Adiponectin is decreased in bipolar depression

Platzer, Martina; Fellendorf, Frederike T.; Bengesser, Susanne; Birner, Armin; Dalkner, Nina; Hamm, Carlo; Hartleb, Riccarda; Queissner, Robert; Pilz, René; Rieger, Alexandra; Maget, Alexander; Mangge, Harald; Zelzer, Sieglinde; Reininghaus, Bernd; Kapfhammer, Hans-Peter; Reininghaus, Eva

doi:10.1080/15622975.2018.1500033

Cited by 23 publications

(13 citation statements)

References 45 publications

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“…Adiponectin also acts on brain to regulate peripheral and systemic processes such as thermogenesis, energy expenditure (Qi et al, 2004) and reproduction (Angelidis et al, 2012). Finally, central adiponectin has been shown to regulate behaviors like food intake (Suyama et al, 2016), locomotor activity (Miyatake et al, 2015) as well as cognition, anxiety and mood (Jeong et al, 2012; Zhang et al, 2017; Cao et al, 2018; Cezaretto et al, 2018; Nicolas et al, 2018; Platzer et al, 2018; Sun et al, 2018). This variety of central effects of adiponectin likely reflects the wide distribution of different adiponectin receptors throughout the brain.…”

Section: Adiponectinmentioning

confidence: 99%

The Role of Leptin and Adiponectin in Obesity-Associated Cognitive Decline and Alzheimer’s Disease

2019

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Cross-talk between adipose tissue and central nervous system (CNS) underlies the increased risk of obese people to develop brain diseases such as cognitive and mood disorders. Detailed mechanisms for how peripheral changes caused by adipose tissue accumulation in obesity impact the CNS to cause brain dysfunction are poorly understood. Adipokines are a large group of substances secreted by the white adipose tissue to regulate a wide range of homeostatic processes including, but not limited to, energy metabolism and immunity. Obesity is characterized by a generalized change in the levels of circulating adipokines due to abnormal accumulation and dysfunction of adipose tissue. Altered adipokine levels underlie complications of obesity as well as the increased risk for the development of obesity-related comorbidities such as type 2 diabetes, cardiovascular and neurodegenerative diseases. Here, we review the literature for the role of adipokines as key mediators of the communication between periphery and CNS in health and disease. We will focus on the actions of leptin and adiponectin, two of the most abundant and well studied adipokines, in the brain, with particular emphasis on how altered signaling of these adipokines in obesity may lead to cognitive dysfunction and augmented risk for Alzheimer’s disease. A better understanding of adipokine biology in brain disorders may prove of major relevance to diagnostic, prevention and therapy.

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Section: Adiponectinmentioning

confidence: 99%

The Role of Leptin and Adiponectin in Obesity-Associated Cognitive Decline and Alzheimer’s Disease

2019

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“…Adiponectin is an adipocyte-secreted protein molecule, whose numerous physiological functions in obesity, diabetes, inflammation, atherosclerosis and cardiovascular diseases have been extensively explored over the past two decades (Bloemer et al, 2018). As a potential marker for bipolar depression, adiponectin expression levels decreased significantly in bipolar disorder patients (Misiak et al, 2019;Platzer et al, 2019). ADN-KO mice displayed not only cognitive impairments, but also LTP deficits of the hippocampal Schaefer collateral pathway and altered levels of key presynaptic and postsynaptic proteins involved in glutamatergic neurotransmission, together suggesting that adiponectin is a crucial regulator of cognition and synaptic function (Bloemer et al, 2019).…”

Section: Discussionmentioning

confidence: 99%

Potential Involvement of Adiponectin Signaling in Regulating Physical Exercise-Elicited Hippocampal Neurogenesis and Dendritic Morphology in Stressed Mice

Wang

Liang

Chen

et al. 2020

Front. Cell. Neurosci.

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Adiponectin, a cytokine secreted by mature adipocytes, proves to be neuroprotective. We have previously reported that running triggers adiponectin up-regulation which subsequently promotes generation of hippocampal neurons and thereby alleviates depression-like behaviors in non-stressed mice. However, under the stressing condition, whether adiponectin could still exert antidepressant-like effects following exercise remained unexplored. In this study, by means of repeated corticosterone injections to mimic stress insult and voluntary wheel running as physical exercise intervention, we examined whether exercise-elicited antidepressive effects might involve adiponectin's regulation on hippocampal neurogenesis and dendritic plasticity in stressed mice. Here we show that repeated injections of corticosterone inhibited hippocampal neurogenesis and impaired dendritic morphology of neurons in the dentate gyrus of both wild-type and adiponectin-knockout mice comparably, which subsequently evoked depression-like behaviors. Voluntary wheel running attenuated corticosterone-suppressed neurogenesis and enhanced dendritic plasticity in the hippocampus, ultimately reducing depressionlike behaviors in wild-type, but not adiponectin-knockout mice. We further demonstrate that such proneurogenic effects were potentially achieved through activation of the AMP-dependent kinase (AMPK) pathway. Our study provides the first evidence that adiponectin signaling is essential for physical exercise-triggered effects on stress-elicited depression by retaining the normal proliferation of neural progenitors and dendritic morphology of neurons in the hippocampal dentate gyrus, which may depend on activation of the AMPK pathway.

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“…Recently, chronic low grade inflammatory processes have been linked to the pathophysiology of BD itself [48-50], and they may also relate to cognitive impairments in BD [51-53], just like in mentally healthy samples [10, 54]. Accordingly, the role of other biomarkers, such as adiponectines, principally leptins, known to associate with cognitive deficits [45], obesity and BD [55, 56], should also be taken into consideration. In addition, abnormalities in white matter microstructure were found in overweight individuals with BD [57].…”

Section: Discussionmentioning

confidence: 99%

Body Mass Index Predicts Decline in Executive Function in Bipolar Disorder: Preliminary Data of a 12-Month Follow-up Study

et al. 2020

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Introduction: Obesity and associated risk factors have been linked to cognitive decline before. Objectives: In the present study, we evaluated potential cumulative negative effects of overweight and obesity on cognitive performance in euthymic patients with bipolar disorder (BD) in a longitudinal design. Methods: Neurocognitive measures (California Verbal Learning Test, Trail Making Test [TMT] A/B, Digit-Symbol-Test, Digit-Span, d2 Test), anthropometrics (e.g., body mass index [BMI]), and clinical ratings (Hamilton Depression Scale, Young Mania Rating Scale) were collected over a 12-month observation period. Follow-up data of 38 patients with BD (mean age 40 years; 15 males, 23 females) were available. Results: High baseline BMI predicted a decrease in the patient’s performance in the Digit-Span backwards task measuring working memory performance. In contrast, cognitive performance was not predicted by increases in BMI at follow-up. Normal weight bipolar patients (n = 19) improved their performance on the TMT B, measuring cognitive flexibility and executive functioning, within 1 year, while overweight bipolar patients (n = 19) showed no change in this task. Conclusions: The results suggest that overweight can predict cognitive performance changes over 12 months.

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Adiponectin is decreased in bipolar depression

Cited by 23 publications

References 45 publications

The Role of Leptin and Adiponectin in Obesity-Associated Cognitive Decline and Alzheimer’s Disease

The Role of Leptin and Adiponectin in Obesity-Associated Cognitive Decline and Alzheimer’s Disease

Potential Involvement of Adiponectin Signaling in Regulating Physical Exercise-Elicited Hippocampal Neurogenesis and Dendritic Morphology in Stressed Mice

Body Mass Index Predicts Decline in Executive Function in Bipolar Disorder: Preliminary Data of a 12-Month Follow-up Study

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