自引率: 暂无数据
被引量: 0
通过率: 暂无数据
审稿周期: 2
版面费用: 暂无数据
国人发稿量: 暂无数据
投稿须知/期刊简介:
The journal provides a focus for communication among neuroscientists geneticists neurodevelopmental pediatricians and behavioral scientists interested in clinical or basic science research in aspects of brain development and function. The journal is an international forum for the exchange of novel and significant information on broad aspects of developmental disabilties. The journal offers timely publication of scientific reviews as well as editorial commentaries and other items of general interest to its readers. As the field of developmental disabilities represents a multi-disciplinary research arena the reviews commentaries and other editorial text must be written in clear authoritative yet accessible and jargon-free prose. The journal is intended for scientists and clinical practitioners in such areas as clinical developmental and rehabilitation psychology; developmental neurobiology; human medical and molecular genetics; molecular biology; neurology; pediatrics; pharmacology; physical medicine and rehabilitation; and psychiatry. Each issue is topic­oriented. Future topics are listed in sufficient time to permit letters of inquiry about proposed articles. Although most articles are invited research reviews by leaders in the field unsolicited proposals will be considered.
-
Pathophysiology, prevention, and potential treatment of neural tube defects.
Neural tube defects (NTD) remain a major cause of morbidity in spite of the reduction in liveborn incidence with periconceptional folic acid. However, the etiology remains unknown. This article reviews studies that address causation and potential treatment of NTD in humans and in animal models that resemble aspects of the common human NTD. Studies of nutritional markers of vitamin B12 and folic acid support a defect in homocysteine metabolism; a thermolabile variant of methylene tetrahydrofolate reductase, an enzyme that remethylates homocysteine to methionine, correlates with a risk of NTD in some human populations. Numerous mouse mutant models of NTD exist, attesting to the ease of disruption of neurulation, and a genetic basis for this malformation. Of these models, the curly tail mouse mutant most closely resembles the common human NTD. Folic acid does not prevent NTD in this model; however inositol supplementation does result in a significant reduction in incidence. Recent advances in fetal surgery, and evidence from mechanically created myelomeningocele in large animals amenable to surgical intervention suggest that the handicaps associated with myelomeningocele and associated Chiari Type II malformation may be prevented by in utero NTD closure. Success will depend on preservation of neurological tissue until such intervention is possible. Further research in animal models at the genetic and cellular levels, together with technological surgical advances, provide hope that prevention of more NTD and the associated handicaps may be possible. MRDD Research Reviews 6:6-14, 2000.
被引量：13 发表：2000
