Schizophrenia: Neural mechanisms for novel therapies

被引：49
作者：
Sawa, A
Snyder, SH
机构：
[1] Johns Hopkins Univ, Sch Med, Dept Neurosci, Baltimore, MD 21205 USA
[2] Johns Hopkins Univ, Sch Med, Dept Psychiat & Behav Sci, Baltimore, MD 21205 USA
[3] Johns Hopkins Univ, Sch Med, Dept Pharmacol & Mol Sci, Baltimore, MD 21205 USA
来源：
MOLECULAR MEDICINE | 2003年 / 9卷 / 1-2期
关键词：
D O I：
10.1007/BF03402101
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
Although valuable antischizophrenic drugs exist, they only partially ameliorate symptoms and elicit substantial side effects. Classic neuroleptic drugs act by blocking dopamine receptors. They can relieve some symptoms but not behavioral withdrawal features that are designated "negative" symptoms. Clozapine and related newer atypical neuroleptics may be more efficacious in relieving negative symptoms. Understandng their actions may facilitate new drug discovery. Agents influencing glutamate neurotransmission and N-methyl-D-aspartate receptors, especially the cotransmitter D-serine, are promising. Stimulation of the alpha7 subtype of nicotinic acetylcholine receptor may also be efficacious. The search for genes linked to schizophrenic has revealed several leads that may permit development of novel therapeutic agents. Promising genes include disrupted-in-schizophrenia-1, dysbindin, and neuregulin.
引用
收藏
页码：3 / 9
页数：7
相关论文
共 44 条
[11]   DOPAMINE RECEPTOR-BINDING PREDICTS CLINICAL AND PHARMACOLOGICAL POTENCIES OF ANTI-SCHIZOPHRENIC DRUGS [J].
CREESE, I ;
BURT, DR ;
SNYDER, SH .
SCIENCE, 1976, 192 (4238) :481-483
[12]   Effect of COMT Val108/158 Met genotype on frontal lobe function and risk for schizophrenia [J].
Egan, MF ;
Goldberg, TE ;
Kolachana, BS ;
Callicott, JH ;
Mazzanti, CM ;
Straub, RE ;
Goldman, D ;
Weinberger, DR .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2001, 98 (12) :6917-6922
[13]   Schizophrenia: The broken P300 and beyond [J].
Ford, JM .
PSYCHOPHYSIOLOGY, 1999, 36 (06) :667-682
[14]   The emerging role of glutamate in the pathophysiology and treatment of schizophrenia [J].
Goff, DC ;
Coyle, JT .
AMERICAN JOURNAL OF PSYCHIATRY, 2001, 158 (09) :1367-1377
[15]   The gene encoding proline dehydrogenase modulates sensorimotor gating in mice [J].
Gogos, JA ;
Santha, M ;
Takacs, Z ;
Beck, KD ;
Luine, V ;
Lucas, LR ;
Nadler, JV ;
Karayiorgou, M .
NATURE GENETICS, 1999, 21 (04) :434-439
[16]   Catechol-O-methyltransferase-deficient mice exhibit sexually dimorphic changes in catecholamine levels and behavior [J].
Gogos, JA ;
Morgan, M ;
Luine, V ;
Santha, M ;
Ogawa, S ;
Pfaff, D ;
Karayiorgou, M .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1998, 95 (17) :9991-9996
[17]   Diet and trophic niche overlap of two ranid species in northern Italy [J].
Guidali, F ;
Scali, S ;
Carettoni, A .
ITALIAN JOURNAL OF ZOOLOGY, 2000, 67 (01) :67-72
[18]   The neuropathology of schizophrenia - A critical review of the data and their interpretation [J].
Harrison, PJ .
BRAIN, 1999, 122 :593-624
[19]   PRODH mutations and hyperprolinemia in a subset of schizophrenic patients [J].
Jacquet, H ;
Raux, G ;
Thibaut, F ;
Hecketsweiler, B ;
Houy, E ;
Demilly, C ;
Haouzir, S ;
Allio, G ;
Fouldrin, G ;
Drouin, V ;
Bou, J ;
Petit, M ;
Campion, D ;
Frébourg, T .
HUMAN MOLECULAR GENETICS, 2002, 11 (19) :2243-2249
[20]  
JAVITT DC, 1991, AM J PSYCHIAT, V148, P1301
12345