287 articles - 08.09.10
1: Am J Clin Nutr. 2010 Aug;92(2):416-21. Epub 2010 Jun 9.
Gopinath B, Flood VM, Rochtchina E, McMahon CM, Mitchell P.
Centre for Vision Research, Department of Ophthalmology, and Westmead Millennium Institute, University of Sydney, Sydney, Australia.
BACKGROUND: Identification of modifiable risk factors that could prevent or slow the development of age-related hearing loss (presbycusis) would be valuable. Dietary polyunsaturated fatty acid (PUFA) intake may be related to age-related hearing loss. OBJECTIVE: We aimed to determine the association between dietary intakes of omega-3 (n-3) PUFAs and fish and the risk of presbycusis. DESIGN: The Blue Mountains Hearing Study is a population-based survey of age-related hearing loss (1997-1999 to 2002-2004). We collected dietary data by using a semiquantitative food-frequency questionnaire and calculated PUFA and fish intakes. In 2956 participants (aged > or =50 y), we measured presbycusis, which we defined as the pure-tone average of frequencies 0.5, 1.0, 2.0, and 4.0 kHz >25 decibels of hearing loss. RESULTS: There was an inverse association between total n-3 PUFA intake and prevalent hearing loss [odds ratio (OR) per SD increase in energy-adjusted n-3 PUFAs: 0.89; 95% CI: 0.81, 0.99]. There was an inverse association between long-chain n-3 PUFAs and incident hearing loss (OR per SD increase in long-chain n-3 PUFAs: 0.76; 95% CI: 0.60, 0.97). Participants who had > or =2 servings of fish/wk compared with participants who had <1 serving of fish/wk had a significantly reduced risk (42%) of developing presbycusis at follow-up (multivariate-adjusted OR: 0.58; 95% CI: 0.35, 0.95). There was an association between consumption of > or =1 to <2 servings/wk of fish and a reduced risk of a progression of hearing loss (OR: 0.53; 95% CI: 0.32, 0.88). CONCLUSIONS: There was an inverse association between higher intakes of long-chain n-3 PUFAs and regular weekly consumption of fish and hearing loss. Dietary intervention with n-3 PUFAs could prevent or delay the development of age-related hearing loss.
Publication Types: Research Support, Non-U.S. Gov't
Links http://www.ncbi.nlm.nih.gov/entrez/queryd.fcgi?cmd=Retrieve&db=PubMed&list_uids=20534742&dopt=ExternalLink
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PMID: 20534742 [PubMed - indexed for MEDLINE]2: J Nutr Health Aging. 2010;14(5):347-51.
Dullemeijer C, Verhoef P, Brouwer IA, Kok FJ, Brummer RJ, Durga J.
Division of Human Nutrition, Wageningen University, P.O. Box 8129, 6700 EV Wageningen, the Netherlands. Carla.Dullemeijer@wur.nl
OBJECTIVES: Age-related hearing loss is a common social and health problem in the older adult population. Up until now, very little scientific attention has been given to the potential role of fatty acids in age-related hearing loss. In this study we investigated whether plasma very long-chain n-3 polyunsaturated fatty acids (PUFAs) are associated with age-related hearing loss over three years. DESIGN: Cross-sectional and 3-year longitudinal analyses. SETTING: Wageningen, the Netherlands. PARTICIPANTS: 720 men and postmenopausal women (50-70 years of age) without middle ear dysfunction or unilateral hearing loss. MEASUREMENTS: Fatty acid proportions were measured in plasma cholesteryl esters. Hearing thresholds (in decibels, dB) at baseline and after three years were measured with pure-tone audiometry. Hearing loss was calculated as the increase in mean hearing thresholds in the low (0.5-kHz, 1-kHz, and 2-kHz) and high (4-kHz, 6-kHz, and 8-kHz) frequencies over three years. RESULTS: Subjects in the highest quartile of plasma very long-chain n-3 PUFA had less hearing loss in the low frequencies over three years than subjects in the lowest quartile (p < 0.01, ANCOVA, difference in mean adjusted hearing thresholds= -1.2 dB). There were no significant differences between the quartiles of plasma very long-chain n-3 PUFA in hearing loss in the high frequencies (p=0.49, ANCOVA). These associations are adjusted for baseline mean hearing thresholds, age, sex, level of education and alcohol consumption. CONCLUSION: This study is the first to show an inverse association between plasma very long-chain n-3 PUFAs and age-related hearing loss. These results are encouraging, but require confirmation from future studies.
Publication Types: Research Support, Non-U.S. Gov't
Links http://www.ncbi.nlm.nih.gov/entrez/queryd.fcgi?cmd=Retrieve&db=PubMed&list_uids=20424800&dopt=ExternalLink
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PMID: 20424800 [PubMed - indexed for MEDLINE]3: Clin Interv Aging. 2010 Apr 7;5:45-61.
Jicha GA, Markesbery WR.
University of Kentucky, Alzheimer's Disease Center and the Sanders-Brown Center on Aging University of Kentucky College of Medicine, Lexington, KY 40536-0230, USA. gajich2@email.uky.edu
Omega-3 fatty acids are essential for brain growth and development. They play an important role throughout life, as critical modulators of neuronal function and regulation of oxidative stress mechanisms, in brain health and disease. Docosahexanoic acid (DHA), the major omega-3 fatty acid found in neurons, has taken on a central role as a target for therapeutic intervention in Alzheimer's disease (AD). A plethora of in vitro, animal model, and human data, gathered over the past decade, highlight the important role DHA may play in the development of a variety of neurological and psychiatric disorders, including AD. Cross sectional and prospective cohort data have demonstrated that reduced dietary intake or low brain levels of DHA are associated with accelerated cognitive decline or the development of incipient dementia, including AD. Several clinical trials investigating the effects of omega-3 fatty acid supplementation in AD have been completed and all failed to demonstrate its efficacy in the treatment of AD. However, these trials produced intriguing data suggesting that the beneficial effects of omega-3 fatty acid supplementation may depend on the stage of disease, other dietary mediators, and apolipoprotein E status.
Publication Types: Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't Review
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PMID: 20396634 [PubMed - indexed for MEDLINE]4: Nat Med. 2010 May;16(5):592-7, 1p following 597. Epub 2010 Apr 11.
Xu ZZ, Zhang L, Liu T, Park JY, Berta T, Yang R, Serhan CN, Ji RR.
Department of Anesthesiology, Sensory Plasticity Laboratory, Pain Research Center, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, USA.
Inflammatory pain, such as arthritis pain, is a growing health problem. Inflammatory pain is generally treated with opioids and cyclooxygenase (COX) inhibitors, but both are limited by side effects. Recently, resolvins, a unique family of lipid mediators, including RvE1 and RvD1 derived from omega-3 polyunsaturated fatty acid, have shown marked potency in treating disease conditions associated with inflammation. Here we report that peripheral (intraplantar) or spinal (intrathecal) administration of RvE1 or RvD1 in mice potently reduces inflammatory pain behaviors induced by intraplantar injection of formalin, carrageenan or complete Freund's adjuvant (CFA), without affecting basal pain perception. Intrathecal RvE1 injection also inhibits spontaneous pain and heat and mechanical hypersensitivity evoked by intrathecal capsaicin and tumor necrosis factor-alpha (TNF-alpha). RvE1 has anti-inflammatory activity by reducing neutrophil infiltration, paw edema and proinflammatory cytokine expression. RvE1 also abolishes transient receptor potential vanilloid subtype-1 (TRPV1)- and TNF-alpha-induced excitatory postsynaptic current increases and TNF-alpha-evoked N-methyl-D-aspartic acid (NMDA) receptor hyperactivity in spinal dorsal horn neurons via inhibition of the extracellular signal-regulated kinase (ERK) signaling pathway. Thus, we show a previously unknown role for resolvins in normalizing the spinal synaptic plasticity that has been implicated in generating pain hypersensitivity. Given the potency of resolvins and the well-known side effects of opioids and COX inhibitors, resolvins may represent new analgesics for treating inflammatory pain.
Publication Types: Research Support, N.I.H., Extramural
Links http://www.ncbi.nlm.nih.gov/entrez/queryd.fcgi?cmd=Retrieve&db=PubMed&list_uids=20383154&dopt=ExternalLink
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PMID: 20383154 [PubMed - indexed for MEDLINE]5: Am J Obstet Gynecol. 2010 May;202(5):469.e1-6. Epub 2010 Mar 31.
Berman DR, Liu YQ, Barks J, Mozurkewich E.
Division of Maternal-Fetal Medicine, Department of Obstetrics and Gynecology, University of Michigan Medical School, Ann Arbor, MI.
OBJECTIVE: Lipopolysaccharide pretreatment potentiates hypoxic ischemic injury. We hypothesized that docosahexaenoic acid pretreatment would improve function and reduce brain volume loss in this rat model of perinatal brain injury and inflammation. STUDY DESIGN: Seven-day-old rats were divided into 3 groups: intraperitoneal docosahexaenoic acid 1 mg/kg and lipopolysaccharide 0.1 mg/kg, 25% albumin and lipopolysaccharide, and normal saline. Injections were given 2.5 hours before carotid ligation, followed by 90 minutes 8% O2. Rats underwent sensorimotor function testing and brain volume loss assessment on postnatal day 14. RESULTS: Docosahexaenoic acid pretreatment improved vibrissae forepaw placing scores compared with albumin/lipopolysaccharide (mean+/-standard deviation weighted score/20: 17.72+/-0.92 docosahexaenoic acid/lipopolysaccharide vs 13.83+/-0.82 albumin/lipopolysaccharide; P<.007). Albumin/lipopolysaccharide rats scores were worse than those of the normal saline/normal saline rats (13.83+/-0.82 vs 17.21+/-0.71; P=.076). No significant differences in brain volume loss were observed among groups. CONCLUSION: Lipopolysaccharide inflammatory stimulation in conjunction with hypoxic ischemic resulted in poorer function than hypoxic ischemic alone. Docosahexaenoic acid pretreatment had significantly improved function in neonatal rats exposed to lipopolysaccharide and hypoxic ischemic. Copyright (c) 2010 Mosby, Inc. All rights reserved.
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PMID: 20356570 [PubMed - indexed for MEDLINE]6: J Inherit Metab Dis. 2010 Apr;33(2):121-7. Epub 2010 Mar 9.
Mazer LM, Yi SH, Singh RH.
Emory University School of Medicine, Atlanta, GA, USA.
Individuals with maple syrup urine disease (MSUD) have impaired metabolism of branched-chain amino acids (BCAA) valine, isoleucine, and leucine. Life-long dietary therapy is recommended to restrict BCAA intake and thus prevent poor neurological outcomes and death. To maintain adequate nutritional status, the majority of protein and nutrients are derived from synthetic BCAA-free medical foods with variable fatty acid content. Given the restrictive diet and the importance of omega-3 fatty acids, particularly docosahexaenoic acid (DHA), in neurological development, this study evaluated the dietary and fatty acid status of females of reproductive age with MSUD attending a metabolic camp. Healthy controls of similar age and sex were selected from existing normal laboratory data. Total lipid fatty acid concentration in plasma and erythrocytes was analyzed using gas chromatography-mass spectroscopy. Participants with MSUD had normal to increased concentrations of plasma and erythrocyte alpha linolenic acid (ALA) but significantly lower concentrations of plasma and erythrocyte docosahexaenoic acid (DHA) as percent of total lipid fatty acids compared with controls (plasma DHA: MSUD 1.03 +/- 0.35, controls 2.87 +/- 1.08; P = 0.001; erythrocyte DHA: MSUD 2.58 +/- 0.58, controls 3.66 +/- 0.80; P = 0.011). Dietary records reflected negligible or no DHA intake over the 3-day period prior to the blood draw (range 0-2 mg). These results suggest females of reproductive age with MSUD have lower blood DHA concentrations than age-matched controls. In addition, the presence of ALA in medical foods and the background diet may not counter the lack of preformed DHA in the diet. The implications of these results warrant further investigation.
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PMID: 20217236 [PubMed - indexed for MEDLINE]7: Biochim Biophys Acta. 2010 Aug;1801(8):791-8. Epub 2010 Mar 6.
Oster T, Pillot T.
Laboratoire Lipidomix (EA 4422), PRES de l'Universite de Lorraine, ENSAIA - INPL, 54505 Vandoeuvre-les-Nancy, France. thierry.oster@ensaia.inpl-nancy.fr
Alzheimer's disease (AD) is a major public health concern due to longer life expectancy in the Western countries. Amyloid-beta (Abeta) oligomers are considered the proximate effectors in the early stages of AD. AD-related cognitive impairment, synaptic loss and neurodegeneration result from interactions of Abeta oligomers with the synaptic membrane and subsequent activation of pro-apoptotic signalling pathways. Therefore, membrane structure and lipid status appear determinant in Abeta-induced toxicity. Numerous epidemiological studies have highlighted the beneficial influence of docosahexaenoic acid (DHA, C22:6 n-3) on the preservation of synaptic function and memory capacities in aged individuals or upon Abeta exposure, whereas its deficiency is presented as a risk factor for AD. An elevated number of studies have been reporting the beneficial effects of dietary DHA supplementation on cognition and synaptic integrity in various AD models. In this review, we describe the important potential of DHA to preserve neuronal and brain functions and classified its numerous molecular and cellular effects from impact on membrane lipid content and organisation to activation of signalling pathways sustaining synaptic function and neuronal survival. DHA appears as one of the most valuable diet ingredients whose neuroprotective properties could be crucial for designing nutrition-based strategies able to prevent AD as well as other lipid- and age-related diseases whose prevalence is progressing in elderly populations. Copyright 2010 Elsevier B.V. All rights reserved.
Publication Types: Review
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PMID: 20211757 [PubMed - indexed for MEDLINE]8: J Nutr. 2010 Apr;140(4):869-74. Epub 2010 Feb 24.
Cole GM, Frautschy SA.
Departments of Medicine and Neurology, University of California, Los Angeles, CA 90095, USA. gmcole@ucla.edu
The risk for dementia, a major contributor to incapacitation and institutionalization, rises rapidly as we age, doubling every 5 y after age 65. Tens of millions of new Alzheimer's disease (AD) and other dementia cases are projected as elderly populations increase around the world, creating a projected dementia epidemic for which most nations are not prepared. Thus, there is an urgent need for prevention approaches that are safe, effective, and affordable. This review addresses the potential of one promising candidate, the (n-3) fatty acid docosahexaenoic acid (DHA), which appears to slow pathogenesis of AD and possibly vascular dementia. DHA is pleiotropic, acting at multiple steps to reduce the production of the beta-amyloid peptide, widely believed to initiate AD. DHA moderates some of the kinases that hyperphosphorylate the tau-protein, a component of the neurofibrillary tangle. DHA may help suppress insulin/neurotrophic factor signaling deficits, neuroinflammation, and oxidative damage that contribute to synaptic loss and neuronal dysfunction in dementia. Finally, DHA increases brain levels of neuroprotective brain-derived neurotrophic factor and reduces the (n-6) fatty acid arachidonate and its prostaglandin metabolites that have been implicated in promoting AD. Clinical trials suggest that DHA or fish oil alone can slow early stages of progression, but these effects may be apolipoprotein E genotype specific, and larger trials with very early stages are required to prove efficacy. We advocate early intervention in a prodromal period with nutrigenomically defined subjects with an appropriately designed nutritional supplement, including DHA and antioxidants.
Publication Types: Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, Non-P.H.S. Review
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PMID: 20181786 [PubMed - indexed for MEDLINE]9: Epilepsy Behav. 2010 Mar;17(3):336-43. Epub 2010 Feb 13.
Taha AY, Jeffrey MA, Taha NM, Bala S, Burnham WM.
Department of Pharmacology and Toxicology, Faculty of Medicine, University of Toronto, Toronto, Ontario, Canada. a.taha@utoronto.ca
OBJECTIVE: Docosahexaenoic acid (DHA), an omega-3 fatty acid, has been reported to raise seizure thresholds. The purpose of the present study was to test the acute anticonvulsant effects of unesterified DHA in rats, using the maximal pentylenetetrazol (PTZ) seizure model, and also to examine DHA incorporation and distribution into blood serum total lipids and brain phospholipids and unesterified fatty acids. Sedation was measured to monitor for the potential toxicity of DHA. METHODS: Male Wistar rats received subcutaneous injections of saline, oleic acid (OA), or DHA. An initial pilot study (Experiment 1) established 400mg/kg as an effective dose of DHA in the maximal PTZ seizure test. A subsequent time-response study, using 400mg/kg (Experiment 2), established 1 hour as an effective postinjection interval for administering DHA subcutaneously. A final study (Experiment 3) comprised two different groups. The first group ("seizure-tested rats") received saline, OA, or DHA (400mg/kg) subcutaneously, and were seizure tested in the maximal PTZ test 1 hour later to confirm the seizure latency measurements at that time. The second group ("assay rats") received identical subcutaneous injections of saline, OA, or DHA (400mg/kg). One hour postinjection, however, they were sacrificed for assay rather than being seizure tested. Assays involved the analysis of serum and brain DHA. Sedation was measured in both Experiment 3 groups during the 1-hour period prior to seizure testing or sacrifice. RESULTS: As noted above, 400mg/kg proved to be an effective subcutaneous dose of DHA (Experiment 1), and 1 hour proved to be the most effective injection-test interval (Experiment 2). In Experiment 3, in the seizure-tested animals, subcutaneous administration of 400mg/kg of DHA significantly increased latency to PTZ seizure onset 1 hour postinjection relative to the saline- and OA-injected controls, which did not differ significantly from each other (P>0.05). In the assay animals, no significant effects of treatment on blood serum total lipids or on brain phospholipid or unesterified fatty acid profiles (P>0.05) were observed. There were also no differences in sedation among the three groups (P>0.05). CONCLUSION: DHA increases resistance to PTZ-induced seizures without altering measures of sedation and, apparently, without changing DHA concentrations in serum or brain. (c) 2010 Elsevier Inc. All rights reserved.
Publication Types: Research Support, Non-U.S. Gov't
Links http://www.ncbi.nlm.nih.gov/entrez/queryd.fcgi?cmd=Retrieve&db=PubMed&list_uids=20153982&dopt=ExternalLink
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PMID: 20153982 [PubMed - indexed for MEDLINE]10: Clin J Pain. 2010 Feb;26(2):168-72.
Ko GD, Nowacki NB, Arseneau L, Eitel M, Hum A.
Canadian Centre for Integrative Medicine and the Physiatry Interventional Pain Clinic, Sunnybrook Health Sciences Centre, University of Toronto, Toronto, Ontario L3P1X2, Canada. drgordko@rogers.com
OBJECTIVE: The aim of this case series study was to investigate and report on patients with neuropathic pain who responded to treatment with omega-3 fatty acids. METHODS: Methods: Five patients with different underlying diagnoses including cervical radiculopathy, thoracic outlet syndrome, fibromyalgia, carpal tunnel syndrome, burn injury were treated with high oral doses of omega 3 fish oil (varying from 2400-7200 mg/day of EPA-DHA). Outcome measures were obtained pretreatment and posttreatment. These included validated surveys (short-form McGill Pain questionnaire, DN4 neuropathic pain scale, Pain Detect Questionnaire), objective clinical tools (Jamar grip strength, Lafayette dynamometry, tender point algometry) and EMG Nerve Conduction studies. RESULTS: These patients had clinically significant pain reduction, improved function as documented with both subjective and objective outcome measures up to as much as 19 months after treatment initiation. No serious adverse effects were reported. CONCLUSIONS: This first-ever reported case series suggests that omega-3 fatty acids may be of benefit in the management of patients with neuropathic pain. Further investigations with randomized controlled trials in a more specific neuropathic pain population would be warranted.
Links http://www.ncbi.nlm.nih.gov/entrez/queryd.fcgi?cmd=Retrieve&db=PubMed&list_uids=20090445&dopt=ExternalLink
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PMID: 20090445 [PubMed - indexed for MEDLINE]11: Curr Alzheimer Res. 2010 May 1;7(3):190-6.
Yurko-Mauro K.
Clinical Research, Martek Biosciences Corporation, Columbia, MD 21045, USA. kyurko@martek.com
Memory loss is a prominent health concern, second only to heart disease for older individuals. Docosahexaenoic acid (DHA), the principle omega-3 fatty acid in brain and heart, plays an important role in neural and cardiac function. Decreases in plasma DHA are associated with cognitive decline in healthy elderly and Alzheimer's patients. Higher DHA intake and plasma levels are inversely correlated with increased relative risk of Alzheimer's disease (AD) and fatal coronary heart disease. DHA provides well known cardiovascular benefits (e.g. lower triglycerides, increased HDL cholesterol, decreased resting heart rate) in older adults. Preclinically, DHA supplementation restores brain DHA levels, enhances learning and memory tasks in aged animals, and significantly reduces beta amyloid, plaques, and tau in transgenic AD models. To date, clinical studies with DHA+EPA supplementation have shown some positive effects in mild cognitive impairment but not in AD, suggesting that early intervention may be a key factor to providing effective therapies. A recent clinical study examined individual effects of 900mg/d algal DHA as a nutritional supplement for age-related cognitive decline (ARCD). This randomized, double blind, placebo controlled study (n=485) found significantly fewer CANTAB Paired Associate Learning errors with algal DHA at six months versus placebo (diff. score -1.63+/-0.76, p=0.03). Positive effects on Verbal Recognition Memory (p<0.02) and significant decreases in resting heart rate with DHA (p<0.03) were observed, indicating improved learning and episodic memory functions and cardiovascular benefits for ARCD. Collectively, data reveal a potentially beneficial role for DHA in preventing or ameliorating cognitive decline and cardiovascular disease in the aged.
Publication Types: Review
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PMID: 20088810 [PubMed - indexed for MEDLINE]12: Curr Pharm Des. 2009;15(36):4173-85.
Carrie I, Abellan Van Kan G, Rolland Y, Gillette-Guyonnet S, Vellas B.
Gerontopole, CHU Toulouse, Department of Geriatric Medicine, Toulouse, France. carrie.i@chu-toulouse.fr
Polyunsaturated fatty acids (PUFA) play a crucial role in cerebral structure and function. Omega-3 PUFA is an exciting area of research, with docosahexaenoic acid (DHA) emerging as a new potential agent for prevention of cognitive decline and treatment of Alzheimer's disease. Preclinical studies suggest that DHA maintains membrane fluidity, improves synaptic and neurotransmitter functioning, enhances learning and memory performances and displays neuroprotective properties. Several epidemiological studies supported the association between Omega-3 PUFA consumption and a lower prevalence of dementia. Although data are divergent, a growing body of evidence supports the view that regular consumption of dietary fish and seafood (which are rich in omega-3 PUFA) prevents cognitive decline. Finally, at present, few data are available from randomized clinical trials (RCTs). on the association between cognition and Omega-3. Ongoing RCTs that assess the effect of Omega-3 might provide new evidence on prevention and treatment of dementia. In this review, we summarize preclinical and clinical research suggesting that DHA exerts beneficial effects on cognitive function with ageing.
Publication Types: Review
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PMID: 20041819 [PubMed - indexed for MEDLINE]13: Neuroscience. 2010 Mar 10;166(1):271-8. Epub 2009 Dec 28.
Arnal E, Miranda M, Barcia J, Bosch-Morell F, Romero FJ.
Fundacion Oftalmologica del Mediterraneo, Valencia, Spain.
The mechanisms underlying diabetic encephalopathy, are largely unknown. Here, we examined whether docosahexaenoic acid (DHA) and lutein could attenuate the oxidative changes of the diabetic cerebral cortex. The levels of malondialdehyde (MDA) were significantly increased and glutathione (GSH) and glutathione peroxidase activity (GPx) were decreased in diabetic rats. The number of 4-hydroxynonenal (4-HNE) positive cells was increased. Treatment with insulin, lutein or DHA and the combination of each antioxidant with insulin, significantly restored all markers concentrations mentioned above, and the increase in 4-HNE inmunofluorescence. We combined 4-HNE immunofluorescence with NeuN (Neuronal Nuclei) staining. The latter demonstrated extensive overlap with the 4-HNE staining in the cortex from diabetic rats. Our findings demonstrate a clear participation of glucose-induced oxidative stress in the diabetic encephalopathy, and that the cells suffering oxidative stress are neurons. Lowering oxidative stress through the administration of different antioxidants may be beneficial for the central nervous tissue in diabetes. Copyright 2010 IBRO. Published by Elsevier Ltd. All rights reserved.
Publication Types: Research Support, Non-U.S. Gov't
Links http://www.ncbi.nlm.nih.gov/entrez/queryd.fcgi?cmd=Retrieve&db=PubMed&list_uids=20036322&dopt=ExternalLink
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PMID: 20036322 [PubMed - indexed for MEDLINE]14: Neurochem Int. 2010 Feb;56(3):501-7. Epub 2009 Dec 22.
Rosenberger TA, Villacreses NE, Weis MT, Rapoport SI.
Department of Pharmacology, Physiology and Therapeutics, University of North Dakota School of Medicine and Health Sciences, Grand Forks, ND 58203, USA. trosenberger@medicine.nodak.edu
In a rat model of neuroinflammation, produced by a 6-day intracerebral ventricular infusion of bacterial lipopolysaccharide (LPS), we reported that the brain concentrations of non-esterified brain arachidonic acid (AA, 20:4 n-6) and its eicosanoid products PGE(2) and PGD(2) were increased, as were AA turnover rates in certain brain phospholipids and the activity of AA-selective cytosolic phospholipase A(2) (cPLA(2)). The activity of Ca(2+)-independent iPLA(2), which is thought to be selective for the release of docosahexaenoic acid (DHA, 22:6 n-3) from membrane phospholipid, was unchanged. In the present study, we measured parameters of brain DHA metabolism in comparable artificial cerebrospinal fluid (control) and LPS-infused rats. In contrast to the reported changes in markers of AA metabolism, the brain non-esterified DHA concentration and DHA turnover rates in individual phospholipids were not significantly altered by LPS infusion. The formation rates of AA-CoA and DHA-CoA in a microsomal brain fraction were also unaltered by the LPS infusion. These observations indicate that LPS-treatment upregulates markers of brain AA but not DHA metabolism. All of which are consistent with other evidence that suggest different sets of enzymes regulate AA and DHA recycling within brain phospholipids and that only selective increases in brain AA metabolism occur following a 6-day LPS infusion. Published by Elsevier Ltd.
Publication Types: Research Support, N.I.H., Intramural
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PMID: 20026368 [PubMed - indexed for MEDLINE]15: Curr Opin Clin Nutr Metab Care. 2010 Mar;13(2):150-5.
Cederholm T, Palmblad J.
Clinical Nutrition and Metabolism, Department of Public Health and Caring Sciences, Uppsala University, Uppsala, Sweden. tommy.cederholm@pubcare.uu.se
PURPOSE OF REVIEW: To report recent data on the potential role of omega-3 fatty acids (n-3 FA) found in oily fish, especially docosahexaenoic acid (DHA), to prevent and treat cognitive decline and Alzheimer's disease. RECENT FINDINGS: Observational studies still provide conflicting results, in which the majority indicate beneficial effects on cognition, both when assessed as a continuous variable or as incident dementia, mainly Alzheimer's disease. Experimental studies have demonstrated potentially ameliorating effects of eicosapentaenoic acid (EPA) and DHA on amyloid fragment formation, signal transduction including upregulation of the apolipoprotein receptor SorLA, as well as on angiogenesis. The role of EPA and DHA metabolites on Alzheimer's disease pathology is under investigation. Recently, three randomized intervention studies, with duration up to 6 months have been reported. In contrast to a small study from Taiwan, no positive overall effects were reported from the Swedish OmegAD Study or from a Dutch study, although post hoc analyses indicate that selected individuals with mild forms of Alzheimer's disease or cognitive decline may respond to treatment. SUMMARY: No firm conclusions can be drawn. Based on epidemiological data, fish including oily fish could be advised as part of a balanced diet for public health purpose, although the evidence for better cognition is only fairly consistent. It is unlikely that n-3 FA will emerge as a treatment option in general for improving cognitive function in patients with Alzheimer's disease. n-3 FA, especially DHA, may turn out as an adjuvant therapy in selected cases. Further long-term intervention studies on individuals with mild cognitive reductions are awaited.
Publication Types: Research Support, Non-U.S. Gov't Review
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PMID: 20019606 [PubMed - indexed for MEDLINE]16: Histol Histopathol. 2010 Feb;25(2):141-51.
Cayli S, Sati L, Seval-Celik Y, Tuncer MA, Yaymaci B, Berkman Z, Altug T, Demir R.
Department of Histology and Embryology, Faculty of Medicine, Akdeniz University, Antalya, Turkey.
The preventive and therapeutic effects of eicosapentaenoic acid (EPA) on diet-induced hyperlipidemia in rabbits have been investigated. Eighteen New Zealand rabbits were randomly divided into three groups of 6 subjects each; experimental group-I (EG-I) was administered a cholesterol rich diet, experimental group-II (EG-II) was treated with EPA (300 mg/kg/d) following a cholesterol-rich diet and the control group (CG) had a standard diet. Blood samples were collected at day 0 and at the 4th and 12th weeks of EG-II to obtain serum levels of total cholesterol (TC), high density lipid-cholesterol (HDL-C), low density lipid-cholesterol (LDL-C) and triglyceride (TG). From each group tissue samples were collected from the carotid artery for immunohistochemistry and electron microscopy. Our results showed that EPA could significantly lower (p<0.001) serum TC, LDL-C, HDL-C and TG levels with a reduction of 35%; 55%; 44% and 51%, respectively. Scanning and transmission electron microscopy results revealed that endothelial damage was more prominent in EG-I when compared to EG-II. The ruptured endothelial lining and damaged cellular surface was increased in EG-I when compared to EG-II. Ultrastructural observations showed that after EPA treatment, the degeneration and cellular surface damage on the endothelium were also decreased. These biochemical and ultrastructural results suggest that EPA is a potential drug which significantly lowers the serum lipid profile and partially repairs endothelial dysfunction due to hyperlipidemia.
Publication Types: Research Support, Non-U.S. Gov't
Links http://www.ncbi.nlm.nih.gov/entrez/queryd.fcgi?cmd=Retrieve&db=PubMed&list_uids=20017101&dopt=ExternalLink
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PMID: 20017101 [PubMed - indexed for MEDLINE]17: Epilepsy Behav. 2010 Jan;17(1):33-8. Epub 2009 Dec 6.
Cysneiros RM, Ferrari D, Arida RM, Terra VC, de Almeida AC, Cavalheiro EA, Scorza FA.
Programa de Pos-graduacao em Disturbios do Desenvolvimento da Universidade Presbiteriana Mackenzie, Sao Paulo, SP, Brazil.
Studies have provided evidence of the important effects of omega-3 fatty acid on the brain in neurological conditions, including epilepsy. Previous data have indicated that omega-3 fatty acids lead to prevention of status epilepticus-associated neuropathological changes in the hippocampal formation of rats with epilepsy. Omega-3 fatty acid supplementation has resulted in extensive preservation of GABAergic cells in animals with epilepsy. This study investigated the interplay of these effects with neurogenesis and brain-derived neurotrophic factor (BDNF). The results clearly showed a positive effect of long-term omega-3 fatty acid supplementation on brain plasticity in animals with epilepsy. Enhanced hippocampal neurogenesis and BDNF levels and preservation of interneurons expressing parvalbumin were observed. Parvalbumin-positive cells were identified as surviving instead of newly formed cells. Additional investigations are needed to determine the electrophysiological properties of the newly formed cells and to clarify whether the effects of omega-3 fatty acids on brain plasticity are accompanied by functional gain in animals with epilepsy. 2009 Elsevier Inc. All rights reserved.
Publication Types: Research Support, Non-U.S. Gov't
Links http://www.ncbi.nlm.nih.gov/entrez/queryd.fcgi?cmd=Retrieve&db=PubMed&list_uids=19969506&dopt=ExternalLink
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PMID: 19969506 [PubMed - indexed for MEDLINE]18: J Neurochem. 2010 Feb;112(4):1054-64. Epub 2009 Dec 3.
Taepavarapruk P, Song C.
Department of Biomedical Sciences, AVC, University of Prince Edward Island, Charlottetown PEC1A4P3, Canada.
Interleukin (IL)-1beta may play an important role in Alzheimer's disease. However, the relationships between glucocorticoids and acetylcholine (ACh), and between neurotrophins and ACh in IL-1-induced memory deficits are unknown. While ethyl-eicosapentaenoate (E-EPA) has recently been reported to reduce inflammation and improve memory, cholinergic and neurotrophic mechanisms by which E-EPA improves memory is unclear. This study evaluated: (i) the correlation between ACh release and memory impairment; (ii) the effect of glucocorticoids on ACh release; (iii) the relationship between nerve growth factor (NGF) and inflammation; and (iv) the effects of E-EPA treatment on IL-1beta-induced changes. Intracerebroventricular IL-1beta administrations produced a significant reduction in hippocampal ACh release in rats fed control diet, which was partially attenuated by mifepristone (RU 486) and completely blocked by IL-1 receptor antagonist. In eight-arm radial maze, significantly less ACh release was correlated with the memory deficits after IL-1beta administrations. mRNA expression of hippocampal NGF was lower, whereas IL-1beta was higher when compared with controls. E-EPA treatment significantly improved the memory, which was correlated with normalizing ACh release, and expressions of NGF and IL-1beta. This study revealed important mechanisms by which IL-1beta impairs, while E-EPA improves memory through IL-1-glucocorticoid-ACh release and IL-1-NGF-ACh release pathways.
Publication Types: Research Support, Non-U.S. Gov't
Links http://www.ncbi.nlm.nih.gov/entrez/queryd.fcgi?cmd=Retrieve&db=PubMed&list_uids=19968753&dopt=ExternalLink
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PMID: 19968753 [PubMed - indexed for MEDLINE]19: Nutr Res. 2009 Dec;29(12):825-30.
Park Y, Park S, Yi H, Kim HY, Kang SJ, Kim J, Ahn H.
Department of Food and Nutrition, College of Human Ecology, Hanyang University, Seoul 133-791, South Korea. yongsoon@hanyang.ac.kr
Evidence suggesting an association between n-3 polyunsaturated fatty acids (PUFA) and stroke risk has been inconsistent, possibly because previous studies have not differentiated between different stroke types. The present study investigated the hypothesis that tissue levels of n-3 PUFA are positively associated with hemorrhagic stroke and negatively associated with ischemic stroke. We recruited 120 subjects for this case-control study, with 40 cases each of hemorrhagic stroke, ischemic stroke, and unaffected controls. Patients with a family history of hemorrhagic stroke had a significantly increased risk for hemorrhagic stroke. Omega-3 Index (20:5n3 + 22:6n3 in erythrocytes) and 22:6n3 were negatively (P < .01) associated with the risk of both hemorrhagic and ischemic stroke in multivariate analyses. Saturated fatty acids 16:0 and 18:0 were positively associated, whereas 18:2n6 and 18:3n6 were negatively (P < .05) associated with risk of ischemic stroke. Monounsaturated fatty acid, 18:1n9, increased (P = .03) the odds of hemorrhagic stroke. Omega-3 Index and docosahexaenoic acid were significantly lower in patients with both subtypes of hemorrhagic stroke, subarachnoid and intracerebral hemorrhage, but only in one subtype of ischemic stroke, small-artery occlusion. Saturated fatty acids 16:0 and 18:0 were significantly higher, but 20:4n6 was significantly lower, in patients with small-artery occlusion. Linoleic acid was significantly lower in patients with small-artery occlusion and large-artery atherosclerosis, whereas 18:1n9 was higher in both subgroups of hemorrhagic stroke. In conclusion, the results of our case-control study suggest that erythrocyte n-3 PUFA may protect against hemorrhagic stroke and ischemic stroke, particularly in the case of small-artery occlusion.
Publication Types: Research Support, Non-U.S. Gov't
Links http://www.ncbi.nlm.nih.gov/entrez/queryd.fcgi?cmd=Retrieve&db=PubMed&list_uids=19963154&dopt=ExternalLink
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PMID: 19963154 [PubMed - indexed for MEDLINE]20: Neurosci Res. 2010 Mar;66(3):256-64. Epub 2009 Nov 24.
Delattre AM, Kiss A, Szawka RE, Anselmo-Franci JA, Bagatini PB, Xavier LL, Rigon P, Achaval M, Iagher F, de David C, Marroni NA, Ferraz AC.
Laboratorio de Neurofisiologia, Departamento de Fisiologia, Universidade Federal do Parana, Curitiba, PR, Brazil.
Omega-3 polyunsaturated fatty acids (omega-3 PUFAs) have been widely associated to beneficial effects over different neuropathologies, but only a few studies associate them to Parkinson's disease (PD). Rats were submitted to chronic supplementation (21-90 days of life) with fish oil, rich in omega-3 PUFAs, and were uni- or bilaterally lesioned with 4microg of the neurotoxin 6-hydroxydopamine (6-OHDA) in the medial forebrain bundle. Although lipid incorporation was evidenced in neuronal membranes, it was not sufficient to compensate motor deficits induced by 6-OHDA. In contrast, omega-3 PUFAs were capable of reducing rotational behavior induced by apomorphine, suggesting neuroprotection over dyskinesia. The beneficial effects of omega-3 PUFAs were also evident in the maintenance of thiobarbituric acid reactive substances index from animals lesioned with 6-OHDA similar to levels from SHAM and intact animals. Although omega-3 PUFAs did not modify the tyrosine hydroxylase immunoreactivity in the substantia nigra pars compacta and in the ventral tegmental area, nor the depletion of dopamine (DA) and its metabolites in the striatum, DA turnover was increased after omega-3 PUFAs chronic supplementation. Therefore, it is proposed that omega-3 PUFAs action characterizes the adaptation of remaining neurons activity, altering striatal DA turnover without modifying the estimated neuronal population.
Publication Types: Evaluation Studies Research Support, Non-U.S. Gov't
Links http://www.ncbi.nlm.nih.gov/entrez/queryd.fcgi?cmd=Retrieve&db=PubMed&list_uids=19941911&dopt=ExternalLink
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PMID: 19941911 [PubMed - indexed for MEDLINE]