We are analyzing https://link.springer.com/article/10.1007/s11064-015-1776-x.

Title:
The Lipoxygenases: Their Regulation and Implication in Alzheimer’s Disease | Neurochemical Research
Description:
Inflammatory processes and alterations of lipid metabolism play a crucial role in Alzheimer’s disease (AD) and other neurodegenerative disorders. Polyunsaturated fatty acids (PUFA) metabolism impaired by cyclooxygenases (COX-1, COX-2), which are responsible for formation of several eicosanoids, and by lipoxygenases (LOXs) that catalyze the addition of oxygen to linolenic, arachidonic (AA), and docosahexaenoic acids (DHA) and other PUFA leading to formation of bioactive lipids, significantly affects the course of neurodegenerative diseases. Among several isoforms, 5-LOX and 12/15-LOX are especially important in neuroinflammation/neurodegeneration. These two LOXs are regulated by substrate concentration and availability, and by phosphorylation/dephosphorylation through protein kinases PKA, PKC and MAP-kinases, including ERK1/ERK2 and p38. The protein/protein interaction also is involved in the mechanism of 5-LOX regulation through FLAP protein and coactosin-like protein. Moreover, non-heme iron and calcium ions are potent regulators of LOXs. The enzyme activity significantly depends on the cell redox state and is differently regulated by various signaling pathways. 5-LOX and 12/15-LOX convert linolenic acid, AA, and DHA into several bioactive compounds e.g. hydroperoxyeicosatetraenoic acids (5-HPETE, 12S-HPETE, 15S-HPETE), which are reduced to corresponding HETE compounds. These enzymes synthesize several bioactive lipids, e.g. leucotrienes, lipoxins, hepoxilins and docosahexaenoids. 15-LOX is responsible for DHA metabolism into neuroprotectin D1 (NPD1) with significant antiapoptotic properties which is down-regulated in AD. In this review, the regulation and impact of 5-LOX and 12/15-LOX in the pathomechanism of AD is discussed. Moreover, we describe the role of several products of LOXs, which may have significant pro- or anti-inflammatory activity in AD, and the cytoprotective effects of LOX inhibitors.
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Keywords {🔍}

pubmed, lox, google, scholar, article, cas, disease, central, alzheimers, lipoxygenase, activity, role, protein, mice, brain, pratico, activation, mapt, cells, level, cox, acid, inhibition, lipid, cell, inhibitors, phosphorylation, effect, inflammatory, inflammation, antiinflammatory, pathway, demonstrated, chu, regulation, loxs, mouse, fig, expression, lipoxygenases, neuronal, microglia, increase, model, amyloid, receptors, γsecretase, human, stress, strosznajder,

Topics {✒️}

nf-κb-sensitive mirna-125b scavenger receptors sr-ai/ii nf-kb-regulated micro rnas pace-asciak cr cpla2/15-lox-dependent pro-survival pathway neuroprotectin d1-mediated anti-inflammatory cox/pge2/ep2 immune pathway article download pdf perk/eif2α/atf4 pathway leading g-protein-coupled hete receptor alzheimer’s-related tau pathology prevented dexamethasone-evoked phosphorylation age-related memory loss genome-wide association studies 17s-dihydroxy-docosa-4z ca2+–zn2+ permeable ampa beta-amyloid-induced neurotoxicity nsaid-induced organ toxicity bis-allylic methylene group peroxynitrite-induced neuronal apoptosis steroidal anti-inflammatory drugs central nervous system lipopolysaccharide-induced memory insult nonsteroidal anti-inflammatory drugs population-based cohort study peroxisome proliferator-activated receptors staging anti-inflammatory therapy apolipoprotein e-deficient mice aspirin-triggered 15-epi-lipoxins γ-secretase-activating protein methyl-dna binding proteins genome-wide association gamma secretase-activating protein gamma-secretase activating protein dexamethasone-evoked mapt phosphorylation bioactive epoxy-hydroxy eicosanoids anti-inflammatory lipid mediators pro-resolving lipid mediators disease-related tau pathology microglial m1/m2 polarization full size image virus-mediated brain delivery attenuates free radical genome-wide analysis polyunsaturated fatty acids aβ25–35-evoked cell death amyloid beta-peptide toxicity 5-lipoxygenase-activating protein inhibitor cyclic amp-mediated inhibition rare missense mutation

Questions {❓}

Zafiriou MP, Deva R, Ciccoli R, Siafaka-Kapadai A, Nigam S (2007) Biological role of hepoxilins: upregulation of phospholipid hydroperoxide glutathione peroxidase as a cellular response to oxidative stress?

Schema {🗺️}

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         headline:The Lipoxygenases: Their Regulation and Implication in Alzheimer’s Disease
         description:Inflammatory processes and alterations of lipid metabolism play a crucial role in Alzheimer’s disease (AD) and other neurodegenerative disorders. Polyunsaturated fatty acids (PUFA) metabolism impaired by cyclooxygenases (COX-1, COX-2), which are responsible for formation of several eicosanoids, and by lipoxygenases (LOXs) that catalyze the addition of oxygen to linolenic, arachidonic (AA), and docosahexaenoic acids (DHA) and other PUFA leading to formation of bioactive lipids, significantly affects the course of neurodegenerative diseases. Among several isoforms, 5-LOX and 12/15-LOX are especially important in neuroinflammation/neurodegeneration. These two LOXs are regulated by substrate concentration and availability, and by phosphorylation/dephosphorylation through protein kinases PKA, PKC and MAP-kinases, including ERK1/ERK2 and p38. The protein/protein interaction also is involved in the mechanism of 5-LOX regulation through FLAP protein and coactosin-like protein. Moreover, non-heme iron and calcium ions are potent regulators of LOXs. The enzyme activity significantly depends on the cell redox state and is differently regulated by various signaling pathways. 5-LOX and 12/15-LOX convert linolenic acid, AA, and DHA into several bioactive compounds e.g. hydroperoxyeicosatetraenoic acids (5-HPETE, 12S-HPETE, 15S-HPETE), which are reduced to corresponding HETE compounds. These enzymes synthesize several bioactive lipids, e.g. leucotrienes, lipoxins, hepoxilins and docosahexaenoids. 15-LOX is responsible for DHA metabolism into neuroprotectin D1 (NPD1) with significant antiapoptotic properties which is down-regulated in AD. In this review, the regulation and impact of 5-LOX and 12/15-LOX in the pathomechanism of AD is discussed. Moreover, we describe the role of several products of LOXs, which may have significant pro- or anti-inflammatory activity in AD, and the cytoprotective effects of LOX inhibitors.
         datePublished:2015-12-16T00:00:00Z
         dateModified:2015-12-16T00:00:00Z
         pageStart:243
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            Arachidonic acid
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            Biochemistry
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      headline:The Lipoxygenases: Their Regulation and Implication in Alzheimer’s Disease
      description:Inflammatory processes and alterations of lipid metabolism play a crucial role in Alzheimer’s disease (AD) and other neurodegenerative disorders. Polyunsaturated fatty acids (PUFA) metabolism impaired by cyclooxygenases (COX-1, COX-2), which are responsible for formation of several eicosanoids, and by lipoxygenases (LOXs) that catalyze the addition of oxygen to linolenic, arachidonic (AA), and docosahexaenoic acids (DHA) and other PUFA leading to formation of bioactive lipids, significantly affects the course of neurodegenerative diseases. Among several isoforms, 5-LOX and 12/15-LOX are especially important in neuroinflammation/neurodegeneration. These two LOXs are regulated by substrate concentration and availability, and by phosphorylation/dephosphorylation through protein kinases PKA, PKC and MAP-kinases, including ERK1/ERK2 and p38. The protein/protein interaction also is involved in the mechanism of 5-LOX regulation through FLAP protein and coactosin-like protein. Moreover, non-heme iron and calcium ions are potent regulators of LOXs. The enzyme activity significantly depends on the cell redox state and is differently regulated by various signaling pathways. 5-LOX and 12/15-LOX convert linolenic acid, AA, and DHA into several bioactive compounds e.g. hydroperoxyeicosatetraenoic acids (5-HPETE, 12S-HPETE, 15S-HPETE), which are reduced to corresponding HETE compounds. These enzymes synthesize several bioactive lipids, e.g. leucotrienes, lipoxins, hepoxilins and docosahexaenoids. 15-LOX is responsible for DHA metabolism into neuroprotectin D1 (NPD1) with significant antiapoptotic properties which is down-regulated in AD. In this review, the regulation and impact of 5-LOX and 12/15-LOX in the pathomechanism of AD is discussed. Moreover, we describe the role of several products of LOXs, which may have significant pro- or anti-inflammatory activity in AD, and the cytoprotective effects of LOX inhibitors.
      datePublished:2015-12-16T00:00:00Z
      dateModified:2015-12-16T00:00:00Z
      pageStart:243
      pageEnd:257
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      keywords:
         Lipoxygenase
         LOX
         Alzheimer’s disease
         Arachidonic acid
         Neurodegeneration
         Neurosciences
         Neurochemistry
         Biochemistry
         general
         Cell Biology
         Neurology
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      affiliation:
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               type:PostalAddress
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      name:Joanna B. Strosznajder
      affiliation:
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            address:
               name:Department of Cellular Signalling, Mossakowski Medical Research Centre Polish Academy of Sciences, Warsaw, Poland
               type:PostalAddress
            type:Organization
      name:Robert P. Strosznajder
      affiliation:
            name:Mossakowski Medical Research Centre Polish Academy of Sciences
            address:
               name:Laboratory of Preclinical Research and Environmental Agents, Department of Neurosurgery, Mossakowski Medical Research Centre Polish Academy of Sciences, Warsaw, Poland
               type:PostalAddress
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      name:Laboratory of Preclinical Research and Environmental Agents, Department of Neurosurgery, Mossakowski Medical Research Centre Polish Academy of Sciences, Warsaw, Poland
      name:Department of Cellular Signalling, Mossakowski Medical Research Centre Polish Academy of Sciences, Warsaw, Poland
      name:Laboratory of Preclinical Research and Environmental Agents, Department of Neurosurgery, Mossakowski Medical Research Centre Polish Academy of Sciences, Warsaw, Poland

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