Abstract
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.
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Key Points
The brain-derived neurotrophic factor (BDNF) can serve as a main regulator of plasticity in an activity-dependent manner in the central nervous system. Nerve growth factor (NGF), BDNF, neurotrophin-3 (NT-3), and neurotrophin-4/5 (NT-4/5) regulate the neuronal architecture and belong to the family of neurotrophins. 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. Clinical studies indicate the role of BDNF as a risk factor for stroke and a marker of the prognosis, mortality, and functional outcome in stroke.
The aim of the study was to evaluate the impact of FFAs and their inflammatory metabolites on the level of BDNF in stroke patients. This is the first study to have analyzed these potential associations. An reverse association between the omega-3 polyunsaturated fatty acid C18:3 linolenic acid and the BDNF level. Although the consumption of ALA by healthy individuals increases the level of BDNF, the association between the level of ALA and BDNF, especially in stroke patients, has been scantily documented. The reverse association between ALA and BDNF detected may reflect diverse metabolic processes in humans compared to animal models or may result from the affected metabolism of BDNF during stroke. 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. There is a pathogenetical association between BDNF and CVD. It can be additionally impacted by nutritional factors such as FFAs and their inflammatory metabolites. FFAs and eicosanoids can interfere with the BDNF level and the risk of CVD by modulating the BDNF metabolism and by affecting the neuroinflammatory status. Our understanding of the role of FFAs and their inflammatory metabolites in BDNF metabolism can add to the search for novel therapies in cardiovascular disorders such as stroke.