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´¦¥Üºñ¯ù´£¨úª«¥i¦¨¬°¯«¸g¬r©Ê§í¨î¾¯ì²z http://med.sina.com/article_detail_103_1_34860.html "Á{§É«eÃÒ¾Úªí©ú¡Aºñ¯ù¯ù¦h×ôªº¥Dn²Õ¦¨³¡¤À³QºÙ¬°EGCG¡]ªí¨S¹¤l¨à¯ù¯À¨S¹¤l»Äà¡^¡A¯à°÷¤zÂZªüº¸¯÷®üÀq¯g±wªÌ¤j¸£¤¤¬r©Ê§C»Eª«ªº²Õ¸Ë§Î¦¨¡A¦b¤À¤l¯ÅÁpªº¦´Á¨BÆJ¡A³o¬O¾ÉP±wªÌ»{ª¾¯à¤O¤U°ªº«n¦]¯À¤§¤@¡C" ³o¦³²§¦±¦P¤u¶Ü? ¶È¨Ñ°Ñ¦Ò ÁÂÁ¤j®a! |
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·|û¡G²q·Q10136148 µoªí®É¶¡:2017/10/16 ¤W¤È 11:41:41²Ä 250 ½g¦^À³
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ªâÄõ¾ÇªÌ¼¶¼gªº " S-ketamine for the treatment of depression " Kaija Järventausta, Olli Kampman, Arvi Yli-Hankala,Esa Leinonen http://www.psykiatriantutkimussaatio.fi/uploads/files/PF_2015/PF2015_ART1.pdf ¨ä¤¤¦³´£¤ÎR-ketamineªºÀø®Ä©M°Æ§@¥Î , ©Î³\¤Þ¥Î¤£¦P¥X³Bµy¦³¬»Ä² , ¤]½Ð¤j®a°Ñ¦Ò ... Clinical efficacy of S-ketamine in major depression In a recent preclinical study, S-ketamine was reported to have a poorer and shorter antidepressant effect than R-ketamine in mice (42). The authors suggested that R-ketamine may be a more potent antidepressant, relative to S-ketamine, and that R-ketamine may also have less psychotomimetic side effects. In another clinical report, however, S-ketamine caused less adverse psychotomimetic effects compared to racemic ketamine in two patients having MDD, although showing a similar antidepressive effect (43) Adverse effects of S-ketamine S-ketamine has been reported to induce more psychotic symptoms, loss of interest and emotional withdrawal compared with R-ketamine in healthy volunteers (30). In a study of ten healthy volunteers receiving R- or S-ketamine, the incidence of subjective side effects was low, but more frequently associated with R- than S-ketamine (38). The most common symptoms were drowsiness, dizziness, drunkenness, sensation of floating, distorted body experience and distorted vision/hearing (38). In repeated S-ketamine infusions in six TRD patient samples, two patients reported pronounced dissociative symptoms (45). Contrarily, S-ketamine has been reported to be better tolerated with fewer adverse psychotomimetic effects than R-ketamine in two depressive patients (43). ... ¶È¨Ñ°Ñ¦Ò ÁÂÁ¤j®a! |
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·|û¡G²q·Q10136148 µoªí®É¶¡:2017/10/16 ¤W¤È 07:01:39²Ä 249 ½g¦^À³
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¹ï¤£°_! §ó¥¿¤@¤U "«Ü´Á«Ý¸ÕªÌ¸Ñ´b ÁÂÁ¤j®a!" §ï¬° «Ü´Á«ÝÃѪ̤j¤j¸Ñ´b ÁÂÁ¤j®a! ÁÂÁ¤j®a! |
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¦³¤@½g2006¥Xª© , ³Q¤Þ¥Î¶W¹L600¦¸ªº½×¤å " Glia-Derived d-Serine Controls NMDA Receptor Activity and Synaptic Memory " http://www.cell.com/cell/fulltext/S0092-8674(06)00506-X As d-serine is released exclusively by astrocytes, we studied the physiological impact of the glial environment on NMDA receptor-dependent activity and plasticity. ¥t¤@½g¥ÑHerman Wolosker, Darrick T. Balu , Joseph T. Coyle ©Ò¼¶¼gªº " The Rise and Fall of the d-Serine-Mediated Gliotransmission Hypothesis " (¥u¦³ºKn) http://www.sciencedirect.com/science/article/pii/S0166223616301187 «oªí©ú d-Serine Is Not a Gliotransmitter ³o¨â½g½×¤å¤¤¶¡ , ¬O§_¦³½Ä¬ð©O? ¤pªºµLªk¬Ý¨ì²Ä¤G½g¥þ¤å , ¤£±o¨ä¸Ñ «Ü´Á«Ý¸ÕªÌ¸Ñ´b ÁÂÁ¤j®a! ¥t¥~½Ð±Ð¤j®a R-ketamine ¦³¦¨Å}©Êªº°ÝÃD¶Ü? ÁÂÁÂ! |
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¤p¨k¤j ¤p§Ìªº¬Ýªk¬O °ò¥»±¤~¬Oªø´Á¥D¾ÉªÑ»ùªºÅQ¥D ¨ä¥L©Î³\¦h¬OªK¸` ¥¼¸g¤½¥qÃҹꪺ¦¨¤À Y±z¦³¿³½ì ½Ð°Ñ¦Ò¬Ý¬Ý Evaluation of cytotoxic, apoptotic, mutagenic, and chemopreventive activities of semi-synthetic esters of gallic acid http://www.sciencedirect.com/science/article/pii/S0278691517302107 In conclusion, our results suggest that alkyl gallates are non-genotoxic, non-mutagenic, and pro-apoptotic agents, which may serve as suitable and promising candidates for preventing chemically-induced chromosomal damage. Gallic acid, one of the components in many plant tissues, is a potential inhibitor for insulin amyloid fibril formation http://www.sciencedirect.com/science/article/pii/S0223523414007260 Gallic acid interacts with £\-synuclein to prevent the structural collapse necessary for its aggregation http://www.sciencedirect.com/science/article/pii/S1570963914001058 Gallic acid is the major component of grape seed extract that inhibits amyloid fibril formation http://www.sciencedirect.com/science/article/pii/S0960894X13011451 ºKn ³\¦h³J¥Õ½è¿ù»~§éÅ|¯e¯f¡A¨Ò¦pªüº¸¯ý®üÀq¯f¡A©¬ª÷´Ë¤ó¯g©M¦ë§Ê¹y³J¥Õ½è¡A¨ä¯S¼x¦b©ó³J¥Õ½è»E¶°Åé¥H¾ý¯»¼Ë³J¥ÕìÅÖºû§Î¦¡ªº¿n²Ö¡C§í¨îìÅÖºû§Î¦¨ªº¤ÑµM²£ª«¬O±´¯ÁªvÀø³o¨Ç¯e¯fªº¦³§Æ±æªº³~®|¡C¦b³o¶µ¬ã¨s¤¤¡A§Ṳ́w¸gÅã¥Ü¡A¨Ï¥ÎÅé¥~²¸³J¥Õ¶À¯ÀT´ú©w©M³z®g¹q¤lÅã·LÃè¡A¸²µå¬ó´£¨úª«§í¨îìÅÖºû§Î¦¨ªº£e-¹T³J¥Õ¡]£e-CN¡^¡A¤@ºØ¦b¥Í²z±ø¥ó¤U¦Ûµo§Î¦¨¾ý¯»¼Ë³J¥ÕìÅÖºûªº¨Å³J¥Õ¡C¦b¸²µå¬ó´£¨úª«ªº¦¨¤À¤¤¡A¨S¹¤l»Ä¬O§í¨î£e-CNìÅÖºû§Î¦¨³Ì¬¡ÅDªº¦¨¤À¡A³q¹Léw£e-CN¥H¨¾¤î¨ä»E¶°¡C¦P®É¡A¨S¹¤l»ÄÅãµÛ°§C£e-CN¹ï¶Ý»Ì²ÓM½F12²ÓMªº¬r©Ê¡C¦¹¥~¡A¨S¹¤l»Ä³q¹L¾ý¯»¼Ë³J¥Õ-£]肽¦³®Ä¦a§í¨îìÅÖºû§Î¦¨¡A¾ý¯»¼Ë£]肽¬Oªüº¸¯ý®üÀq¯f¤¤ªº±À©wªºP¯f¦]¤l¡Cµ²½×¬O¨S¹¤l»Äೡ¤À¨ã¦³ìÅÖºû§í¨î¬¡©Ê¡C(goole ½Ķ) ¶È¨Ñ°Ñ¦Ò ÁÂÁ¤j®a! |
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ÁÂÁ Vela ¤j¤jµy¨Ó¼öÄËÄ˪º°T®§ «e´X¤Ñ¤p§Ì¤~è¬Ý¨ìintepirdine¤T´ÁÁ{§Én¸Ñª¼ªº·s»D µL©`¤µ¤Ñ´N¶Ç¥X¥¢±Ñªº®ø®§ ³oÓ¤T´Á¶W¹L1300¤H¤j«¬Á{§ÉªºIntepirdine¦b¤G´ÁÁ{§É®É ¬O¥Ñ¤j¼tGSK°µªº Axovant±µ¤â¤T´Á ±ÂÅvªº±ø¥óÁÙ¤£®t If intepirdine receives marketing approval, AXON will have to share some of the spoils with GlaxoSmithKline, including $155 million in milestones, which are payable upon approval and following achievement of $1.2 billion in annual revenue from intepirdine, as well as a 12.5% royalty on net sales. µM¦Óintepirdine¤G´ÁÁ{§É¼Æ¾Ú ªíÆ[¨Ó¬Ý¦n¹³¥u¦³¥¥ ½Ð°Ñ¤U¦C¤åÄm Double-blind, controlled phase II study of a 5-HT6 receptor antagonist, SB-742457, in Alzheimer¡¦s disease https://www.ncbi.nlm.nih.gov/pubmed/20043816 RESULTS: 371 subjects were randomized. In the ITT population (n=357), linear trend analysis at Week 24 suggested a dose response for CIBIC+ with a mean slope of -0.05 points/5-mg dose increase (95% confidence interval [CI]: -0.09, -0.01; p=0.016). The dose response slope for change from baseline in ADAS-Cog was -0.22 points/5-mg dose increase (95% CI: -0.45, 0.01; p=0.059). The adjusted mean treatment difference from placebo at Week 24 for SB-742457 35 mg (-0.31) was significant on CIBIC+ (95% CI: -0.62, -0.00; p=0.047) but non-significant on ADAS-Cog (-1.28 [95% CI: -2.96, 0.40]; p=0.135). Adverse events occurred in 24-37% in the SB-742457 groups vs 29% for placebo; 11-16% discontinued SB-742457 vs 15% for placebo. ¦A¨Ó¬Ý¤ß®®ªºSND14ªºII(a)¼Æ¾Ú ¥ÑÂÅ¥ý¤¸±Ð±Â©MªL¼äªY³Õ¤hÂå®v©Ò¥Ó½Ðªº±M§Q¤å¥ó http://appft1.uspto.gov/netacgi/nph-Parser?Sect1=PTO1&Sect2=HITOFF&d=PG01&p=1&u=/netahtml/PTO/srchnum.html&r=1&f=G&l=50&s1=20170216234.PGNR. Á{§É¼Æ¾Ú Outcome Measures [0059] The mean.+-.SD scores of both primary and secondary outcomes--including ADAS-cog, additional cognition composite, and CIBIC-plus--of the two groups of patients are shown in FIG. 3, Table 2. At week 0 (baseline), there were no significant differences between the two groups in ADAS-cog and additional cognition composite (p=.75 and p=.2.7, respectively). [0060] For the primary outcome, sodium benzoate produced greater improvement in ADAS-cog score than the placebo therapy throughout the study (mean differences from baseline were 3.8, 5.4, 5.9, and 5.9 in the benzoate group and 2.4, 1.7, 2.7, and 1.7 in the placebo group, at weeks 8, 16, 24, and endpoint; p=.3730, p=.0021, p=.0116, and p=.0031, respectively), with effect size of .86 at the end of the study (FIG. 3, Table 2). The results were similar when the baseline ADAS-cog score was controlled in the GEE model (FIG. 7, Table 6). [0061] For the secondary outcomes, sodium benzoate was better than placebo in the additional cognition composite at endpoint (p=.007, effect size=.78). Benzoate treatment also produced greater improvement m CIBC-plus score than placebo therapy at week 16 (p=.015), week 24 (p=.016), and endpoint (p=.012, effect size=.73 at endpoint) (FIG. 3, Table 2). [0062] The dropout rate (3.3%) of the sodium benzoate group tended to be lower than that (16.7%) of the placebo group, yet insignificantly (p=.195). [0063] For subgroup analysis, we further examined efficacy of sodium benzoate versus placebo in CDR .5 and CDR 1 subgroups. For ADAS-cog, sodium benzoate produced greater improvement than placebo therapy at weeks 16 and 24 and endpoint (p=0151, p=.0387, and p=.0092, respectively) in the CDR 1 subgroup. However, sodium benzoate was not superior to the placebo therapy in the CDR .5 subgroup throughout the study (p>.05) (FIG. 4, Table 3). [0064] Sodium benzoate showed better efficacy in the CDR 1 subgroup (p=.041) and borderline significance in the CDR .5 subgroup (p=.063) in improving the additional cognition composite (FIG. 5, Table 4). For CIBIC-plus, sodium benzoate produced greater improvement than placebo therapy at week 24 and endpoint (p=.040 and p=.018, respectively) in the CDR 1 subgroup but not in the CDR .5 subgroup (FIG. 6, Table 5).
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NaBen ªº¦hºØ§@¥Î¤w¦p«ez , ³o¬ONaBen¦Û¤vnµo´§ªº¥»¨Æ ¦Ó¦w¼¢¾¯ªº®ÄÀ³¬On¥ÎSPCD¨Ó°§C¥¦ªº¼vÅT "REDUCING THE RISK, TIME AND COST OF CLINICAL R&D WITH TRIMENTUM(TM) SEQUENTIAL PARALLEL COMPARISON DESIGN TRIALS "¤å³¹ùØ»¡¨ì http://c.eqcdn.com/_b4bc1d9f9ee3090c76740b4712627618/vistagen/db/263/503/pdf/TrimentumWhitepaper+Final+June2016.pdf " In every study, the placebo response was markedly reduced in Stage 2 compared to Stage 1. This serves to demonstrate the effectiveness of Trimentum Stage 1 in identifying non-responders within the placebo arm, as well as the continued lower placebo response among Stage 1 placebo non-responders in Stage 2. ¦Ó Trimentum™ ´N¬O¦Ñ¥v¤j¤j´£°_ªº (Sequential Parallel Comparison Design, SPCD; Fava et al., 2003) ©Ò¥HNaBen Y¯à¦Û¤vµo´§ÃÄ®Ä , ¥[½ÑÁ{§ÉSPCD³]p´î§C¦w¼¢¾¯ªº®ÄÀ³ §Ú̧ƱæSND1¨t¦C ¦¤é¦¨¥\ ³yºÖ¤H¸s ¶È¨Ñ°Ñ¦Ò ÁÂÁ¤j®a |
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¤S§ä¨ì¤@Ó 2017/8/8 Core-shell particles, preparation process thereof, and composition containing the same http://patft.uspto.gov/netacgi/nph-Parser?Sect1=PTO2&Sect2=HITOFF&p=1&u=%2Fnetahtml%2FPTO%2Fsearch-bool.html&r=1&f=G&l=50&co1=AND&d=PTXT&s1=%22SYNEURX+INTERNATIONAL+CORP%22&OS= Inventors: Shieh; Dar-Bin (Tainan, TW) Assignee: SYNEURX INTERNATIONAL CORP. (Taipei, TW) |
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²q·Q¤j¡A SND5¬O¹wpnªvÀøÄY«¥¢´¼¯g¡A ±Ð±Â¦b¤µ¦~ªÑªF·|®É¡A«Ü¿³¾Äªº»¡SND5¬O¨ì¥Ø«e¬°¤î¥L©Ò¬Ý¨ì°Êª«¹êÅ礤°T¸¹³Ì±jªº¡A ¤ñ²{¦b¤ß®®Âi±¤WªºÃĪ«ÁÙn±j¡C ¥L¤]nªÑªF¬Û«H¥Lªº§PÂ_¡A¦Ó¥Lªº§PÂ_¦Ü¤µ¨S¦³¥¢·Ç¹L¡C ¥H±Ð±Â¦b¾Ç¬É»PÂå¬É¤è±²Ö¿nªº¸ê¾ú¡A¤p§Ì¬Û«H¥Lªº§PÂ_¡C |
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Åý§Ú̦A½Æ²ß¤@¤Uf¥Ò»Ä¶uªvÀø¦´Áªü¯÷®üÀq¯gªºÁ{§É³ø§i Benzoate, a D-Amino Acid Oxidase Inhibitor, for the Treatment of Early-Phase Alzheimer Disease: A Randomized, Double-Blind, Placebo-Controlled Trial Chieh-Hsin Lin, Ping-Kun Chen, Yue-Cune Chang, Liang-Jen Chuo, Yan-Syun Chen, Guochuan E. Tsai, Hsien-Yuan Lane http://www.biologicalpsychiatryjournal.com/article/S0006-3223(13)00739-7/fulltext |
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2015.3µoªíªºGlyx-13(Rapastinel¡B2016.1.31ÀòBTD)ªºphase2aÁ{§É³ø§i«Ü¦³·N«ä¡A§Ú¤£¬On¤À¨Éµw±õ±õªºÁ{§É¼Æ¾Ú ³o½g³ø§i¦³·N«ä¤§³B¬O¤@¶}©l´N´£¨ìºë¯«¬ìÃĪ«¶}µoªº²{¹ê§x¹Ò¡G¡u·í§ó¦hªº¤½¥q¤¤¤î¬ã¨sºë¯«¯e¯f¥ÎÃĮɡK¡K¡vAs more companies have discontinued psychiatric drug research, early POC(proof of concept) studies have assumed increasing importance for those companies that continue to do research in this area by guiding decisions as to whether further investment in a molecule or a mechanism of action is justified¡C©Ò¥HPOCÁ{§É«Ü«n¡A¥i¥H´£¨ÑÃļt¨M©w¬O§_§ë¤J§ó¦hªºª÷¿ú¶i¦æ§ó¤j³W¼Òªº¤HÅéÁ{§É¡Cµ²½×¤S¦A¤@¦¸´£¨ì¡APOC studies, such as the one described here, play a pivotal role in allowing drug researchers to decide whether to move forward with larger and more expensive studies and enable them to focus available resources on those molecules that appear to have the most therapeutic promise¡C¶}µoGlyx-13ªº³o®a¤½¥q¨S¦h¤[´N³QAllergan¬Ý¤W¤F ¤W¤å§@ªÌSheldon Preskorn¨Ó¦Û³ôÂÄ´µ¤j¾ÇÂå¾Ç°|¡A¥L¦b2014¦~¤@¤ëªº¤å³¹´N¤w´£¨ìºë¯«¬ìÃĪ«¶}µoªº§x¹Ò¡¨In the last several years, a number of pharmaceutical companies have reduced or altogether stopped efforts to develop new psychiatric medications. The reasons are cost and the speculative nature of such development programs, due to the absence of substantive knowledge of the pathophysiology and pathoetiology underlying specific psychiatric illnesses¡¨³Ìªñ³o´X¦~¡A³\¦hÃļt´î¤Ö±N¤ß¤O©ñ¦b·sªººë¯«¬ìÃĪ«¬ãµo¤W¡A¬Æ¦Ü¬O§¹¥þ°±¤î§V¤O¤F ·í2005¦~¤@¤ëºë¯«¤Àµõ¯f«¶q¯ÅªºCATIEµ²ªG¥XÄl«á¡Aunder intensifying pressure to rein in costs, several large companies, including London-headquartered AstraZeneca and GlaxoSmithKline, chose to pull out of psychiatric pharmacology altogether.¦b¥[±j±±¨î¦¨¥»ªºÀ£¤O¤U¡A«Ü¦h¤jÃļt©ñ±ó¤£·F¤F¡A¦pªü´µ¯S±¶§Q±d©M¸¯Äõ¯À ³o¼Ë¥i¥H²z¸ÑCNS BTDªº¬Ã¶Q§a¡A¦pªG²{¹ê¤@ÂI±q¤jÃļtªº¨¤«×¨Ó¬Ý¡ACNS BTDªº»ùÈÀ³¸Ó§ó¡K¡K ¥u¥i±¤¡u¤Ñ¨ÏÌ¡v¤£À´¡A«D±`¨S¦³«H¤ß¡K¡K |
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·|û¡GVela10140988 µoªí®É¶¡:2017/9/8 ¤U¤È 07:45:58²Ä 82 ½g¦^À³
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·|û¡G³¯ÀR10141886 µoªí®É¶¡:2017/9/8 ¤U¤È 01:59:57²Ä 81 ½g¦^À³
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»OÆWªº¥Í§Þ§ë¸êªÌ¡]³Ð§ë¡B¤Ñ¨Ï¡B¦P·~¡^¦³´XÓ¯S©Ê¡G§ë¸êÃB«×¤p¡]¥Í§Þ¤½¥qµLªk²Ö¿n»È¼u½Ä¨ë¶i«×¡B¤Ï³Qn¨Dn¦³±ÂÅv¡B¦³¦¬¤J¡^¡A§ë¸ê´Á¶¡µu¡B¹ê»Ú±¡§Î¬O³y¦¨¥Í§Þ¤½¥qÄw½X±¹³³QÅ]°§k¨ì¡A»¡¬O¡u¤Ñ¨Ï¡v§ë¸ê¤H¦³¨Ç·¸¬ü¤F¡C¤ß®®¤d±i¥H¤Wªº½æ®a¤Ö»¡¤]¦³¤¦ì¡B¬Ý°_¨Ó¬O¼µ¹L¤FÅ]°¤§§k¡C |
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·|û¡G¤j¤á¤H®a10140174 µoªí®É¶¡:2017/9/8 ¤U¤È 12:11:50²Ä 80 ½g¦^À³
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½Ð°Ý¦³¤H¦³ª¾¹D©Î¬Opºâ³o¨Çì©lªÑªF©M³Ð§ë¤j·§ÁÙ¦³¦h¤Ö±in½æ? ¥xÆW³o¨Ç¤Ñ¨Ï§ë¸ê¤H°µªº¯uªº¬O¦³°÷µuªº,¤@¤W¿³Âd´N¶}©l½æ,½æ¤F¤@¦~¦hÁÙ¦b½æ.¤@°Æ´N¬On½æ¥úªº¼Ë¤l,¤@ÂI·ÀI³£¤£·Q©Ó¾á. |
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·|û¡G²q·Q10136148 µoªí®É¶¡:2017/9/8 ¤W¤È 08:36:43²Ä 79 ½g¦^À³
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¤ß®®ªºÁ{§É¸ÕÅç±N¤ÏÀ³ªÌ©w¸q¦b PANSS total score ¦³ 20% §ïµ½ªº±wªÌ ³oÀ³¸Ó¬O°Ñ¦Ò³s¥ý¤¸±Ð±Âªº NaBen ªºÁ{§É¼Æ¾Ú 21% ¦Ó¨Ó ·Q½Ð±Ð¤j®aªº¬O 21% À³¬O¤@Ó¥§¡È ¤]´N¬O»¡PANSS§ïµ½´T«×¦b21%¤W©Î¤Uªº¾÷·| ¦U¬ù¬°50% ³o¼Ë¬O§_¥i¥H»¡¤ß®® NaBen ªº¤ÏÀ³²v¬O³]©w¦b50%©O? ÁÂÁ¤j®a! |
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·|û¡G²q·Q10136148 µoªí®É¶¡:2017/9/7 ¤W¤È 08:39:01²Ä 78 ½g¦^À³
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¥ý¦æÁÂÁÂliaw6575 ¤jªº¸ÑªR ¤ß®®Á{§É¸ÕÅ窺SPCD³]p http://liawbf.pixnet.net/blog/post/47509275-spcd-%E6%98%AF%E5%BA%95 |
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·|û¡G²q·Q10136148 µoªí®É¶¡:2017/9/5 ¤U¤È 05:06:27²Ä 77 ½g¦^À³
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Extensive study on antidepressants in the US http://www.goinpharma.com/en/extensive-study-antidepressants-the-us/ A study on ketamine, among the most widely used molecules in neurology http://www.goinpharma.com/en/study-ketamine-among-the-most-widely-used-molecules-neurology/ ®a²À\¯N ÁÂÁ¤j®a! |
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·|û¡G²q·Q10136148 µoªí®É¶¡:2017/9/4 ¤U¤È 09:49:14²Ä 76 ½g¦^À³
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ÁÂÁ¦ѥv¤j¤jªº«ü¾É»¡©ú ¬Ý¨ì±z¹ï¤ß®®ÃĪ«ªº¬ã¨s¦p¼Æ®a¬Ã ¥H¥v¾Ç®aªººë¯«°O¿ýµÛºë¯«¬ìÃĪ«¾÷¨îªºµo®i¥v §óÅý¤H´Ü¨Øªº¬O±z¦b²³¦h½×¤å¤¤ªº²z¸Ñ ¤ÀªR»P¾ã¦Xªº¯à¤O ²`«pªº©³Ä¦b¤å³¹¤¤¦ÛµM¬yÅS ¹ï©ó¨ô¤å¡A¤p§ÌºÉ¯à¤O¦a¬Ý¡A¬ÝÀ´ªº©Î¬Ý¤£À´ªº ¥un¦³±zªº¥[«ù¡A¦³¨º¤@¥y«nªºµ²½×«K¦æ ¡u...¤]´N·|§ó¥[²z¸ÑSND14ªºMOA²Ï¹ê¡v ·PÁ±z¡I §ó¬ß±æ±z¦h¦h¬°¤å¨Ó±Ð¾É¤j®a¡A²¦³º¡AªY½à¤å³¹n¦³©¯ºÖªº·P°Ê¬O«ÜÃø±oªº ¦A¤@¦¸·P®¦¡I |
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·|û¡G¦Ñ¥v10140531 µoªí®É¶¡:2017/9/4 ¤U¤È 08:56:08²Ä 75 ½g¦^À³
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²q·Q¤jô £]-amyloidªº¨I¿n»Pªü¯÷®üÀq¯fªºÃö«Y«Ü½ÆÂø¡C«Ü¦h°·±dªøªÌ¸£¤¤¤]³Qµo²{«Ü¦h£]-amyloid¡Aµ¥¯Å¤£¨È©óªü¯÷®üÀq±wªÌ¡C ¶Ç²Î¬O¥Î¬t¡Ð18¼Ð°O¥h®ñ¸²µå¿}ªº¥¿¤l³y¼v¡A³o¥u¯àÆ[¹î¤ñ¸û±ß´ÁªºAD¡A¦pªGn¦bµo¯f«e´N³Q¶EÂ_¥X¨Ó¡A¥²¶·¦³§óÆF±Óºë±Kªº§Þ³N¡C2004¦~¤Ç¯÷³ù¤j¾ÇMathis »P Klunkµ¥¤H±N¥¿¤l³y¼v§Þ³N¤j¤j´£¤Éºë½T«×«á(Pittsburgh Compound-B¡BPIB-PET)³Q©^¬°¶Àª÷¼Ð·Ç¡CBerkeleyªºWilliam J. Jagust¦³¦h½g¤å³¹´N¬O§Q¥ÎPIB-PET°Q½×£]-amyloid plaques¡A§Ú¤Þ¤@¬q2011¦~10¤ëªº¤å¦r¡¨Applying the cutoff value of 1.6, we found that iPIB-PET(+) status was present in 89.6% (n = 17 out of n = 19) of the AD subjects, 69.8% (n = 43 out of n = 63) of the MCI subjects, and 47.9% (n = 9 out of n = 19) of the HC(healthy control)¡¨¡¨ Among all subjects, iPIB-PET(+) was present in 92.0% (n = 103 out of n = 112) of the AD subjects, 72.5% (n = 166 out of n = 229) of the MCI subjects, and 41.1% (n = 51 out of n = 124) of the HC¡¨¤j¬ù¤E¦¨ªºªü¯÷®üÀq¯f¤H¡B¤C¦¨MCI·|¥X²{PIB-PET(+)¡A¦ý¤]°ª¹F¥|¦¨¦hªº°·±dªøªÌ§e²{PIB-PET(+)¡A©ó¬Oµ²½×´£¨ì¡¨ Thus, elevated brain A£] levels alone are unlikely to explain typical AD dementia-associated patterns of brain atrophy, and additional factors downstream or independent of the A£] cascade may be necessary to cause the devastating brain atrophy in AD¡¨³æ³æ¥Î£]-amyloid¨I¿n¼W¥[¬O¤£¤Ó¥i¯à¸ÑÄÀªü¯÷®üÀq¬ÛÃöªº¤j¸£µäÁY¡AÀ³¸ÓÁÙ¦³¨ä¥Lªºì¦]¡C¨Ò¦p¥H¦â¦C¥x©Ôºû¤Ò¤j¾ÇDavid Gurwitz´N´£¥XRGS2³oÓ°ò¦] ±qWilliam J. Jagust¦b2011¦~ªº¤å³¹¥i¥H©¹«e«ä¦Ò1991¦~John Hardy°Ñ¦Òð¤ó¯g´£¥Xªº£]-amyloid precursor proteinªº°²»¡¦n¹³¤£°÷©P¥þ¡A¤]¥i¥H«ä¦Ò¤jÃļtªñ¤G¤Q¦~¼®¤O©ó©Þ°£¹Ó¸O¡B¦Z¤g¸O¦n¹³¨«¿ù¸ô¤F¡CµM«á¦A·Q·QSND14«P¶iNMDARªº¾÷Âà¡A¦pªG¯à±q1987¦~Timothy GreenamyreªºGlutamate transmission and toxicity in Alzhelmer¡¦s diseaseŪ°_¡A´N·|²M·¡¦ó¥H90¦~¥N«Ü¦h±M®a±qglycine site¹Á¸ÕD-cycloserine¡A¤]´N·|§ó¥[²z¸ÑSND14ªºMOA²Ï¹ê¡C |
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·|û¡G¤p·ç10140606 µoªí®É¶¡:2017/9/4 ¤W¤È 10:41:24²Ä 73 ½g¦^À³
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²q·Q¤j±z¦n, ¤p§Ì¤]¨Ó®¥¶P²q·Q¤j¶}ª©¡A¤p§Ì¯E¤Í¨¤À¡A«á¨Ó¦¨¬°¸Î¤Í¡A²{¦b«h¦h¤F¤ß¤Íªº¨¤À¡A¤@ª½ÀqÀq¸òÀH¥²´IªO¤W½Ñ¦ì«e½úªº¸}¨B¡A¤]·PÁªO¤W³\¦h±M·~ªº«e½ú¡A¦p : cliff¤j¡B¥v¤j¡A©M§ë¸êÆ[©À¤j®v : «¼CµL¾W¤j¡A¤@ª½¥H¨Óªº¤À¨É¡AÅý§Ú̳o¨Ç¤p´²¤á¥i¥H¦¨ªø©M¾Ç²ß¡A¤p§Ì¨ÃµL¥Í§ÞI´º±M·~¡A¥u¯à´N¦Û¤v¬Ý¨ì¦³·N«äªº¤å³¹©M¤j®a¤À¨É¡A³Ìªñ¬Ý¤F¤@½g¥x¤jºë¯«¬ìªL·Ô°aÂå®v©Ò¼¶¤pÃļtªº¬ãµo¶Ç©_¡G²Ä¤@Ó®ÖãªvÀø¡u¿ðµo©Ê¤£¦Û¥D¹B°Ê¡vªº·sÃÄ Valbenazine¡AÅý¤p§Ìı±o«D±`®¶¾Ä¡A½Ð¦U¦ì¤j¤j°Ñ¦Ò~ ³sµ²¦p¤U : pansci.asia/archives/119808 |
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