The interrelationship of metabolic syndrome and neurodegenerative diseases with focus on brain-derived neurotrophic factor (BDNF): Kill two birds with one stone

Motamedi, Shima; Karimi, Isaac; Jafari, Fariba

doi:10.1007/s11011-017-9997-0

Cited by 75 publications

(54 citation statements)

References 62 publications

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“…Indeed, BDNF haploinsufficiency [13,14] or missense mutations in its receptor, TrkB [15,16], are associated with hyperfagia, weight gain, and obesity both in human and in mouse models. In line with these observations, both exogenous BDNF administration and BDNF gene transfer in a mouse model of obesity and type 2 diabetes mellitus restore normal food intake, inducing weight loss and decreasing insulin resistance [17,18], which supports the concept that BDNF deficit in the brain induces a metabotropic impairment leading to obesity [19,20]. …”

Section: Introductionmentioning

confidence: 56%

“…The current opinion that obesity is associated with lower levels of circulating BDNF [11,19], and that restoring its physiological levels by administration of exogenous BDNF may prevent the detrimental effect of the metabolic syndrome [11] should be considered carefully.…”

Section: Discussionmentioning

confidence: 99%

“…In this context, a significant reduction of circulating BDNF levels in obese subjects versus controls was found [28,29], suggesting a negative association between circulating BDNF and this pathology [11,19]. However, in the last few years this relationship was called into question.…”

Section: Introductionmentioning

confidence: 99%

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Association between Obesity and Circulating Brain-Derived Neurotrophic Factor (BDNF) Levels: Systematic Review of Literature and Meta-Analysis

Sandrini

Minno

Amadio

et al. 2018

IJMS

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Reduction in brain-derived neurotrophic factor (BDNF) expression in the brain as well as mutations in BDNF gene and/or of its receptor are associated to obesity in both human and animal models. However, the association between circulating levels of BDNF and obesity is still not defined. To answer this question, we performed a meta-analysis carrying out a systematic search in electronic databases. Ten studies (307 obese patients and 236 controls) were included in the analysis. Our data show that obese patients have levels of BDNF similar to those of controls (SMD: 0.01, 95% CI: −0.28, 0.30, p = 0.94). The lack of difference was further confirmed both in studies in which BDNF levels were assessed in serum (MD: −0.93 ng/mL, 95% CI: −3.34, 1.48, p = 0.45) and in plasma (MD: 0.15 ng/mL, 95% CI: −0.09, 0.39, p = 0.23). Data evaluation has shown that some bias might affect BDNF measurements (e.g., subject recruitment, procedures of sampling, handling, and storage), leading to a difficult interpretation of the results. Standardization of the procedures is still needed to reach strong, affordable, and reliable conclusions.

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Section: Introductionmentioning

confidence: 56%

Section: Discussionmentioning

confidence: 99%

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Association between Obesity and Circulating Brain-Derived Neurotrophic Factor (BDNF) Levels: Systematic Review of Literature and Meta-Analysis

Sandrini

Minno

Amadio

et al. 2018

IJMS

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“…Manipulating central and peripheral BDNF levels modified metabolic dysfunction in an animal study (Lyons et al 1999). BDNF was also suggested to play a crucial role in the pathophysiology of obesity and metabolic syndrome in neurodegenerative disorder such as depression (Motamedi et al 2017) because low plasma levels of BDNF were reported in patients with metabolic syndrome (Chaldakov et al 2004). Therefore, the relationship between metabolic abnormality and BD might be a consequence of aberrant inflammatory and neural networks.…”

mentioning

confidence: 99%

Combination of dextromethorphan and memantine in treating bipolar spectrum disorder: a 12-week double-blind randomized clinical trial

Lee

Wang

Chang

et al. 2020

Int J Bipolar Disord

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Background: The aim of this study is to determine whether adding combination of agents with anti-inflammatory and neurotrophic effects is more efficacious than mood stabilizer alone in improving clinical symptoms, plasma brainderived neurotrophic factor (BDNF), cytokine levels, and metabolic profiles in patients with bipolar spectrum disorder. Methods:In a randomized, double-blind, controlled 12-week clinical trial, patients with moderate mood symptoms (HDRS ≥ 18 or YMRS ≥ 14) were recruited. The patients were randomly assigned to a group while still undergoing regular valproate (VPA) treatments: VPA + dextromethorphan (DM) (30 mg/day) + memantine (MM) (5 mg/day) (DM30 + MM5) (n = 66), VPA + DM (30 mg/day) (DM30) (n = 69), VPA + MM (5 mg/day) (MM5) (n = 66), or VPA + Placebo (Placebo) (n = 69). Symptom severity, immunological parameters [plasma tumor necrosis factor (TNF)-α and C-reactive protein (CRP)] and plasma brain-derived neurotrophic factor (BDNF) were regularly examined. Metabolic profiles [cholesterol, triglycerides, glycosylated hemoglobin (HbA1C), fasting serum glucose, body mass index (BMI)] were measured at baseline and at 2, 8, and 12 weeks.Results: Depression scores were significantly (P = 0.03) decreases and BDNF levels significantly (P = 0.04) increased in the DM30 + MM5 group than in the Placebo group. However, neither depressive scores nor BDNF levels were significantly different between the DM30, MM5, and Placebo groups. Changes in certain plasma cytokine and BDNF levels were significantly correlated with metabolic parameters. Conclusion:We concluded that add-on DM30 + MM5 was significantly more effective than placebo for clinical symptoms and plasma BDNF levels. Additional studies with larger samples and mechanistic studies are necessary to confirm our findings.Trial registration NCT03039842 (https ://regis ter.clini caltr ials.gov/). Trial date was -Retrospectively registered, https ://clini caltr ials.gov/ct2/show/NCT03 03984 2?term=NCT03 03984 2&rank=1.

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“…BDNF is a member of the neurotrophin family that includes nerve growth factor, neurotrophin-3, and neutorophin-4. BDNF is a widely investigated marker related to mental illness and plays an important role in the pathophysiology of depression (Karege et al, 2002;Motamedi, Karimi, & Jafari, 2017). BDNF is broadly expressed in the central nervous system and supports the survival of neurons during development (Huang & Reichardt, 2001).…”

Section: R Ole Of N Eu R Otr Op Hi C Fa Ct Ors I N D Ep R E Ssion Amentioning

confidence: 99%

Sonic hedgehog, Wnt, and brain‐derived neurotrophic factor cell signaling pathway crosstalk: potential therapy for depression

Tayyab

Shahi

Farheen

et al. 2017

J of Neuroscience Research

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There are various theories to explain the pathophysiology of depression and support its diagnosis and treatment. The roles of monoamines, brain-derived neurotrophic factor (BDNF), and Wnt signaling are well researched, but sonic hedgehog (Shh) signaling and its downstream transcription factor Gli1 are not well studied in depression. Shh signaling plays a fundamental role in embryonic development and adult hippocampal neurogenesis and also involved in the growth of cancer. In this article, we summarize the evidence for the Shh signaling pathway in depression and the potential crosstalk of Shh with Wnt and BDNF. Antidepressants are known to upregulate the adult hippocampal neurogenesis to treat depression. Shh plays an important role in adult hippocampal neurogenesis, and its downstream signaling components regulate the synthesis of Wnt proteins.

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The interrelationship of metabolic syndrome and neurodegenerative diseases with focus on brain-derived neurotrophic factor (BDNF): Kill two birds with one stone

Cited by 75 publications

References 62 publications

Association between Obesity and Circulating Brain-Derived Neurotrophic Factor (BDNF) Levels: Systematic Review of Literature and Meta-Analysis

Association between Obesity and Circulating Brain-Derived Neurotrophic Factor (BDNF) Levels: Systematic Review of Literature and Meta-Analysis

Combination of dextromethorphan and memantine in treating bipolar spectrum disorder: a 12-week double-blind randomized clinical trial

Sonic hedgehog, Wnt, and brain‐derived neurotrophic factor cell signaling pathway crosstalk: potential therapy for depression

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