Selfish brain and selfish immune system interplay: A theoretical framework for metabolic comorbidities of mood disorders

Yamagata, Ana S.; Mansur, Rodrigo B.; Rizzo, Lucas B.; Rosenstock, Tatiana R.; McIntyre, Roger S.; Brietzke, Elisa

doi:10.1016/j.neubiorev.2016.11.010

Cited by 25 publications

(22 citation statements)

References 124 publications

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“…Major preconditioning risk factors such as cardio‐vascular dysfunction, diabetes, metabolic syndrome, traumatic brain injury, and stroke are shared by the sporadic AD (Biessels and Reagan, ; Chakrabarti et al, ; de la Torre, ; Patterson et al, ) and PD (Athauda and Foltynie ; Daneshvar et al, ; Jabir et al, ; Jha et al, ; Santiago and Potashkin, ; Santiago and Potashkin, ), in addition to being associated with AE (Chou et al, ; Kalra et al, ; Ono and Galanopoulou, ; Pitkanen et al, ; Verrotti et al, ; Waldbaum and Patel, ). These factors are characterized by common brain pathologies such as chronic hypoperfusion (Scholz and Hanefeld, ; Zlokovic, ), neuro‐inflammation, and insulin resistance (Rosales‐Corral et al, ; Straub ; Yamagata et al, ), all leading to energy deficiency and oxidative stress. At the same time, the major genetic risk factors for sporadic AD, APOE ε4 allele (Liu et al, ; Zlokovic, ), and TREM2 mutations (Guerreiro et al, ; Jonsson et al, ), and a‐synuclein gene, MAPT, LRRK2, and GBA for PD (Deleidi and Gasser, ; Kalinderi et al, ) also lead to neurovascular dysfunction and neuro‐inflammation.…”

Section: Short Outline Of Main Glucose Functionsmentioning

confidence: 99%

The vicious circle of hypometabolism in neurodegenerative diseases: Ways and mechanisms of metabolic correction

Zilberter

2017

J of Neuroscience Research

182

139

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Hypometabolism, characterized by decreased brain glucose consumption, is a common feature of many neurodegenerative diseases. Initial hypometabolic brain state, created by characteristic risk factors, may predispose the brain to acquired epilepsy and sporadic Alzheimer's and Parkinson's diseases, which are the focus of this review. Analysis of available data suggests that deficient glucose metabolism is likely a primary initiating factor for these diseases, and that resulting neuronal dysfunction further promotes the metabolic imbalance, establishing an effective positive feedback loop and a downward spiral of disease progression. Therefore, metabolic correction leading to the normalization of abnormalities in glucose metabolism may be an efficient tool to treat the neurological disorders by counteracting their primary pathological mechanisms. Published and preliminary experimental results on this approach for treating Alzheimer's disease and epilepsy models support the efficacy of metabolic correction, confirming the highly promising nature of the strategy. V C 2017 Wiley Periodicals, Inc.

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Section: Short Outline Of Main Glucose Functionsmentioning

confidence: 99%

The vicious circle of hypometabolism in neurodegenerative diseases: Ways and mechanisms of metabolic correction

Zilberter

2017

J of Neuroscience Research

182

139

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“…It is widely acknowledged that type 2 diabetes mellitus (DM2) incidence is significantly higher in patients with schizophrenia compared to the general population (McIntyre et al, ; Mitchell, Vancampfort, De Herdt, Yu, & De Hert, ; Vancampfort et al, ). Several factors, including adverse effects of antipsychotic medications, altered inflammatory processes and possibly shared genetic links between schizophrenia and DM2 likely contribute to comorbidity between these two disorders (Calkin, Gardner, Ransom, & Alda, ; Ferentinos & Dikeos, ; Garcia‐Rizo, Kirkpatrick, Fernandez‐Egea, Oliveira, & Bernardo, ; Perry, McIntosh, Weich, Singh, & Rees, ; Yamagata et al, ). Research dating back to the pre‐anti‐psychotic era (Henneman, Altschule, & Goncz, ) as well as findings from treatment‐naïve, first episode psychosis (FEP) patients suggest a pre‐diabetic condition with impaired glucose metabolism at the onset of the psychotic illness (Arranz et al, ; Greenhalgh et al, ; Misiak et al, ; Perry et al, ; Ryan, Collins, & Thakore, ; Spelman, Walsh, Sharifi, Collins, & Thakore, ).…”

Section: Introductionmentioning

confidence: 99%

Glucose metabolism dysregulation at the onset of mental illness is not limited to first episode psychosis: A systematic review and meta‐analysis

Küçükgöncü

Košir

Zhou

et al. 2018

Early Intervention Psych

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Aim: To compare the differences of glucose metabolism outcomes between treatment-naïve, patients with first episode psychosis (FEP) and mood disorders.Methods: We conducted a systematic review and meta-analysis of glucose intolerance in treatment-naïve, first episode patients with severe mental illnesses (SMIs). Results:We identified 31 eligible studies. Compared to healthy controls, FEP group have higher insulin and insulin resistance levels, and both groups have higher glucose tolerance test results.No significant differences were found in glucose metabolism outcomes between FEP and mood disorder groups.Conclusions: Our results highlight impaired glucose metabolism at the onset of SMIs, suggesting both patients with psychosis and mood disorders are high-risk groups for diabetes development. K E Y W O R D Sdiabetes, first episode, insulin, mood disorders, psychosis

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“…In BD, obesity has been associated with greater illness severity and cognitive dysfunction, and even suicide attempts (Goldstein et al 2011;Yim et al 2012). One main link between metabolic disturbance and BD was postulated as inflammation (Yamagata et al 2017). Manipulating central and peripheral BDNF levels modified metabolic dysfunction in an animal study (Lyons et al 1999).…”

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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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Selfish brain and selfish immune system interplay: A theoretical framework for metabolic comorbidities of mood disorders

Cited by 25 publications

References 124 publications

The vicious circle of hypometabolism in neurodegenerative diseases: Ways and mechanisms of metabolic correction

The vicious circle of hypometabolism in neurodegenerative diseases: Ways and mechanisms of metabolic correction

Glucose metabolism dysregulation at the onset of mental illness is not limited to first episode psychosis: A systematic review and meta‐analysis

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

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