Abstract
Recent work has suggested that the ovarian steroid hormone, 17β-estradiol (E2), at physiological concentrations, may exert protective effects in neurodegenerative disorders such as Alzheimer's disease, Parkinson's disease and acute ischemic stroke. While physiological concentrations of E2 have consistently been shown to be protective in vivo, direct protection of neurons remains controversial, suggesting that while direct protection of neurons may occur in some instances, an alternative or parallel pathway for protection may exist which could involve another cell type in the brain. In the present review, we summarize the data in support of a possible role for astrocytes in the mediation of neuroprotection by E2. We also summarize the data suggesting a non-classical estrogen receptor may underlie some of the protective effects of E2 by activating cellular signaling pathways, such as extracellular-regulated kinase (ERK) and phosphatidylinositol 3-kinase/Akt. A possible indirect pathway involving astrocytes may act in concert with the proposed direct pathway to achieve a widespread, global protection of both ER positive and negative neurons.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 70-75 |
| Number of pages | 6 |
| Journal | Experimental Gerontology |
| Volume | 42 |
| Issue number | 1-2 |
| DOIs | |
| State | Published - Jan 1 2007 |
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Keywords
- Astrocyte
- Cerebral ischemia
- Estrogen
- TGF-β
ASJC Scopus subject areas
- Aging
- Medicine(all)
Cite this
Role of astrocytes in estrogen-mediated neuroprotection. / Dhandapani, Krishnan Michael; Brann, Darrell W.
In: Experimental Gerontology, Vol. 42, No. 1-2, 01.01.2007, p. 70-75.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Role of astrocytes in estrogen-mediated neuroprotection
AU - Dhandapani, Krishnan Michael
AU - Brann, Darrell W
PY - 2007/1/1
Y1 - 2007/1/1
N2 - Recent work has suggested that the ovarian steroid hormone, 17β-estradiol (E2), at physiological concentrations, may exert protective effects in neurodegenerative disorders such as Alzheimer's disease, Parkinson's disease and acute ischemic stroke. While physiological concentrations of E2 have consistently been shown to be protective in vivo, direct protection of neurons remains controversial, suggesting that while direct protection of neurons may occur in some instances, an alternative or parallel pathway for protection may exist which could involve another cell type in the brain. In the present review, we summarize the data in support of a possible role for astrocytes in the mediation of neuroprotection by E2. We also summarize the data suggesting a non-classical estrogen receptor may underlie some of the protective effects of E2 by activating cellular signaling pathways, such as extracellular-regulated kinase (ERK) and phosphatidylinositol 3-kinase/Akt. A possible indirect pathway involving astrocytes may act in concert with the proposed direct pathway to achieve a widespread, global protection of both ER positive and negative neurons.
AB - Recent work has suggested that the ovarian steroid hormone, 17β-estradiol (E2), at physiological concentrations, may exert protective effects in neurodegenerative disorders such as Alzheimer's disease, Parkinson's disease and acute ischemic stroke. While physiological concentrations of E2 have consistently been shown to be protective in vivo, direct protection of neurons remains controversial, suggesting that while direct protection of neurons may occur in some instances, an alternative or parallel pathway for protection may exist which could involve another cell type in the brain. In the present review, we summarize the data in support of a possible role for astrocytes in the mediation of neuroprotection by E2. We also summarize the data suggesting a non-classical estrogen receptor may underlie some of the protective effects of E2 by activating cellular signaling pathways, such as extracellular-regulated kinase (ERK) and phosphatidylinositol 3-kinase/Akt. A possible indirect pathway involving astrocytes may act in concert with the proposed direct pathway to achieve a widespread, global protection of both ER positive and negative neurons.
KW - Astrocyte
KW - Cerebral ischemia
KW - Estrogen
KW - TGF-β
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U2 - 10.1016/j.exger.2006.06.032
DO - 10.1016/j.exger.2006.06.032
M3 - Article
VL - 42
SP - 70
EP - 75
JO - Experimental Gerontology
JF - Experimental Gerontology
SN - 0531-5565
IS - 1-2
ER -