G2Cdb::Human Disease report

Disease id
D00000104
Name
Angiomatoid fibrous histiocytoma
Nervous system disease
no

Genes (1)

Gene Name/Description Mutations Found Literature Mutations Type Genetic association?
G00002162 FUS
fused in sarcoma
Y (11063972) Translocation fusion (with another gene) (TF) Y

References

  • The possibility of neurotoxicity in the hippocampus in major depression: a primer on neuron death.

    Sapolsky RM

    Department of Biological Sciences, Stanford University School of Medicine, Stanford University, California 94305, USA.

    A number of studies indicate that prolonged, major depression is associated with a selective loss of hippocampal volume that persists long after the depression has resolved. This review is prompted by two ideas. The first is that overt neuron loss may be a contributing factor to the decrease in hippocampal volume. As such, the first half of this article reviews current knowledge about how hippocampal neurons die during insults, focusing on issues related to the trafficking of glutamate and calcium, glutamate receptor subtypes, oxygen radical generation, programmed cell death, and neuronal defenses. This is meant to orient the reader toward the biology that is likely to underlie any such instances of neuron loss in major depression. The second idea is that glucocorticoids, the adrenal steroids secreted during stress, may play a contributing role to any such neuron loss. The subtypes of depression associated with the hippocampal atrophy typically involve significant hypersecretion of glucocorticoids, and the steroid has a variety of adverse effects in the hippocampus, including causing overt neuron loss. The second half of this article reviews the steps in this cascade of hippocampal neuron death that are regulated by glucocorticoids.

    Biological psychiatry 2000;48;8;755-65

Literature (1)

Pubmed - human_disease

  • The possibility of neurotoxicity in the hippocampus in major depression: a primer on neuron death.

    Sapolsky RM

    Department of Biological Sciences, Stanford University School of Medicine, Stanford University, California 94305, USA.

    A number of studies indicate that prolonged, major depression is associated with a selective loss of hippocampal volume that persists long after the depression has resolved. This review is prompted by two ideas. The first is that overt neuron loss may be a contributing factor to the decrease in hippocampal volume. As such, the first half of this article reviews current knowledge about how hippocampal neurons die during insults, focusing on issues related to the trafficking of glutamate and calcium, glutamate receptor subtypes, oxygen radical generation, programmed cell death, and neuronal defenses. This is meant to orient the reader toward the biology that is likely to underlie any such instances of neuron loss in major depression. The second idea is that glucocorticoids, the adrenal steroids secreted during stress, may play a contributing role to any such neuron loss. The subtypes of depression associated with the hippocampal atrophy typically involve significant hypersecretion of glucocorticoids, and the steroid has a variety of adverse effects in the hippocampus, including causing overt neuron loss. The second half of this article reviews the steps in this cascade of hippocampal neuron death that are regulated by glucocorticoids.

    Biological psychiatry 2000;48;8;755-65

© G2C 2014. The Genes to Cognition Programme received funding from The Wellcome Trust and the EU FP7 Framework Programmes:
EUROSPIN (FP7-HEALTH-241498), SynSys (FP7-HEALTH-242167) and GENCODYS (FP7-HEALTH-241995).

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