component accounts for some cases of MDD, it is now clearly established that MDD results from strong gene and environment interactions. Such interactions could be mediated by epigenetic mechanisms, defined as chromatin and DNA modifications that alter gene expression without changing the DNA structure itself. Some epigenetic mechanisms have recently emerged as particularly relevant molecular substrates, promoting vulnerability or resilience to the development of depressive-like symptoms. Although the role of brainderived neurotrophic factor (BDNF) in the pathophysiology of MDD remains unclear, its modulation of the efficacy of antidepressants is clearly established. Therefore, in this review, we focus on the epigenetic mechanisms regulating the expression of BDNF in humans and in animal models of depression, and discuss their role in individual differences in vulnerability to depression and response to antidepressant drugs. KEY WORDS: BDNF, Epigenetics, Individual differences IntroductionMajor depressive disorder (MDD) is a common debilitating disorder (Bromet et al., 2011) affecting many aspects of the patient's life and family. In addition to its high comorbidity with other neuropsychiatric conditions and increased rate of suicide, depression has a variety of socioeconomic consequences, including low education, unstable employment, reduced work performance and marital dysfunction (Kessler and Bromet, 2013). In 2000, the economic costs of depression in the United States alone were estimated at $83.1 billion, encompassing direct medical costs, suicide-related mortality costs, as well as indirect workplace costs (Greenberg et al., 2003). Moreover, the prevalence of depressive disorders is expected to continue its growth and become by the year 2030 the second leading cause of disease burden among the World Health Organization member states (Mathers and Loncar, 2006). Despite extensive research efforts in past decades, the etiology of REVIEW Department of Biomedical Sciences, Neuroscience Program, Florida State University, Tallahassee, FL 32306, USA.*Author for correspondence (mohamed.kabbaj@med.fsu.edu) depression remains elusive, its diagnosis uncertain and the pharmacotherapy inefficient. Indeed, the antidepressants currently used, which target the monoaminergic pathways, require weeks to months of treatment and exhibit very poor or no response in nearly 50% of patients (Magni et al., 2013;Trivedi et al., 2006;Warden et al., 20...

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Section: Florian Duclot and Mohamed Kabbaj*mentioning

confidence: 99%

Epigenetic mechanisms underlying the role of brain-derived neurotrophic factor in depression and response to antidepressants

Duclot

Kabbaj

2015

Journal of Experimental Biology

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“…Second, BDNF and IGF-1 facilitate lipid oxidation in muscles [53] and glucose metabolism [1], which are essential for energy regulation during submaximal activity [54]. Peripheral production of neurotrophins and growth factors can lead to effects on the central nervous system (CNS) because they all cross the blood -brain barrier, resulting in correlated peripheral and CNS concentrations [55]. It is possible that growth factors are upregulated in the periphery for their beneficial effects on metabolic and vascular systems, and then cross the blood -brain barrier, triggering neurogenic actions.…”

Section: (A) Neurotrophins and Growth Factorsmentioning

confidence: 99%

Linking brains and brawn: exercise and the evolution of human neurobiology

2013

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The hunting and gathering lifestyle adopted by human ancestors around 2 Ma required a large increase in aerobic activity. High levels of physical activity altered the shape of the human body, enabling access to new food resources (e.g. animal protein) in a changing environment. Recent experimental work provides strong evidence that both acute bouts of exercise and long-term exercise training increase the size of brain components and improve cognitive performance in humans and other taxa. However, to date, researchers have not explored the possibility that the increases in aerobic capacity and physical activity that occurred during human evolution directly influenced the human brain. Here, we hypothesize that proximate mechanisms linking physical activity and neurobiology in living species may help to explain changes in brain size and cognitive function during human evolution. We review evidence that selection acting on endurance increased baseline neurotrophin and growth factor signalling (compounds responsible for both brain growth and for metabolic regulation during exercise) in some mammals, which in turn led to increased overall brain growth and development. This hypothesis suggests that a significant portion of human neurobiology evolved due to selection acting on features unrelated to cognitive performance.

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“…Since BDNF crosses the blood-brain barrier in both directions (Pan et al, 1998) and can be measured in serum and plasma (Fujimura et al, 2002), serum BDNF levels may reflect brain BDNF levels (Klein et al, 2011). The first study assessing BDNF in cocaine addicts found no difference in BDNF serum levels in 15 cocaine addicts and a group of healthy controls (Angelucci et al, 2007).…”

Section: Introductionmentioning

confidence: 99%

Brain-derived neurotrophic factor serum levels in cocaine-dependent patients during early abstinence

Corominas-Roso

Roncero

Eiroá-Orosa

et al. 2013

European Neuropsychopharmacology

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Cite as: Corominas-Roso, M., Roncero, C., Eiroa-Orosa, F. J., Gonzalvo, B., Grau-Lopez, L., Ribases, M., … Casas, M. (2013). Brain-derived neurotrophic factor serum levels in cocaine-dependent patients during early abstinence. European Neuropsychopharmacology, 23(9) completed a two-week detoxification program at an inpatient facility. Two serum samples were collected for each patient at baseline and at the end of the protocol.Serum samples were also collected for 46 healthy controls (aged 35.52 ± 9.37 years).Demographic, consumption and clinical data were recorded for all patients.Significantly lower serum BDNF levels (p<.0001) were observed for cocaine-dependent patients at baseline compared to healthy controls. Serum BDNF levels increased significantly across 12 days of early abstinence (p = .030). Baseline BDNF levels correlated with craving (p = .034). Post-detoxification BDNF levels correlated with craving (p = .018), loss of control (p < .000), abstinence measures (p = 0.031), depression (p = 0.036), and anxiety (p = 0.036). Post-detoxification BDNF levels also had predictive value for the loss of control measure of craving. Chronic cocaine use is associated with decreased serum BDNF. A progressive increase in serum BDNF levels during early abstinence correlates with cocaine craving and abstinence symptoms and may reflect increasing BDNF levels in different brain regions. These findings suggest that serum BDNF may be a biomarker for cocaine addiction.

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Blood BDNF concentrations reflect brain-tissue BDNF levels across species

Cited by 588 publications

References 24 publications

Epigenetic mechanisms underlying the role of brain-derived neurotrophic factor in depression and response to antidepressants

Epigenetic mechanisms underlying the role of brain-derived neurotrophic factor in depression and response to antidepressants

Linking brains and brawn: exercise and the evolution of human neurobiology

Brain-derived neurotrophic factor serum levels in cocaine-dependent patients during early abstinence

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