Journal
BIOCHIMICA ET BIOPHYSICA ACTA-GENERAL SUBJECTS
Volume 1800, Issue 10, Pages 1113-1120Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.bbagen.2009.11.013
Keywords
Estrogen; Estradiol; Non-feminizing estrogens; Mitochondria; Neuroprotection; Estrogen receptor; Alzheimer's disease
Categories
Funding
- NIH [P01 AG10485, P01 AG22550, P01 AG27956]
- NATIONAL INSTITUTE ON AGING [P01AG010485, P01AG027956, P01AG022550] Funding Source: NIH RePORTER
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Mitochondria have become a primary focus in our search not only for the mechanism(s) of neuronal death but also for neuroprotective drugs and therapies that can delay or prevent Alzheimer's disease and other chronic neurodegenerative conditions. This is because mitochrondria play a central role in regulating viability and death of neurons, and mitochondrial dysfunction has been shown to contribute to neuronal death seen in neurodegenerative diseases. In this article, we review the evidence for the role of mitochondria in cell death and neurodegeneration and provide evidence that estrogens have multiple effects on mitochondria that enhance or preserve mitochondrial function during pathologic circumstances such as excitotoxicity, oxidative stress, and others. As such, estrogens and novel non-hormonal analogs have come to figure prominently in our efforts to protect neurons against both acute brain injury and chronic neurodegeneration. (C) 2009 Elsevier B.V. All rights reserved.
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