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Review
. 1997 Nov;77(3):F165-70.
doi: 10.1136/fn.77.3.f165.

Apoptosis in neural development and disease

N D Mazarakis  1 , A D Edwards, H Mehmet
Affiliations
Review

Apoptosis in neural development and disease

N D Mazarakis et al. Arch Dis Child Fetal Neonatal Ed. 1997 Nov.
No abstract available

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Figures

Figure 1
Figure 1
A model of apoptosis in neural cells. Neurotrophin withdrawal leads to death by a default mechanism through as yet uncharacterised pathways. Gene mutations, inappropriate production of neurotransmitters, such as glutamate, free radical generation, and mitochondrial damage also trigger apoptosis as do engagement of death receptors. In the latter case oligomerisation of Fas/Apo-1 or TNF receptors or the p75 NGF receptor results in the recruitment of death domain proteins, which in turn activate members of the caspase family of cysteine proteases in an organised proteolytic cascade. Bcl-2 family members and inhibitor of apoptosis proteins (IAPs) control the decision to commit cell suicide, depending on whether pro- or anti-apoptotic partners predominate. In the later stages, specific endonucleases cleave DNA as part of the packaging process. Finally, cells are phagocytosed by healthy neighbours (not shown). Arrows indicate the flow of events and do not necessarily denote direct interactions.
See this image and copyright information in PMC

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