Guest guest Posted November 16, 2005 Report Share Posted November 16, 2005 I have been doing some homework on this topic by request; especially pay attention to the last few sentences of the abstracts for a summary. The abstract itself is a summary of the research, and the last sentence or two is supposed to recap the main point. I am posting several on this. I found many areas of the brain and body that are benefitted by fatty acid supplementation, according to the research. There were many on cardio health, for example, and peripheral neuroapathy, esp in diabetics. Also some on the benefits for reducing the damage to the brain by alcohol. Hope you all enjoy the reading. ;-) ______________________________________________________ : J Mol Neurosci. 2001 Apr-Jun;16(2-3):263-72; discussion 279-84. Related Articles, Links ? Plasmalogens, phospholipase A2, and docosahexaenoic acid turnover in brain tissue. Farooqu AA, Horrocks LA. Department of Molecular and Cellular Biochemistry The Ohio State University, Columbus 43210, USA. Plasmalogens are glycerophospholipids of neural membranes containing vinyl ether bonds. Their synthetic pathway is located in peroxisomes and endoplasmic reticulum. The rate-limiting enzymes are in the peroxisomes and are induced by docosahexaenoic acid (DHA). Plasmalogens often contain arachidonic acid (AA) or DHA at the sn-2 position of the glycerol moiety. The receptor-mediated hydrolysis of plasmalogens by cytosolic plasmalogen-selective phospholipase A2 generates AA or DHA and lysoplasmalogens. AA is metabolized to eicosanoids. The mechanism of signaling with DHA is not known. The plasmalogen-selective phospholipase A2 differs from other intracellular phospholipases A2 in molecular mass, kinetic properties, substrate specificity, and response to glycosaminoglycans, gangliosides, and sialoglycoproteins. A major portion of [3H]DHA incorporated into neural membranes is found at the sn-2 position of ethanolamine glycerophospholipids. Studies with a mutant cell line defective in plasmalogen biosynthesis indicate that the incorporation of DHA is reduced in this RAW 264.7 cell line by 50%. In contrast, the incorporation of AA remains unaffected. This is reversed completely when the growth medium is supplemented with sn-1-hexadecylglycerol, suggesting that DHA can be selectively targeted for incorporation into plasmalogens. We suggest that deficiencies of DHA and plasmalogens in peroxisomal disorders, Alzheimer's disease (AD), depression, and attention deficit hyperactivity disorders (ADHD) may be responsible for abnormal signal transduction associated with learning disability, cognitive deficit, and visual dysfunction. These abnormalities in the signal-transduction process can be partially corrected by supplementation with a diet enriched with DHA. Publication Types: • Review • Review, Tutorial PMID: 11478381 [PubMed - indexed for MEDLINE] *************** 1: J Neurochem. 2004 Oct;91(1):20-9. Related Articles, Links ? Neuroprotective actions of eicosapentaenoic acid on lipopolysaccharide-induced dysfunction in rat hippocampus. Lonergan PE, DS, Horrobin DF, Lynch MA. Trinity College Institute of Neuroscience, Department of Physiology, Trinity College, Dublin, Ireland. Eicosapentaenoic acid (EPA) protects hippocampus from age-related and irradiation- induced changes that lead to impairment in synaptic function; the evidence suggests that this is due to its anti-inflammatory effects, specifically preventing changes induced by the proinflammatory cytokine, interleukin-1beta (IL-1beta). In this study, we have investigated the possibility that EPA may prevent the effects of lipopolysaccharide (LPS) administration, which have been shown to lead to deterioration of synaptic function in rat hippocampus. The data indicate that treatment of hippocampal neurones with EPA abrogated the LPS- induced increases in phosphorylation of the mitogen-activated protein kinase, c-Jun N- terminal kinase (JNK), the transcription factor, c-Jun and the mitochondrial protein, Bcl-2. In parallel, we report that intraperitoneal administration of LPS to adult rats increases phosphorylation of JNK, c-Jun and Bcl-2 in hippocampal tissue and that these changes are coupled with increased IL-1beta concentration. Treatment of rats with EPA abrogates these effects and also blocks the LPS-induced impairment in long-term potentiation in perforant path-granule cell synapses that accompanies these changes. We propose that the neuroprotective effect of EPA may be dependent on its ability to inhibit the downstream consequences of JNK activation. PMID: 15379883 [PubMed - indexed for MEDLINE] *************** 1: J Nutr. 1998 Feb;128(2 Suppl):427S-433S. Related Articles, Links Comment in: • J Nutr. 1999 Feb;129(2):446. ? The slow discovery of the importance of omega 3 essential fatty acids in human health. Holman RT. Hormel Institute, University of Minnesota, Austin 55912, USA. Although linoleic and linolenic acids have been known to be necessary for normal growth and dermal function since 1930, the omega 3 essential fatty acids (EFA) have not received much attention until recently. The two families of acids are metabolized by the same enzymes, making them competitive. Gross deficiencies of omega 6 plus omega 3 EFA have been observed in humans, induced by attempts at total parenteral nutrition (TPN) with preparations devoid of lipids. Deficiency of omega 3 acids has been induced by TPN containing high omega 6 and low omega 3 fatty acids. In natural human populations, a wide range of omega 3 and omega 6 proportions have been found, ranging from high omega 3 and low omega 6 content to low omega 3 and high omega 6 content, showing inverse correlation between sigma omega 6 and sigma omega 3. In humans with neuropathy or impairment of the immune system, significant deficits of omega 3 EFA have been measured. Publication Types: • Review • Review, Tutorial PMID: 9478042 [PubMed - indexed for MEDLINE] ***************************** ??????1: Eur J Clin Invest. 2005 Nov;35(11):691-9. Related Articles, Links ? Cognitive and physiological effects of Omega-3 polyunsaturated fatty acid supplementation in healthy subjects. Fontani G, Corradeschi F, Felici A, Alfatti F, Migliorini S, Lodi L. University of Siena, Siena, Italy. Background It has been reported that Omega-3 fatty acids may play a role in nervous system activity and that they improve cognitive development and reference memory- related learning, increase neuroplasticity of nerve membranes, contribute to synaptogenesis and are involved in synaptic transmission. The aim of this study was to examine the effects of Omega-3 supplementation on some cognitive and physiological parameters in healthy subjects. Materials and methods Subjects were tested at the beginning of the experiment and after 35 days. In this period they were supplemented with Omega-3 polyunsaturated fatty acids. A group was supplemented with olive oil (placebo). Tests involving different types of attention were used, i.e. Alert, Go/No-Go, Choice and Sustained Attention. For each test, the reaction time, the event-related potentials by electroencephalogram (EEG) and the electromyography (EMG) of the forefinger flexor muscle were recorded. The Profile of Mood States test (POMS) was also administered. Results Blood analyses showed that after Omega-3 supplementation the arachidonic acid/eicosapentaenoic acid ratio (AA/EPA) was strongly reduced. The mood profile was improved after Omega-3 with increased vigour and reduced anger, anxiety and depression states. This was associated with an effect on reactivity with a reduction of reaction time in the Go/No-Go and Sustained Attention tests. The latency of EMG activation was concomitantly reduced in the same tests plus Choice. An EEG frequency shift towards the theta and alpha band were recorded in all the tests after Omega-3. Conclusions Omega-3 supplementation is associated with an improvement of attentional and physiological functions, particularly those involving complex cortical processing. These findings are discussed in terms of the influence of Omega-3 on the central nervous system. Eur J Clin Invest 2005; 35 (11): 691-699. PMID: 16269019 [PubMed - in process] ******************************************************************* Quote Link to comment Share on other sites More sharing options...
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