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| 1 | A new look at auranofin,dextromethorphan and rosiglitazone for reduction of glia-mediated inflammation in neurodegenerative diseases显示文摘Neurodegenerative disorders including Alzheimer's disease are characterized by chronic inflammation in the central nervous system. The two main glial types involved in inflammatory reactions are microglia and astrocytes. While these cells normally protect neurons by providing nutrients and growth factors, disease specific stimuli can induce glial secretion of neurotoxins. It has been hypothesized that reducing glia-mediated inflammation could diminish neuronal loss. This hypothesis is supported by observations that chronic use of non-steroidal anti-inflammatory drugs(NSAIDs) is linked with lower incidences of neurodegenerative disease. It is possible that the NSAIDs are not potent enough to appreciably reduce chronic neuroinflammation after disease processes are fully established. Gold thiol compounds, including auranofin, comprise another class of medications effective at reducing peripheral inflammation. We have demonstrated that auranofin inhibits human microglia- and astrocyte-mediated neurotoxicity. Other drugs which are currently used to treat peripheral inflammatory conditions could be helpful in neurodegenerative disease. Three different classes of anti-inflammatory compounds, which have a potential to inhibit neuroinflammation are highlighted below. | Jocelyn M.Madeira Stephanie M.Schindler Andis Klegeris | 2015 | Neural Regeneration Research2015，10，3： | 3 |
| 2 | Regulation of neuroimmune processes by damage-and resolution-associated molecular patterns显示文摘Sterile inflammatory processes are essential for the maintenance of central nervous system homeostasis,but they also contribute to various neurological disorders,including neurotrauma,stroke,and demyelinating or neurodegenerative diseases.Immune mechanisms in the central nervous system and periphery are regulated by a diverse group of endogenous proteins,which can be broadly divided into the pro-inflammatory damageassociated molecular patterns(DAMPs)and anti-inflammatory resolution-associated molecular patterns(RAMPs),even though there is notable overlap between the DAMPand RAMP-like activities for some of these molecules.Both groups of molecular patterns were initially described in peripheral immune processes and pathologies;however,it is now evident that at least some,if not all,of these immunomodulators also regulate neuroimmune processes and contribute to neuroinflammation in diverse central nervous system disorders.The review of recent literature demonstrates that studies on DAMPs and RAMPs of the central nervous system still lag behind the much broader research effort focused on their peripheral counterparts.Nevertheless,this review also reveals that over the last five years,significant advances have been made in our understanding of the neuroimmune functions of several well-established DAMPs,including high-mobility group box 1 protein and interleukin 33.Novel neuroimmune functions have been demonstrated for other DAMPs that previously were considered almost exclusively as peripheral immune regulators;they include mitochondrial transcription factor A and cytochrome C.RAMPs of the central nervous system are an emerging area of neuroimmunology with very high translational potential since some of these molecules have already been used in preclinical and clinical studies as candidate therapeutic agents for inflammatory conditions,such as multiple sclerosis and rheumatoid arthritis.The therapeutic potential of DAMP antagonists and neutralizing antibodies in central nervous system neuroinflammatory diseases is also supported by several of the identified studies.It can be concluded that further studies of DAMPs and RAMPs of the central nervous system will continue to be an important and productive field of neuroimmunology. | Andis Klegeris | 2021 | Neural Regeneration Research2021，16，3： | 3 |
| 3 | Improvement in generic prob- lem-solving abilities of students by use of tutor-less problem-based learning in a large classroom setting 显示文摘 | Klegeris A Bahniwal M Hurren H | 2013 | CBE Life Sci Educ2013，12，1： | 1 |
| 4 | Impact of problem-based learning in a large classroom setting: student perception and problem-solving skills显示文摘 | Klegeris A Hurren H | 2011 | Adv Physiol Educ2011，35，4： | 1 |
| 5 | Inflammation,the complement system and the diseases of aging显示文摘 | McGeer EG Klegeris A McGeer PL | 2005 | Neurobiol Aging2005，26，1： | 1 |
| 6 | Impact of problem-based learning in a large classroom setting:student perception and problem-solving skills显示文摘 | Klegeris A Hurren H | 2011 | Adv Physiol Educ2011，35，4： | 1 |
| 7 | beta-amyloid protein enhances macrophage production ofoxygen free radicals and glutamate 显示文摘 | Klegeris A McGeer PL | 1997 | J Neurosci1997，49，2： | 1 |
| 8 | Inflammation,the complement system and the diseases of aging显示文摘 | McGeer EG Klegeris A McGeer PL | | 0，，1： | 1 |
| 9 | Therapeutic approaches to in-flammation in neurodegenerative disease显示文摘 | Klegeris A McGeer EG McGeer PL | 2007 | Curr Opin Neurol2007，20，： | 1 |
| 10 | Proton pump inhibitorsreduce interferon-γ-induced neurotoxicity and STAT3phos-phorylation of human astrocytes显示文摘 | Hashioka S Klegeris A McGeer PL | 2011 | Glia2011，59，5： | 1 |
| 11 | Interaction of Alzheimer' s beta-amyloid peptidewith the human monocytic cell line THP-1results in a protein kinase C-dependent secretionof tumor necrosis factor-alpha显示文摘 | Klegeris A Walker DG McGeer PL | 1997 | Brain Res1997，747，1： | 1 |
| 12 | Chymotrypsin-like proteases contribute to human monocytic THP-1 cell as well as human microglial neurotoxicity显示文摘 | Klegeris A McGeer PL | 2005 | Glia2005，51，1： | 1 |
| 13 | Impact of problem - based learning in a largeclassroom setting: student perception and problem - solving skills 显示文摘 | Klegeris A Hurren H | 2011 | Adv Physiol Educ2011，35，4： | 1 |
| 14 | Severe vascular disturbance in a case of familial brain calcinosis显示文摘 | Judit Miklossy Ian R. Mackenzie Katerina Dorovini-Zis Donald B. Calne Zbigniew K. Wszolek Andis Klegeris Patrick L. McGeer | 2005 | Acta Neuropathologica2005，，6： | 1 |
| 15 | α-Synuclein activates kinases and induces neurotoxic responses In human THP-1 and microglial cells显示文摘 | Klegeris A Pelech S Giasson BI | 2008 | NeurobiolAging2008，29，5： | 1 |
| 16 | Improvement in generic problem-solving abilities of students by use of tutor-less problem- based learning in a large classroom setting显示文摘 | Klegeris A Bahniwal M Hurren H | 2013 | CBE Life SciEduc2013，12，1： | 1 |
| 17 | Modulation of microglial functions by methyl jasmonate显示文摘Neuroinflammation contributes to the neurodegenerative processes in Alzheimer's disease(AD);therefore,characterization of novel drug candidates aimed at combatting inflammation in the central nervous system is one of the potential avenues for the development of effective AD treatment and prevention strategies.Non-neuronal microglial cells orchestrate neuroinflammatory reactions,and their adverse activation has been linked to AD pathogenesis.Methyl jasmonate(MJ) has anti-cancer properties and has also been shown to reduce peripheral inflammation in pre-clinical models.Recently,anti-neuroinflammatory activity of MJ was demonstrated in mice,but the exact cellular and molecular mechanisms responsible for this beneficial effect are unknown.We hypothesized that MJ can regulate select microglial functions,and used two different in vitro models of microglia to test this hypothesis.MJ inhibited the production of damaging reactive oxygen species by differentiated human HL-60 promyelocytic leukemia cells without reducing their viability.MJ also selectively upregulated phagocytic activity of murine BV-2 microglia,but had no effect on nitric oxide secretion by these cells.Since microglial phagocytosis can be beneficial for clearance of amyloid β aggregates in AD,the observed upregulation of phagocytic activity by MJ,combined with its inhibitory effect on reactive oxygen species production,supports continued studies of MJ as a candidate drug for managing adverse neuroinflammation in AD. | Jordan A.McKenzie Andis Klegeris | 2018 | Neural Regeneration Research2018，13，7： | 1 |
| 18 | Therapeutic approaches to inflammation in neurodegenerative disease显示文摘 | Klegeris A McGeer EG McGeer PL | 2007 | Curr Opin Neurol2007，20，3： | 1 |
| 19 | Expression of complement messenger RNAs and proteins by human oligodendro- glial cells显示文摘 | HosokawaM Klegeris A Maguire J etal | 2003 | Glia2003，42，： | 1 |
| 20 | Antidepressants inhibit interferon-gamma-induced microglial production of IL-6 and nitric oxide显示文摘 | Hashioka S Klegeris A Monji A Kato T Sawada M Mcgeer PL | 2007 | Exp Neurol2007，206，1： | 1 |
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