BDNF/NF-κB Signaling in the Neurobiology of Depression

Caviedes, Ariel; Lafourcade, Carlos; Soto, Claudio A. Telléz; Wyneken, Úrsula

doi:10.2174/1381612823666170111141915

Cited by 184 publications

(120 citation statements)

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“…The anti-depressant activity of WY14643 appeared to involve activation of the brain derived neurotropic factor (BDNF) signaling cascade [44], a pathway implicated in a range of neuronal processes (depicted in Figure 1) [75][76][77][78]. It is well known that BDNF levels are found to be decreased in the hippocampus of depressed individuals and in animal models of this disorder [79][80][81][82]. Furthermore, the action of antidepressants, like fluoxetine, increase BDNF levels, which in turn correlates with an improvement of behavioral dysfunction [83].…”

Section: Mood Disordersmentioning

confidence: 99%

Is There a Future for PPARs in the Treatment of Neuropsychiatric Disorders?

Tufano

Pinna

2020

Molecules

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Recently, peroxisome proliferator-activated receptor (PPAR)-α and γ isoforms have been gaining consistent interest in neuropathology and treatment of neuropsychiatric disorders. Several studies have provided evidence that either the receptor expression or the levels of their endogenously-produced modulators are downregulated in several neurological and psychiatric disorders and in their respective animal models. Remarkably, administration of these endogenous or synthetic ligands improves mood and cognition, suggesting that PPARs may offer a significant pharmacological target to improve several neuropathologies. Furthermore, various neurological and psychiatric disorders reflect sustained levels of systemic inflammation. Hence, the strategy of targeting PPARs for their anti-inflammatory role to improve these disorders is attracting attention. Traditionally, classical antidepressants fail to be effective, specifically in patients with inflammation. Non-steroidal anti-inflammatory drugs exert potent antidepressant effects by acting along with PPARs, thereby strongly substantiating the involvement of these receptors in the mechanisms that lead to development of several neuropathologies. We reviewed running findings in support of a role for PPARs in the treatment of neurological diseases, including Alzheimer’s disease or psychiatric disorders, such as major depression. We discuss the opportunity of targeting PPARs as a future pharmacological approach to decrease neuropsychiatric symptoms at the same time that PPAR ligands resolve neuroinflammatory processes.

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Section: Mood Disordersmentioning

confidence: 99%

Is There a Future for PPARs in the Treatment of Neuropsychiatric Disorders?

Tufano

Pinna

2020

Molecules

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“…In addition to its functions in the immune system, NF-Kβ regulates neurogenesis and synaptic plasticity. 35 BDNF has been shown to activate NF-kβ which enhances both dendritic spine and excitatory synapse density. 18 Impairment in spatial learning has been seen in mice lacking in the NF-kβ p50 subunit.…”

Section: Bdnf and Viral Proteinsmentioning

confidence: 99%

“…There is a positive feedback loop between NF-kβ and BDNF since NF-kβ also regulates BDNF expression. 35 BDNF has been shown to be neuroprotective by enhancing mitochondrial biogenesis, transport and overall mitochondrial health. 24 HIV-1 tat and gp120 alter mitochondrial fission, mitochondrial transport and mitophagy in neurons and microglial cells.…”

Section: Bdnf and Viral Proteinsmentioning

confidence: 99%

<p>The Role of Brain Derived Neurotrophic Factor in HIV-Associated Neurocognitive Disorder: From the Bench-Top to the Bedside</p>

Michael

Mpofana

Ramlall

et al. 2020

NDT

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Human immunodeficiency virus (HIV)-associated neurocognitive disorder (HAND) remains prevalent in the anti-retroviral (ART) era. While there is a complex interplay of many factors in the neuropathogenesis of HAND, decreased neurotrophic synthesis has been shown to contribute to synaptic degeneration which is a hallmark of HAND neuropathology. Brain derived neurotrophic factor (BDNF) is the most abundant and synaptic-promoting neurotrophic factor in the brain and plays a critical role in both learning and memory. Reduced BDNF levels can worsen neurocognitive impairment in HIV-positive individuals across several domains. In this paper, we review the evidence from pre-clinical and clinical studies showing the neuroprotective roles of BDNF against viral proteins, effect on co-morbid mental health disorders, altered human microbiome and ART in HAND management. Potential applications of BDNF modulation in pharmacotherapeutic, cognitive and behavioral interventions in HAND are also discussed. Finally, research gaps and future research direction are identified with the aim of helping researchers to direct efforts to make these BDNF driven interventions improve the quality of life of patients living with HAND.

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“…It is well established that alterations in these intracellular signaling have profound effects on synaptic transmission and plasticity. This was documented repeatedly for ERK [110,111,112], AKT [113,114,115], and NFκB [116,117,118] activations.…”

Section: Na+ K+-atpase Signaling and Bdmentioning

confidence: 71%

Na+, K+-ATPase Signaling and Bipolar Disorder

Lichtstein¹,

Ilani²,

Rosen³

et al. 2018

IJMS

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Bipolar disorder (BD) is a severe and common chronic mental illness characterized by recurrent mood swings between depression and mania. The biological basis of the disease is poorly understood and its treatment is unsatisfactory. Although in past decades the “monoamine hypothesis” has dominated our understanding of both the pathophysiology of depressive disorders and the action of pharmacological treatments, recent studies focus on the involvement of additional neurotransmitters/neuromodulators systems and cellular processes in BD. Here, evidence for the participation of Na+, K+-ATPase and its endogenous regulators, the endogenous cardiac steroids (ECS), in the etiology of BD is reviewed. Proof for the involvement of brain Na+, K+-ATPase and ECS in behavior is summarized and it is hypothesized that ECS-Na+, K+-ATPase-induced activation of intracellular signaling participates in the mechanisms underlying BD. We propose that the activation of ERK, AKT, and NFκB, resulting from ECS-Na+, K+-ATPase interaction, modifies neuronal activity and neurotransmission which, in turn, participate in the regulation of behavior and BD. These observations suggest Na+, K+-ATPase-mediated signaling is a potential target for drug development for the treatment of BD.

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BDNF/NF-κB Signaling in the Neurobiology of Depression

Cited by 184 publications

References 0 publications

Is There a Future for PPARs in the Treatment of Neuropsychiatric Disorders?

Is There a Future for PPARs in the Treatment of Neuropsychiatric Disorders?

<p>The Role of Brain Derived Neurotrophic Factor in HIV-Associated Neurocognitive Disorder: From the Bench-Top to the Bedside</p>

Na+, K+-ATPase Signaling and Bipolar Disorder

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