The DOI matches its Crossref record; 9 of the 9 references it cites were found in a registry or an index.
Neural apoptosis
Abstract
Apoptosis is a mode of cell death in which the cell plays an active role in its own demise. The study of neural apoptosis, the identification of genes controlling apoptosis, and the examination of the mechanisms by which these genes achieve their effects have assumed increasing importance over the past few years. This is because (1) neural apoptosis occurs not only in development, but also in pathophysiological states such as stroke, glutamate toxicity, and β‐amyloid peptide toxicity; (2) genes that control apoptotic cell death, such as bcl‐2, p35, p53, and p75NTR, also modulate necrotic neural death in some cases; (3) the emerging mechanisms by which these genes control apoptosis may be relevant for understanding neurodegenerative processes, and for the design of therapeutic agents; and (4) the findings that the cell plays an active role in its own demise, and that specific gene products are involved, suggest that therapeutic intervention may be feasible.
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Add Alzheimer's disease to the list of autoimmune diseases
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Metadata
- Authors
- Bredesen, D. E.
- Venue
- Annals of Neurology
- Publisher
- Wiley
- Published
- 1995-12
- Volume
- 38
- Issue
- 6
- Pages
- 839-851
- ISSN
- 0364-5134 (ISSN-L)
- 1531-8249
- OpenAlex
- W4211045864
- Cited by
- 484
- References
- 9
- FWCI
- 15.75
- Type
- journal article
- Language
- en
- Open access
- closed
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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
