Free Fatty Acids and Their Inflammatory Derivatives Affect BDNF in Stroke Patients.

Dariusz Kotlega,Malgorzata Szczuko,Przemyslaw Nowacki,Agnieszka Zembron-Lacny,Barbara Morawin,Monika Golab-Janowska,Raffaele Capasso

doi:10.1155/2020/6676247

Abstract

Objective The neurotrophin brain-derived neurotrophic factor (BDNF) affects poststroke functional outcome, neurogenesis, neuroprotection, and neuroplasticity. Its level is related to the diet and nutritional status, and more specifically, it is free fatty acids (FFAs) and eicosanoids that can have an impact on the BDNF level. The aim of this study was to analyze the potential impact of FFAs and eicosanoids on the BDNF level in stroke patients. Material and Methods. Seventy-three ischemic stroke patients were prospectively enrolled in the study. Laboratory tests were performed in all subjects, including the levels of FFAs, eicosanoids, and BDNF. FFAs and inflammatory metabolites were determined by gas chromatography and liquid chromatography, while BDNF was evaluated by the immune-enzymatic method (ELISA). Results The plasma level of BDNF negatively correlated with C22:1n9 13 erucic acid, C18:3n3 linolenic acid (ALA), and lipoxin A4 15-epi-LxA4. A direct association was observed in relation to BDNF and C16:1 palmitoleic acid and C20:3n6 eicosatrienoic acid (dihomo-gamma-linolenic acid (DGLA)). Conclusions Saturated fatty acids and omega-3 and omega-9 erucic acids can affect signaling in the BDNF synthesis resulting in the decrease in BDNF. There is a beneficial effect of DGLA on the BDNF level, while the effect of ALA on BDNF can be inhibitory. Specialized proresolving lipid mediators can play a role in the BDNF metabolism. BDNF can interact with inflammation as the risk factor in the cardiovascular disorders, including stroke.

Highlights

brain-derived neurotrophic factor (BDNF) is expressed in hippocampal neurons to a large extent, and it binds to the tropomyosin receptor kinase B (TrkB), regulates synaptic plasticity, and supports regulation of neuronal morphology and circuits involved in the processes of memory and learning
A negative association was detected between lipoxin A4 15-epi-LxA4 and BDNF level, which means that lipoxin level decreases with the increasing levels of BDNF
Changes in blood BDNF levels and signaling may be a potential common factor for the metabolic syndrome and atherosclerosis playing a role in the development of cardiovascular disorders

Summary

Introduction

The receptors of tropomyosin receptor kinase (Trk) mediate the impact of neurotrophins on signaling pathways This leads to the activation of survival, differentiation, and growth [2]. The memory and learning processes are connected with the modulation of the synaptic excitatory strength that can be regulated by neurotrophins. They regulate hippocampal long-term potentiation [1]. BDNF is expressed in hippocampal neurons to a large extent, and it binds to the tropomyosin receptor kinase B (TrkB), regulates synaptic plasticity, and supports regulation of neuronal morphology and circuits involved in the processes of memory and learning. BDNF promotes myelination, differentiation, and proliferation of oligodendroglia through the oligodendrocyte precursor cells (OPC) [5]

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Discussion

Conclusion