Neuronal cell death : a demise with different shapes

Nicotera, Pierluigi; Leist, Marcel; Manzo, Luigi

Neuronal cell death : a demise with different shapes

Dateien

Zu diesem Dokument gibt es keine Dateien.

Datum

1999

Autor:innen

Nicotera, Pierluigi

Leist, Marcel

Manzo, Luigi

Publikationstyp

Zeitschriftenartikel

Publikationsstatus

Published

Erschienen in

Trends in Pharmacological Sciences. 1999, 20(2), pp. 46-51. ISSN 0165-6147. Available under: doi: 10.1016/S0165-6147(99)01304-8

Zusammenfassung

Severe neuronal loss is common to many neurodegenerative diseases. Although necrotic features are often prevalent in neuropathological conditions, there is now increasing evidence to show that apoptosis can significantly contribute to neuronal demise in neurodegenerative diseases, including Huntington's and Alzheimer's diseases and HIV-associated dementia. Furthermore, a role in other disorders such as stroke, trauma, Parkinson's disease, multiple sclerosis and amyotrophic lateral sclerosis has been suggested from animal studies1. Nevertheless, it is unclear which of the two types of demise, apoptosis or necrosis, prevail in acute and slowly developing neurogenerative disorders, and whether the mode of cell death is relevant for the ultimate progression of the disease.
The debate on the occurrence and prevalence of either type of death in pathological conditions such as stroke or neurotoxic injury could be resolved in part by considering that different types of cell death within a tissue reflect either the complete or the partial execution of a common death programme. Some endogenous mediators might modulate the shape (morphological appearance) of cells in the death process; such modulation could have implications for the neighbouring tissue by interfering with the execution of apoptosis-specific subroutines, thereby changing apoptosis to necrosis.

Fachgebiet (DDC)

570 Biowissenschaften, Biologie

Schlagwörter

Pharmacology, Cell biology, apoptosis, nitric Oxide, necrosis, excitotoxicity, neurodegeneration, caspase, ATP

Zitieren

ISO 690

NICOTERA, Pierluigi, Marcel LEIST, Luigi MANZO, 1999. Neuronal cell death : a demise with different shapes. In: Trends in Pharmacological Sciences. 1999, 20(2), pp. 46-51. ISSN 0165-6147. Available under: doi: 10.1016/S0165-6147(99)01304-8

BibTex

@article{Nicotera1999Neuro-20161,
  year={1999},
  doi={10.1016/S0165-6147(99)01304-8},
  title={Neuronal cell death : a demise with different shapes},
  number={2},
  volume={20},
  issn={0165-6147},
  journal={Trends in Pharmacological Sciences},
  pages={46--51},
  author={Nicotera, Pierluigi and Leist, Marcel and Manzo, Luigi}
}

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    <dcterms:abstract xml:lang="eng">Severe neuronal loss is common to many neurodegenerative diseases. Although necrotic features are often prevalent in neuropathological conditions, there is now increasing evidence to show that apoptosis can significantly contribute to neuronal demise in neurodegenerative diseases, including Huntington's and Alzheimer's diseases and HIV-associated dementia. Furthermore, a role in other disorders such as stroke, trauma, Parkinson's disease, multiple sclerosis and amyotrophic lateral sclerosis has been suggested from animal studies1. Nevertheless, it is unclear which of the two types of demise, apoptosis or necrosis, prevail in acute and slowly developing neurogenerative disorders, and whether the mode of cell death is relevant for the ultimate progression of the disease.&lt;br /&gt;The debate on the occurrence and prevalence of either type of death in pathological conditions such as stroke or neurotoxic injury could be resolved in part by considering that different types of cell death within a tissue reflect either the complete or the partial execution of a common death programme. Some endogenous mediators might modulate the shape (morphological appearance) of cells in the death process; such modulation could have implications for the neighbouring tissue by interfering with the execution of apoptosis-specific subroutines, thereby changing apoptosis to necrosis.</dcterms:abstract>
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