Effects of Docosahexaenoic Acid on Neurotransmission

Tanaka, Kazuhiro; Farooqui, Akhlaq A.; Siddiqi, Nikhat J.; Alhomida, Abdullah S.; Ong, Wei‐Yi

doi:10.4062/biomolther.2012.20.2.152

Cited by 76 publications

(48 citation statements)

References 64 publications

(78 reference statements)

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“…This supplement is mostly needed for the synaptic membranes which contain high levels of phospholipids [33]. Findings from animal and clinical studies support the role of ω-3 PUFA as essential nutrients for maintaining normal brain function [34].…”

Section: Discussionmentioning

confidence: 99%

Comparative study on the independent and combined effects of omega-3 and vitamin B12 on phospholipids and phospholipase A2 as phospholipid hydrolyzing enzymes in PPA-treated rats as a model for autistic traits

et al. 2018

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BackgroundAbnormal phospholipid metabolism is a major component of many neurodevelopmental disorders including autism. Oral administration of propionic acid (PPA) can produce behavioral abnormalities and biochemical features in rodents similar to those observed in autism and can thus be used as a model to understand impaired brain fatty acid metabolism in autism.MethodsThe present study was designed to understand alterations in phospholipid metabolism in the brain of a rodent model of autism and to explore omega-3 and vitamin B12 as remedies. Five groups of rats were selected: Group 1 was the control. Group 2 was the rodent model of autism treated with a neurotoxic dose of PPA. Group 3 was given vitamin B12 cobalamin (16.7 mg/kg/day) for 30 days after PPA treatment. Group 4 was given pharmaceutical grade Omega-3 (200 mg cholesterol free-DHA/kg body weight/day), a product of Madre lab, Germany, for 30 days after PPA treatment for 3 days. Group 5 was given a combined dose of ω-3 + Vitamin B12 for the same duration post-PPA treatment. Phospholipid levels and Phospholipase A2 were measured in the brain homogenates of all the groups. ELISA and western blotting were used to detect the cPLA2 protein level.ResultsA significant decrease in phospholipid levels and a significant increase in cPLA2 were found in brain tissue of PPA-treated rats; however, both ω-3 and vitamin B12 were efficient in ameliorating the neurotoxic effect of PPA.ConclusionBoth ω-3 and vitamin B12 may play a role in ameliorating impaired phospholipid metabolism in autism; however, proper clinical trials are needed.

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Section: Discussionmentioning

confidence: 99%

Comparative study on the independent and combined effects of omega-3 and vitamin B12 on phospholipids and phospholipase A2 as phospholipid hydrolyzing enzymes in PPA-treated rats as a model for autistic traits

et al. 2018

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“…The polyunsaturated fatty acids could play the pro-oxidant role in the oxidative tensions and encounter the lipid peroxidation of neuronal cells (37). It can also decrease the inflammatory factors, suppress neuronal apoptosis as well as enhance nitric oxide generation causing improvement in cerebrovascular endothelial function (3839).…”

Section: Discussionmentioning

confidence: 99%

Protective effect of vitamin C, vitamin B12 and omega-3 on lead-induced memory impairment in rat

et al. 2016

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Lead belongs to the heavy metal group and is considered as an environmental contaminant. Acute or chronic contact to lead can change the physiological function of human organs. One of the most important disorders following the lead exposure is neurotoxicity. Lead neurotoxicity consists of the neurobehavioral disturbances like cognitive impairment. The aim of the current study is to evaluate the possible protective effect of vitamin C (Vit C), vitamin B12 (Vit B12), omega 3 (ω-3), or their combination on the lead-induced memory disorder. Adult wistar rats were orally administered Vit C (120 mg/kg/day) or Vit B12 (1 mg/kg/day) or ω-3 (1000 mg/kg/day) or their combination for 3 weeks in groups of 7 animals each. Then lead acetate (15 mg/kg/day) was injected intraperitoneally for one week to all pretreated animals. The control group received normal saline as a vehicle while the positive control for cognitive impairment received just lead acetate. At the end of treatments animal memories were evaluated in Object Recognition Task. The results showed, although 15 mg/kg lead acetate significantly declines the memory-evaluating parameters, pretreatment with Vit C, Vit B12, ω-3, or their combination considerably inverted the lead induced reduction in discrimination (d2) index (P < 0.001) and recognition (R) index (P < 0.001, P < 0.05, P < 0.05, and P < 0.001, respectively). Our findings indicate while lead acetate impairs spatial memory in rat, administration of Vit C, Vit B12, ω-3, or their combination prior to the lead exposure inhibits the lead induced cognitive loss. There was no remarkable difference in this effect between the used supplements.

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“…26 Our data are in line with previous findings demonstrating that the expression of these markers as well as their related learning and memory functions is modulated by omega-3 fatty acids in the adult brain. 36,48,49 However, although decreases in BDNF and Arc-1 expression are commonly linked to the development of longterm cognitive and behavioral alterations 11,13,50,51 and their reduction in the prefrontal cortex are associated with depression, 50 the mechanism underlying brain DHA reductions and behavioral alterations are still a matter of debate. In addition, considering the substantial evidence regarding the importance of DHA during brain development and on resulting cognitive functions, further investigations are needed to assess a functional relationship between cognitive/behavioral alterations and DHA deficiency in Elovl2 −/− mice.…”

Section: Discussionmentioning

confidence: 99%

Impairment of DHA synthesis alters the expression of neuronal plasticity markers and the brain inflammatory status in mice

Talamonti

Sasso

et al. 2019

FASEB j.

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Docosahexaenoic acid (DHA) is a ω‐3 fatty acid typically obtained from the diet or endogenously synthesized through the action of elongases (ELOVLs) and desaturases. DHA is a key central nervous system constituent and the precursor of several molecules that regulate the resolution of inflammation. In the present study, we questioned whether the impaired synthesis of DHA affected neural plasticity and inflammatory status in the adult brain. To address this question, we investigated neural and inflammatory markers from mice deficient for ELOVL2 (Elovl2−/−), the key enzyme in DHA synthesis. From our findings, Elovl2−/− mice showed an altered expression of markers involved in synaptic plasticity, learning, and memory formation such as Egr‐1, Arc1, and BDNF specifically in the cerebral cortex, impacting behavioral functions only marginally. In parallel, we also found that DHA‐deficient mice were characterized by an increased expression of pro‐inflammatory molecules, namely TNF, IL‐1β, iNOS, caspase‐1 as well as the activation and morphologic changes of microglia in the absence of any brain injury or disease. Reintroducing DHA in the diet of Elovl2−/− mice reversed such alterations in brain plasticity and inflammation. Hence, impairment of systemic DHA synthesis can modify the brain inflammatory and neural plasticity status, supporting the view that DHA is an essential fatty acid with an important role in keeping inflammation within its physiologic boundary and in shaping neuronal functions in the central nervous system.

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Effects of Docosahexaenoic Acid on Neurotransmission

Cited by 76 publications

References 64 publications

Comparative study on the independent and combined effects of omega-3 and vitamin B12 on phospholipids and phospholipase A2 as phospholipid hydrolyzing enzymes in PPA-treated rats as a model for autistic traits

Comparative study on the independent and combined effects of omega-3 and vitamin B12 on phospholipids and phospholipase A2 as phospholipid hydrolyzing enzymes in PPA-treated rats as a model for autistic traits

Protective effect of vitamin C, vitamin B12 and omega-3 on lead-induced memory impairment in rat

Impairment of DHA synthesis alters the expression of neuronal plasticity markers and the brain inflammatory status in mice

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