The influence of orally administered docosahexaenoic acid on cognitive ability in aged mice

Jiang, Lufang; Shi, Yan; Wang, Lisheng; Yang, Zhipeng

doi:10.1016/j.jnutbio.2008.07.003

Cited by 69 publications

(44 citation statements)

References 48 publications

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“…Alongside the increase in peripheral inflammation, BD has been associated with a decrease in brain-derived neurotrophic factor (BDNF) levels (20, 21). Neurotrophins, such as BDNF, are a group of secreted proteins that are essential for neuron survival and synaptic functioning (22–25). …”

Section: Introductionmentioning

confidence: 99%

Inflammatory mediators of cognitive impairment in bipolar disorder

Bauer

Pascoe

Wollenhaupt-Aguiar

et al. 2014

Journal of Psychiatric Research

106

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Objectives Recent studies have pointed to neuroinflammation, oxidative stress and neurotrophic factors as key mediators in the pathophysiology of mood disorders. Little is however known about the cascade of biological episodes underlying the cognitive deficits observed during the acute and euthymic phases of bipolar disorder (BD). The aim of this review is to assess the potential association between cognitive impairment and biomarkers of inflammation, oxidative stress and neurotrophic activity in BD. Methods Scopus (all databases), Pubmed and Ovid Medline were systematically searched with no language or year restrictions, up to November 2013, for human studies that collected both inflammatory markers and cognitive data in BD. Selected search terms were bipolar disorder, depression, mania, psychosis, inflammatory, cognitive and neurotrophic. Results Ten human studies satisfied the criteria for consideration. The findings showed that high levels of peripheral inflammatory-cytokine, oxidative stress and reduced brain derived neurotrophic factor (BDNF) levels were associated with poor cognitive performance. The BDNF val66met polymorphism is a potential vulnerability factor for cognitive impairment in BD. Conclusions Current data provide preliminary evidence of a link between the cognitive decline observed in BD and mechanisms of neuroinflammation and neuroprotection. The identification of BD specific inflammatory markers and polymorphisms in inflammatory response genes may be of assistance for therapeutic intervention.

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Section: Introductionmentioning

confidence: 99%

Inflammatory mediators of cognitive impairment in bipolar disorder

Bauer

Pascoe

Wollenhaupt-Aguiar

et al. 2014

Journal of Psychiatric Research

106

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“…Beside its positive effect on cognition in human subjects, several investigations listed below in Table 1 focused on studying the effects of DHA administration in old rodents, its distribution in brain regions, its outcomes and effects on cognition. Such studies support the fact that DHA supplemented diet, as observed in humans, could improve the cognitive dysfunction due to aging [56][57][58][59][60][61][62]. In the study of Pan and colleagues, DHA (150 or 300 mg/kg/d) was also found to significantly improve learning and memory in young rats while a higher dose of DHA (600 mg/kg) increased the risk of memory impairment [63].…”

Section: Effect Of Dha In Normal Agingmentioning

confidence: 53%

“…Another example of potent neuroprotective activity comes from the observation that DHA is able to regulate neurotrophic factors like BDNF via a p38 MAPK-dependent mechanism leading to its potential therapeutic efficacy for neuronal survival [57,170]. Similarly, oral administration of DHA activates the GDNF-MAPK-CERB pathway in hippocampus of natural aged rat [58]. …”

Section: Anti-apoptotic Effects In the Brainmentioning

confidence: 99%

The pleiotropic effects of omega-3 docosahexaenoic acid on the hallmarks of Alzheimer's disease

Belkouch¹,

Hachem²,

Elgot³

et al. 2016

The Journal of Nutritional Biochemistry

105

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“…Some further investigations will be necessary to elucidate whether the increase in DHA was a common response to a neuronal stress, itself coming from either the odd-chain fatty acids and the cholesterol metabolism or the neurotransmitter disorders. The diet has been reported to modulate the brain PUFA level and consequently biogenic amine metabolism (Lavialle et al 2008;Jiang et al 2009). The high level of EPA and DHA in red blood cells is associated with a slowed hippocampal and overall brain atrophy in humans (Pottala et al 2014).…”

Section: Discussionmentioning

confidence: 99%

Combined Sepiapterin Reductase and Methylmalonyl-CoA Epimerase Deficiency in a Second Patient: Cerebrospinal Fluid Polyunsaturated Fatty Acid Level and Follow-Up Under l-DOPA, 5-HTP and BH4 Trials

et al. 2015

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Objective/context: We describe the second patient presenting the combination of two homoallelic homozygous nonsense mutations in two genes distant from 1.8 Mb in the chromosome 2p13-3, the methylmalonyl-CoA epimerase gene (MCEE) and the sepiapterin reductase gene (SPR).Case report: The patient was born from consanguineous parents. He has presented a moderate but constant methylmalonic acid (MMA) excretion in urine associated with a mental retardation. The first homozygous mutation was identified in the MCEE gene (c.139C>T; p.Arg47*). Progressive dystonia and cataplexy narcolepsy led to diagnose the second homozygous mutation in the SPR gene: c.751A>T; p.Lys251*. Sepiapterin reductase deficiency (SRD) was characterized by a defect in tetrahydrobiopterin (BH4), the cofactor of several hydroxylases needed for the synthesis of neurotransmitters. A treatment with L-DOPA/carbidopa and 5-HTP dramatically improved the dystonic posture, the mood and the hypersomnia, proving that the pathogenesis was due to SRD. A supplementation with BH4 did not induce additional clinical benefit, although HVA and HIAA increased in CSF. The polyunsaturated fatty acids were measured in CSF as the markers of the neuronal stress. We have shown that DHA and its precursor EPA were high before and during the time course of the different treatments.In conclusion: The patient has inherited two copies of the two mutations from his consanguineous parents in the MCEE and SPR genes in the chromosome 2p13-3. DHA and EPA increased in CSF as a response to the neuronal stress induced by the defect in neurotransmitters or the altered metabolism of the odd-chain fatty acids and cholesterol.

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The influence of orally administered docosahexaenoic acid on cognitive ability in aged mice

Cited by 69 publications

References 48 publications

Inflammatory mediators of cognitive impairment in bipolar disorder

Inflammatory mediators of cognitive impairment in bipolar disorder

The pleiotropic effects of omega-3 docosahexaenoic acid on the hallmarks of Alzheimer's disease

Combined Sepiapterin Reductase and Methylmalonyl-CoA Epimerase Deficiency in a Second Patient: Cerebrospinal Fluid Polyunsaturated Fatty Acid Level and Follow-Up Under l-DOPA, 5-HTP and BH4 Trials

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