Role Of Lipids In Brain Injury And Diseases

Bibliography

• Wenk MR: The emerging field of lipidomics. Nat. Rev. Drug Discov. 4(7), 594–610 (2005).
   Google Scholar
• Excellent comprehensive review on various aspects of lipidomics and bioinformatics.
   Google Scholar
• Fahy E, Subramaniam S, Brown HA et al.: A comprehensive classification system for lipids. J. Lipid Res. 46(5), 839–862 (2005).
   Google Scholar
• Comprehensive classification of lipids with a common platform that is compatible with informatics requirements for the hard-core lipid community.
   Google Scholar
• Adibhatla RM, Hatcher JF, Dempsey RJ: Lipids and lipidomics in brain injury and diseases. AAPS J. 8(2), E314–E321 (2006).
   Google Scholar
• Adibhatla RM, Hatcher JF: Phospholipase A2, reactive oxygen species, and lipid peroxidation in cerebral ischemia. Free Radic. Biol. Med. 40(3), 376–387 (2006).
   Google Scholar
• Jiang J, Borisenko GG, Osipov A et al.: Arachidonic acid-induced carbon-centered radicals and phospholipid peroxidation in cyclo-oxygenase-2-transfected PC12 cells. J. Neurochem. 90(5), 1036–1049 (2004).
   Google Scholar
• Simmons DL, Botting RM, Hla T: Cyclooxygenase isozymes: The biology of prostaglandin synthesis and inhibition. Pharmacol Rev. 56(3), 387–437 (2004).
   Google Scholar
• Comprehensive review on cyclooxygenease (COX) enzymes and prostaglandin synthesis.
   Google Scholar
• Kunz A, Anrather J, Zhou P, Orio M, Iadecola C: Cyclooxygenase-2 does not contribute to postischemic production of reactive oxygen species. J. Cereb. Blood Flow Metab. 27(3), 545–551 (2007).
   Google Scholar
• First report showing that COX-2 does not contribute to reactive oxygen species (ROS) production.
   Google Scholar
• Delacourte A, Sergeant N, Champain D et al.: Nonoverlapping but synergetic tau and APP pathologies in sporadic Alzheimer’s disease. Neurology. 59(3), 398–407 (2002).
   Google Scholar
• Highlights the missing link between synergetic tau and A pathologies.
   Google Scholar
• Ehehalt R, Keller P, Haass C, Thiele C, Simons K: Amyloidogenic processing of the Alzheimer -amyloid precursor protein depends on lipid rafts. J. Cell Biol. 160(1), 113–123 (2003).
   Google Scholar
• Suggests that cleavage of the different amyloid precursor protein (APP) pools by α- versus β-secretases depends on distribution of APP to lipid rafts.
   Google Scholar
• Mandavilli A: The amyloid code. Nat. Med. 12(7), 747–751 (2006).
   Google Scholar
• Provocative commentary on the current amyloid theories in Alzheimer’s disease (AD).
   Google Scholar
• Herrup K, Neve R, Ackerman SL, Copani A: Divide and die: Cell cycle events as triggers of nerve cell death. J. Neurosci. 24(42), 9232–9239 (2004).
   Google Scholar
• Critical review on neuronal cell cycle and death and transgenic models in AD.
   Google Scholar
• Schwab C, Hosokawa M, McGeer PL: Transgenic mice over-expressing amyloid beta protein are an incomplete model of Alzheimer disease. Exp. Neurol. 188(1), 52–64 (2004).
   Google Scholar
• Transgenic models over-expressing Aβ alone are incomplete models for AD and have limited use.
   Google Scholar
• Gotz J, Streffer JR, David D et al.: Transgenic animal models of Alzheimer’s disease and related disorders: histopathology, behavior and therapy. Mol. Psychiatry 9(7), 664–683 (2004).
   Google Scholar
• Puglielli L: Aging of the brain, neurotrophin signaling, and Alzheimer’s disease: Is IGF1- R the common culprit? Neurobiol. Aging doi: 10.1016/j.neurobiolaging.2007.01.010 (2007).
   Google Scholar
• Puglielli L, Tanzi RE, Kovacs DM: Alzheimer’s disease: the cholesterol connection. Nature Neurosci. 6(4), 345–351 (2003).
   Google Scholar
• Presents the connection between cholesterol and Aβ and how statins lower Aβ in experimental models by inhibiting cholesterol synthesis.
   Google Scholar
• Whitfield JF: Can statins put the brakes on Alzheimer’s disease? Expert Opin. Investig. Drugs. 15(12), 1479–1485 (2006).
   Google Scholar
• Review suggests more clinical trials are needed to specifically assess the statin effects on sporadic AD.
   Google Scholar
• Grimm MOW, Grimm HS, Patzold AJ et al.: Regulation of cholesterol and sphingomyelin metabolism by amyloid- and presenilin. Nat. Cell Biol. 7(11), 1118–1123 (2005).
   Google Scholar
• Model suggesting the combined effects of cellular cholesterol and sphingomyelin levels regulate α-secretase activity in APP cleavage.
   Google Scholar
• Mattson MP, Cutler RG, Jo DG: Alzheimer peptides perturb lipid-regulating enzymes. Nat. Cell Biol. 7(11), 1045–1047 (2005).
   Google Scholar
• Caballero J, Nahata M: Do statins slow down Alzheimer’s disease? A review. J. Clin. Pharm. Ther. 29(3), 209–213 (2004).
   Google Scholar
• Moses GS, Jensen MD, Lue LF et al.: Secretory PLA2-IIA: A new inflammatory factor for Alzheimer’s disease. J. Neuroinflammation. 3(1), doi: 10.1186/1742–2094–1183–1128 (2006).
   Google Scholar
• First report showing the expression of sPLA2 IIA (inflammatory PLA2) in AD brains.
   Google Scholar
• Williams TI, Lynn BC, Markesbery WR, Lovell MA: Increased levels of 4- hydroxynonenal and acrolein, neurotoxic markers of lipid peroxidation, in the brain in mild cognitive impairment and early Alzheimer’s disease. Neurobiol. Aging 27(8), 1094–1099 (2006).
   Google Scholar
• Liu X, Lovell MA, Lynn BC: Development of a method for quantification of acroleindeoxyguanosine adducts in DNA using isotope dilution-capillary LC/MS/MS and its application to human brain tissue. Anal. Chem. 77(18), 5982–5989 (2005).
   Google Scholar
• Mariani E, Polidori MC, Cherubini A, Mecocci P: Oxidative stress in brain aging, neurodegenerative and vascular diseases: an overview. J. Chromatog. B. 827(1), 65–75 (2005).
   Google Scholar
• Oddo S, Billings L, Kesslak JP, Cribbs DH, LaFerla FM: A immunotherapy leads to clearance of early, but not late, hyperphosphorylated tau aggregates via the proteasome. Neuron 43(3), 321–332 (2004).
   Google Scholar
• Farooqui AA, Ong W-Y, Horrocks LA: Inhibitors of brain phospholipase A2 activity: their neuropharmacological effects and therapeutic importance for the treatment of neurologic disorders. Pharmacol Rev. 58(3), 591–620 (2006).
   Google Scholar
• Hauser RA, Zesiewicz TA: Advances in the pharmacologic management of early Parkinson disease. Neurologist 13(3), 126–132 (2007).
   Google Scholar
• Welch K, Yuan J: -Synuclein oligomerization: a role for lipids? Trends Neurosci. 26(10), 517–519 (2003).
   Google Scholar
• Discusses the relationship between polyunsaturated fatty acid (PUFA) and α-synuclein multimerization in PD.
   Google Scholar
• Sharon R, Bar-Joseph I, Frosch MP, Walsh DM, Hamilton JA, Selkoe DJ: The formation of highly soluble oligomers of - synuclein is regulated by fatty acids and enhanced in Parkinson’s disease. Neuron. 37(4), 583–595 (2003).
   Google Scholar
• Samadi P, Grègoire L, Rouillard C et al.: Docosahexaenoic acid reduces levodopainduced dyskinesias in 1-methyl-4-phenyl- 1,2,3,6-tetrahydropyridine monkeys. Ann. Neurol. 59(2), 282–288 (2006).
   Google Scholar
• Horinouchi K, Erlich S, Perl DP et al.: Acid sphingomyelinase deficient mice - a model of types A and B Niemann-Pick disease. Nature Genetics 10(3), 288–293 (1995).
   Google Scholar
• An animal model for Niemann-Pick types A and B diseases was developed.
   Google Scholar
• Futerman AH, van Meer G: The cell biology of lysosomal storage disorders. Nat. Rev. Mol. Cell Biol. 5(7), 554–565 (2004).
   Google Scholar
• Larsen EC, Hatcher JF, Adibhatla RM: Effect of tricyclodecan-9-yl potassium xanthate (D609) on phospholipid metabolism and cell death during oxygenglucose deprivation in PC12 cells. Neuroscience 146(3), 946–961 (2007).
   Google Scholar
• Report showing that the loss of phosphatidylcholine (PC) is a cause rather than a result of cell death.
   Google Scholar
• Vance JE: Lipid imbalance in the neurological disorder, Niemann-Pick C disease. FEBS Lett. 580(23), 5518–5524 (2006).
   Google Scholar
• Maxfield FR, Tabas I: Role of cholesterol and lipid organization in disease. Nature 438(7068), 612–621 (2005).
   Google Scholar
• This review is more biophysical in nature and discusses the importance of cholesterol in membrane phospholipid organization.
   Google Scholar
• Aarli JA: Role of cytokines in neurological disorders. Curr. Med. Chem. 10, 1931–1937 (2003).
   Google Scholar
• Carlson NG, Rose JW: Antioxidants in multiple sclerosis: do they have a role in therapy? CNS Drugs 20(6), 433–441 (2006).
   Google Scholar
• Kalyvas A, David S: Cytosolic phospholipase A2 plays a key role in the pathogenesis of multiple sclerosis-like disease. Neuron. 41(3), 323–335 (2004).
   Google Scholar
• First report showing the cytosolic phospholipase A2 (cPLA2) role in multiple sclerosis (MS).
   Google Scholar
• Marusic S, Leach MW, Pelker JW et al.: Cytosolic phospholipase A2a-deficient mice are resistant to experimental autoimmune encephalomyelitis. J. Exp. Med. 202(6), 841–851 (2005).
   Google Scholar
• Heller RA, Kronke M: TNF receptormediated signaling pathways. J. Cell Biol. 126, 5–9 (1994).
   Google Scholar
• Kronke M, Adam-Klages S: Role of caspases in TNF-mediated regulation of cPLA2. FEBS Lett. 531(1), 18–22 (2002).
   Google Scholar
• Cunningham TJ, Yao L, Oetinger M, Cort L, Blankenhorn EP, Greensteinm JI: Secreted phospholipase A2 activity in experimental autoimmune encephalomyelitis and multiple sclerosis. J. Neuroinflammation 3 doi: 10.1186/1742–2094–3-26, (2006).
   Google Scholar
• Aktas O, Waiczies S, Zipp F: Neurodegeneration in autoimmune demyelination: Recent mechanistic insights reveal novel therapeutic targets. J. Neuroimmunol. 184(1–2), 17–26 (2007).
   Google Scholar
• Maccarrone M, Battista N, Centonze D: The endocannabinoid pathway in Huntington’s disease: A comparison with other neurodegenerative diseases. Prog. Neurobiol. 81(5–6), 349–379 (2007).
   Google Scholar
• Review discusses the endocannabinoid pathway in AD, parkinson’s disease (PD), Huntington disease (HD) and MS. Agonists/antagonists of endocannabinoid receptors and inhibitors of endocannabinoid metabolism are discussed in detail.
   Google Scholar
• Pacher P, Batkai S, Kunos G: The endocannabinoid system as an emerging target of pharmacotherapy. Pharmacol. Rev. 58(3), 389–462 (2006).
   Google Scholar
• Degroot A, Nomikos GG: In vivo neurochemical effects induced by changes in endocannabinoid neurotransmission. Curr. Opin. Pharmacol. 7(1), 62–68 (2007).
   Google Scholar
• Battista N, Fezza F, Finazzi-Agro A, Maccarrone M: The endocannabinoid system in neurodegeneration. Ital. J. Biochem. 55(3–4), 283–289 (2006).
   Google Scholar
• Clifford JJ, Drago J, Natoli AL et al.: Essential fatty acids given from conception prevent topographies of motor deficit in a transgenic model of Huntington’s disease. Neuroscience 109(1), 81–88 (2002).
   Google Scholar
• Puri BK, Leavitt BR, Hayden MR et al.: Ethyl-EPA in Huntington disease: a double-blind, randomized, placebocontrolled trial. Neurology 65(2), 286–292 (2005).
   Google Scholar
• Muma NA: Transglutaminase is linked to neurodegenerative diseases. J. Neuropathol. Exp. Neurol. 66(4), 258–263 (2007).
   Google Scholar
• Stack EC, Smith KM, Ryu H et al.: Combination therapy using minocycline and coenzyme Q10 in R6/2 transgenic Huntington’s disease mice. Biochim. Biophys. Acta. 1762(3), 373–380 (2006).
   Google Scholar
• Kunst CB: Complex genetics of amyotrophic lateral sclerosis. Am. J. Hum. Genet. 75(6), 933–947 (2004).
   Google Scholar
• Thorough review of amyotrophic lateral sclerosis (ALS) genetics.
   Google Scholar
• Bruijn LI, Miller TM, Cleveland DW: Unraveling the mechanisms involved in motor neuron degeneration in ALS. Ann. Rev. Neurosci. 27(1), 723–749 (2004).
   Google Scholar
• Nirmalananthan N, Greensmith L: Amyotrophic lateral sclerosis: recent advances and future therapies. Curr. Opin. Neurol. 18(6), 712–719 (2005).
   Google Scholar
• This articles discusses clinical trials in ALS. Despite intense research, riluzole, an antiglutamate agent, still remains the only treatment for ALS.
   Google Scholar
• Minghetti L: Cyclooxygenase-2 (COX-2) in inflammatory and degenerative brain diseases. J. Neuropath. Exp. Neurol. 63(9), 901–910 (2004).
   Google Scholar
• Agar J, Durham H: Relevance of oxidative injury in the pathogenesis of motor neuron diseases. Amyotroph. Lateral Scler. Other Motor Neuron Disord. 4(4), 232–242 (2003).
   Google Scholar
• Simpson EP, Henry YK, Henkel JS, Smith RG, Appel SH: Increased lipid peroxidation in sera of ALS patients: A potential biomarker of disease burden. Neurology 62(10), 1758–1765 (2004).
   Google Scholar
• Horrobin D: The lipid hypothesis of schizophrenia. In: Brain Lipids and Disorders in Biological Psychiatry. Skinner ER (Ed.), Elsevier Science, Amsterdam, The Netherlands 39–52 (2002).
   Google Scholar
• Role of lipids in schizophrenia is elegantly presented in this book chapter.
   Google Scholar
• Berger GE, Smesny S, Amminger GP: Bioactive lipids in schizophrenia. Int. Rev. Psychiatry. 18(2), 85–98 (2006).
   Google Scholar
• Hakak Y, Walker JR, Li C et al.: Genome-wide expression analysis reveals dysregulation of myelination-related genes in chronic schizophrenia. Proc. Natl. Acad. Sci. USA 98(8), 4746–4751 (2001).
   Google Scholar
• Papandreou D, Pavlou E, Kalimeri E, Mavromichalis I: The ketogenic diet in children with epilepsy. Br. J. Nutr. 95(1), 5–13 (2006).
   Google Scholar
• LaRoche SM: A new look at the secondgeneration antiepileptic drugs: a decade of experience. Neurologist. 13(3), 133–139 (2007).
   Google Scholar
• Bialer M, Johannessen SI, Kupferberg HJ, Levy RH, Perucca E, Tomson T: Progress report on new antiepileptic drugs: a summary of the Eigth Eilat Conference (EILAT VIII). Epilepsy Research 73(1), 1–52 (2007).
   Google Scholar
• Review of the new generation anti-epileptic drugs.
   Google Scholar
• Klotz U: The role of pharmacogenetics in the metabolism of antiepileptic drugs: pharmacokinetic and therapeutic implications. Clin. Pharmacokinet. 46(4), 271–279 (2007).
   Google Scholar
• Gasior M, Rogawski MA, Hartman AL: Neuroprotective and disease-modifying effects of the ketogenic diet. Behav. Pharmacol. 17(5–6), 431–439 (2006).
   Google Scholar
• Bough KJ, Rho JM: Anticonvulsant mechanisms of the ketogenic diet. Epilepsia. 48(1), 43–58 (2007).
   Google Scholar
• Presents a view of how the ketogenic diet exerts anticonvulsant effects, summarizing key insights from experimental and clinical studies. PUFAs are generated after ketogenic diet that up-regulate various energy metabolism genes and mitochondrial biogenesis that reduces ROS generation and increase energy production.
   Google Scholar
• Savitz SI: A critical appraisal of the NXY- 059 neuroprotection studies for acute stroke: A need for more rigorous testing of neuroprotective agents in animal models of stroke. Exp. Neurol. 205(1), 20–25 (2007).
   Google Scholar
• A critical appraisal of failed Stroke Acute Ischemic NXY-059 Treatment (SAINT) II Phase III stroke clinical trial.
   Google Scholar
• Adibhatla RM, Hatcher JF: Cytidine 5’- diphosphocholine (CDP-choline) in stroke and other CNS disorders. Neurochem. Res. 30(1), 15–23 (2005).
   Google Scholar
• Review on CDP-choline actions in stroke and its possible effect in regulating proinflammatory cytokines such as TNF-α and IL-1β.
   Google Scholar
• Adibhatla RM, Hatcher JF, Larsen EC, Chen X, Sun D, Tsao F: CDP-choline significantly restores the phosphatidylcholine levels by differentially affecting phospholipase A2 and CTPphosphocholine cytidylyltransferase after stroke. J. Biol. Chem. 281(10), 6718–6725 (2006).
   Google Scholar
• First report showing the loss of PC due to activation of sPLA2 and loss of CCT; CDPcholine restored PC levels by opposing these actions in stroke model.
   Google Scholar
• Mehta SL, Manhas N, Raghubir R: Molecular targets in cerebral ischemia for developing novel therapeutics. Brain Res. Rev. 54(1) 34–66, (2007).
   Google Scholar
• Comprehensive review of molecular mechanisms in cerebral ischemia.
   Google Scholar
• Liu T, Clark RK, McDonnell PC et al.: TNF- expression in ischemic neurons. Stroke 25(7), 1481–1488 (1994).
   Google Scholar
• Wang CX, Shuaib A: Involvement of inflammatory cytokines in central nervous system injury. Prog. Neurobiol. 67(2), 161–172 (2002).
   Google Scholar
• Loddick SA, Rothwell NJ: Neuroprotective effects of human recombinant interleukin-1 receptor antagonist in focal cerebral ischaemia in the rat. J. Cereb. Blood Flow Metab. 16(5), 932–940 (1996).
   Google Scholar
• Wang X, Yue TL, Barone FC, White RF, Gagnon RC, Feuerstein GZ: Concomitant cortical expression of TNF- and IL-1 mRNAs follows early response gene expression in transient focal ischemia. Mol. Chem. Neuropath. 23(2–3), 103–114 (1994).
   Google Scholar
• Adibhatla RM, Dempsey RJ, Hatcher JF: Integration of cytokine biology and lipid metabolism in stroke. Front Neurosurg. Res. (under the aegis of Front Biosci). (2007) (In Press).
   Google Scholar
• Secades JJ, Lorenzo JL: Citicoline: Pharmacological and clinical review, 2006 update. Methods Find. Exp. Clin. Pharmacol. 28, 1–56 (2006).
   Google Scholar
• Savitz SI, Fisher M: Future of neuroprotection for acute stroke: In the aftermath of the SAINT trials. Ann. Neurol. 61(5), 396–402 (2007).
   Google Scholar
• Critical issues and Stroke Therapy Academic Industrial Roundtable (STAIR) guidelines for future stroke clinical trials are discussed in the aftermath of failed SAINT-II NXY-059 stroke trails.
   Google Scholar
• Crack PJ, Taylor JM: Reactive oxygen species and the modulation of stroke. Free Radic. Biol. Med. 38(11), 1433–1444 (2005).
   Google Scholar
• Liu KJ, Rosenberg GA: Matrix metalloproteinases and free radicals in cerebral ischemia. Free Radic. Biol. Med. 39(1), 71–80 (2005).
   Google Scholar
• Margaill I, Plotkine M, Lerouet D: Antioxidant strategies in the treatment of stroke. Free Radic. Biol. Med. 39(4), 429–443 (2005).
   Google Scholar
• Tomitori H, Usui T, Saeki N et al.: Polyamine oxidase and acrolein as novel biochemical markers for diagnosis of cerebral stroke. Stroke 36(12), 2609–2613 (2005).
   Google Scholar
• First report showing acrolein, a highly toxic aldehyde (100-times more potent than HNE), in plasma of stroke patients. So far accumulation of acrolein in stroke brains had not been demonstrated.
   Google Scholar
• Rigg JL, Zafonte RD: Corticosteroids in TBI: is the story closed? J. Head Trauma Rehab. 21(3), 285–288 (2006).
   Google Scholar
• Ariza M, Pueyo R, Matarin MdM et al.: Influence of APOE polymorphism on cognitive and behavioral outcome in moderate and severe traumatic brain injury. J. Neurol. Neurosurg. Psychiatry. 77(10), 1191–1193 (2006).
   Google Scholar
• Interesting clinical study demonstrating that performance of neuropsychological tasks is worse in patients with APOE 4 allele after TBI.
   Google Scholar
• Iwata A, Browne KD, Chen X-H, Yuguchi T, Smith DH: Traumatic brain injury induces biphasic upregulation of ApoE and ApoJ protein in rats. J. Neurosci. Res. 82(1), 103–114 (2005).
   Google Scholar
• Fluid percussion injury showed Aaccumulation and increased ApoE mRNA expression in rats.
   Google Scholar
• Jellinger KA: Head injury and dementia. Curr Opin Neurol. 17(6), 719–723 (2004).
   Google Scholar
• Starkstein SE, Jorge R: Dementia after traumatic brain injury. Int. Psychogeriatr. 17(Suppl. 1), S93–S107 (2005).
   Google Scholar
• Smith C, Graham DI, Murray LS, Stewart J, Nicoll JAR: Association of APOE e4 and cerebrovascular pathology in traumatic brain injury. J. Neurol. Neurosurg. Psychiatry 77(3), 363–366 (2006).
   Google Scholar
• Mahmood A, Lu D, Qu C, Goussev A, Chopp M: Treatment of traumatic brain injury with a combination therapy of marrow stromal cells and atorvastatin in rats. Neurosurgery 60(3), 546–554 (2007).
   Google Scholar
• Lynch JR, Wang H, Mace B et al.: A novel therapeutic derived from apolipoprotein E reduces brain inflammation and improves outcome after closed head injury. Exp. Neurol. 192(1), 109–116 (2005).
   Google Scholar
• Hall ED, Springer JE: Neuroprotection and acute spinal cord injury: a reappraisal. NeuroRx 1(1), 80–100 (2004).
   Google Scholar
• Kim H-Y: Novel metabolism of docosahexaenoic acid in neural cells. J. Biol. Chem. 282(26), 18861–18665 (2007).
   Google Scholar
• Marcheselli VL, Hong S, Lukiw WJ et al.: Novel docosanoids inhibit brain ischemiareperfusion- mediated leukocyte infiltration and pro-inflammatory gene expression. J. Biol. Chem. 278(44), 43807–43817 (2003).
   Google Scholar
• Bazan N: The onset of brain injury and neurodegeneration triggers the synthesis of docosanoid neuroprotective signaling. Cell. Mol. Neurobiol. 26(4–6), 901–913 (2006).
   Google Scholar
• Ariel A, Serhan CN: Resolvins and protectins in the termination program of acute inflammation. Trends Immunol. 28(4), 176–183 (2007).
   Google Scholar
• Belayev L, Marcheselli VL, Khoutorova L et al.: Docosahexaenoic acid complexed to albumin elicits high-grade ischemic neuroprotection. Stroke 36(1), 118–123 (2005).
   Google Scholar
• Lukiw WJ, Cui J-G, Marcheselli VL et al.: A role for docosahexaenoic acid-derived neuroprotectin D1 in neural cell survival and Alzheimer disease. J. Clin. Invest. 115(10), 2774–2783 (2005).
   Google Scholar
• Balazy M: Eicosanomics: targeted lipidomics of eicosanoids in biological systems. Prostaglandins Other Lipid Mediat. 73(3–4), 173–180 (2004).
   Google Scholar
• Hillard CJ: Lipids and drugs of abuse. Life Sci. 77(14), 1531–1542 (2005).
   Google Scholar
• Senn C, Hangartner C, Moes S, Guerini D, Hofbauer KG: Central administration of small interfering RNAs in rats: a comparison with antisense oligonucleotides. Eur. J. Pharmacol. 522(1–3), 30–37 (2005).
   Google Scholar
• Cejka D, Losert D, Wacheck V: Short interfering RNA (siRNA): tool or therapeutic? Clin. Sci. (Lond). 110(1), 47–58 (2006).
   Google Scholar
• This review and the following one by Dykxhoorn et al. discuss the technology of RNA silencing, potential obstacles and possibilities for clinical applications.
   Google Scholar
• Dykxhoorn DM, Palliser D, Lieberman J: The silent treatment: siRNAs as small molecule drugs. Gene Ther. 13, 541–552 (2006).
   Google Scholar
• Adibhatla RM, Hatcher JF, Tureyen K: CDP-choline liposomes provide significant reduction in infarction over free CDPcholine in stroke. Brain Res. 1058(1–2), 193–197 (2005).
   Google Scholar
• Efficient delivery of CDP-choline to the brain using liposome encapsulation substantially improves the outcome after stroke. The route of administration is very important in clinical trials, which has been ignored in US trials.
   Google Scholar
• Adibhatla RM: Mechanistic aspects of CDP-choline (Citicoline) action in stroke. In: 4th Asia Pacific Conference Against Stroke (APCAS March 30-April 1, 2007). Conference Secretariat, APCAS New Delhi, India (2007).
   Google Scholar
• Adibhatla RM, Hatcher JF: Citicoline mechanisms and clinical efficacy in cerebral ischemia. J. Neurosci. Res. 70(2), 133–139 (2002).
   Google Scholar
• Wolozin B: Cholesterol, statins and dementia. Curr. Opin. Lipidol. 15(6), 667–672 (2004).
   Google Scholar
• Lane RM, Farlow MR: Lipid homeostasis and apolipoprotein E in the development and progression of Alzheimer’s disease. J. Lipid Res. 46(5), 949–968 (2005).
   Google Scholar
• Farooqui AA, Horrocks LA, Farooqui T: Modulation of inflammation in brain: a matter of fat. J. Neurochem. 101(3), 577–599 (2007).
   Google Scholar
• Mukherjee S, Maxfield FR: Lipid and cholesterol trafficking in NPC. Biochim. Biophys. Acta. 1685(1–3), 28–37 (2004).
   Google Scholar
• Miranda SRP, He X, Simonaro CM et al.: Infusion of recombinant human acid sphingomyelinase into Niemann-Pick disease mice leads to visceral, but not neurological, correction of the pathophysiology. FASEB J. 14(13), 1988–1995 (2000).
   Google Scholar
• Kanter JL, Narayana S, Ho PP et al.: Lipid microarrays identify key mediators of autoimmune brain inflammation. Nat. Med. 12(1), 138–143 (2006).
   Google Scholar
• Centonze D, Finazzi-Agro A, Bernardi G, Maccarrone M: The endocannabinoid system in targeting inflammatory neurodegenerative diseases. Trends Pharmacol. Sci. 28(4), 180–187 (2007).
   Google Scholar
• Lin T-N, Wang Q, Simonyi A et al.: Induction of secretory phospholipase A2 in reactive astrocytes in response to transient focal cerebral ischemia in the rat brain. J. Neurochem. 90(3), 637–645 (2004).
   Google Scholar
• Reid RC: Inhibitors of secretory phospholipase A2 group IIA. Curr. Med. Chem. 12(25), 3011–3026 (2005).
   Google Scholar
• Presents the structurally diverse array of available sPLA2 group IIA inhibitors, their associated biological activity in animal models and evaluation of therapeutic potential in Phase II clinical trials.
   Google Scholar
• Narayan RK, Michel ME, Ansell B et al.: Clinical trials in head injury. J. Neurotrauma 19(5), 503–557 (2002).
   Google Scholar
• Despite promising preclinical data, most of the clinical TBI trials that have been performed in recent years have failed to demonstrate any significant improvement in outcomes. This report summarizes the key points of a workshop sponsored by NIH/National Institute of Neurological Disorders and Stroke (NINDS) to evaluate problems of past trials and insights into proper planning of future clinical trials.
   Google Scholar