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Titolo:
Apoptosis and brain development
Autore:
Roth, KA; DSa, C;
Indirizzi:
Washington Univ, Sch Med, Dept Pathol & Immunol, St Louis, MO 63110 USA Washington Univ St Louis MO USA 63110 l & Immunol, St Louis, MO 63110 USA
Titolo Testata:
MENTAL RETARDATION AND DEVELOPMENTAL DISABILITIES RESEARCH REVIEWS
fascicolo: 4, volume: 7, anno: 2001,
pagine: 261 - 266
SICI:
1080-4013(2001)7:4<261:AABD>2.0.ZU;2-8
Fonte:
ISI
Lingua:
ENG
Soggetto:
PROGRAMMED CELL-DEATH; BCL-2 GENE FAMILY; X-DEFICIENT MICE; CYTOCHROME-C; NEURONAL DEATH; CEREBRAL-CORTEX; NERVOUS-SYSTEM; IN-VIVO; BAX; MITOCHONDRIA;
Keywords:
programmed cell death; apoptosis; Bcl-2; caspase; telencephalon; neurodevelopment;
Tipo documento:
Review
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Citazioni:
53
Recensione:
Indirizzi per estratti:
Indirizzo: Roth, KA Washington Univ, Sch Med, Dept Pathol & Immunol, Campus Box 8118,660 S Euclid Ave, St Louis, MO 63110 USA Washington Univ Campus Box 8118,660 S Euclid Ave St Louis MO USA 63110
Citazione:
K.A. Roth e C. D'Sa, "Apoptosis and brain development", MENT RET D, 7(4), 2001, pp. 261-266

Abstract

Neuronal cell death in the embryonic brain was first recognized almost a century ago. Its significance for normal nervous system development and function has been a major focus of neuroscientific investigation ever since. Remarkable progress has been made in defining the cellular processes controlling neuronal cell death and studies performed over the last ten years have revealed extensive homology between the molecules regulating programmed cell death in Caenorhabdids elegans and apoptosis in mammalian cells. Targetedgene disruptions of members of the bcl-2 and caspase gene families have demonstrated particularly significant roles for bcl-x, bax, caspase-9 and caspase-3 in mammalian brain development. As expected from previous studies ofsynapse-bearing neurons and neurotrophic factors, reduced neuronal cell death in mice bearing mutations in key pro-apoptotic molecules resulted in increased numbers of neurons in a variety of neuronal subpopulations. However, targeted gene disruptions also demonstrated a heretofore underappreciatedsignificance of neural precursor cell death and immature neuron death in nervous system development. Pathological activation of apoptotic death pathways may lead to neuroanatomic abnormalities and possibly to developmental disabilities. (C) 2001 Wiley-Liss, Inc.

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Documento generato il 02/04/20 alle ore 02:55:36