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Titolo:
Neuronal cell death in nervous system development, disease, and injury (Review)
Autore:
Martin, LJ;
Indirizzi:
Johns Hopkins Univ, Sch Med, Div Neuropathol & Neurosci, Dept Pathol, Baltimore, MD 21205 USA Johns Hopkins Univ Baltimore MD USA 21205 Pathol, Baltimore, MD 21205 USA
Titolo Testata:
INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE
fascicolo: 5, volume: 7, anno: 2001,
pagine: 455 - 478
SICI:
1107-3756(200105)7:5<455:NCDINS>2.0.ZU;2-O
Fonte:
ISI
Lingua:
ENG
Soggetto:
AMYOTROPHIC-LATERAL-SCLEROSIS; AMYLOID PRECURSOR PROTEIN; TRANSIENT CEREBRAL-ISCHEMIA; FAMILIAL ALZHEIMERS-DISEASE; RETINAL GANGLION-CELLS; BCL-X-L; INTERNUCLEOSOMAL DNA CLEAVAGE; MITOCHONDRIAL CYTOCHROME-C; HIPPOCAMPAL CA1 NEURONS; TUMOR-SUPPRESSOR P53;
Keywords:
Alzheimer's disease; amyotrophic lateral sclerosis; cell death; cerebral ischemia; motor neuron degeneration; stroke; traumatic brain injury; apoptosis-necrosis continuum;
Tipo documento:
Review
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
211
Recensione:
Indirizzi per estratti:
Indirizzo: Martin, LJ Johns Hopkins Univ, Sch Med, Div Neuropathol & Neurosci, Dept Pathol, 720 Rutland Ave, Baltimore, MD 21205 USA Johns Hopkins Univ 720 Rutland Ave Baltimore MD USA 21205 5 USA
Citazione:
L.J. Martin, "Neuronal cell death in nervous system development, disease, and injury (Review)", INT J MOL M, 7(5), 2001, pp. 455-478

Abstract

Neuronal death is normal during nervous system development but is abnormalin brain and spinal cord disease and injury. Apoptosis and necrosis are types of cell death. They are generally considered to be distinct forms of cell death. The re-emergence of apoptosis may contribute to the neuronal degeneration in chronic neurodegenerative disease, such as amyotrophic lateral sclerosis and Alzheimer's disease, and in neurological injury such as cerebral ischemia and trauma. There is also mounting evidence supporting an apoptosis-necrosis cell death continuum. In this continuum, neuronal death can result from varying contributions of coexisting apoptotic and necrotic mechanisms; thus, some of the distinctions between apoptosis and necrosis are becoming blurred. Cell culture and animal model systems are revealing the mechanisms of cell death. Necrosis can result from acute oxidative stress. Apoptosis can be induced by cell surface receptor engagement, growth factor withdrawal, and DNA damage. Several families of proteins and specific biochemical signal-transduction pathways regulate cell death. Cell death signaling can involve plasma membrane death receptors, mitochondrial death proteins, proteases, kinases, and transcription factors. Players in the cell death and cell survival orchestra include Pas receptor, Bcl-2 and Bar (and their homologues), cytochrome c, caspases, p53, and extracellular signal-regulated protein kinases. Some forms of cell death require gene activation, RNA synthesis, and protein synthesis, whereas others forms are transcriptionally-translationally-independent and are driven by posttranslational mechanisms such as protein phosphorylation and protein translocation. A better understanding of the molecular mechanisms of neuronal cell death in nervous systemdevelopment, injury and disease can lead to new therapeutic approaches forthe prevention of neurodegeneration and neurological disabilities and willexpand the field of cell death biology.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 18/01/20 alle ore 11:23:41