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Steroidogenic acute regulatory protein (StAR): evidence of gonadotropin-induced steroidogenesis in Alzheimer disease.

Publication ,  Journal Article
Webber, KM; Stocco, DM; Casadesus, G; Bowen, RL; Atwood, CS; Previll, LA; Harris, PLR; Zhu, X; Perry, G; Smith, MA
Published in: Mol Neurodegener
October 3, 2006

BACKGROUND: Alzheimer disease (AD) is clinically characterized by progressive memory loss, impairments in behavior, language and visual-spatial skills and ultimately, death. Epidemiological data reporting the predisposition of women to AD has led to a number of lines of evidence suggesting that age-related changes in hormones of the hypothalamic-pituitary-gonadal (HPG) axis following reproductive senescence, may contribute to the etiology of AD. Recent studies from our group and others have reported not only increases in circulating gonadotropins, namely luteinizing hormone (LH) in individuals with AD compared with control individuals, but also significant elevations of LH in vulnerable neuronal populations in individuals with AD compared to control cases as well as the highest density of gonadotropin receptors in the brain are found within the hippocampus, a region devastated in AD. However, while LH is higher in AD patients, the downstream consequences of this are incompletely understood. To begin to examine this issue, here, we examined the expression levels of steroidogenic acute regulatory (StAR) protein, which regulates the first key event in steroidogenesis, namely, the transport of cholesterol into the mitochondria, and is regulated by LH through the cyclic AMP second messenger pathway, in AD and control brain tissue. RESULTS: Our data revealed that StAR protein was markedly increased in both the cytoplasm of hippocampal pyramidal neurons as well as in the cytoplasm of other non-neuronal cell types from AD brains when compared with age-matched controls. Importantly, and suggestive of a direct mechanistic link, StAR protein expression in AD brains colocalized with LH receptor expression. CONCLUSION: Therefore, our findings suggest that LH is not only able to bind to its receptor and induce potentially pathogenic signaling in AD, but also that steroidogenic pathways regulated by LH may play a role in AD.

Duke Scholars

Published In

Mol Neurodegener

DOI

EISSN

1750-1326

Publication Date

October 3, 2006

Volume

1

Start / End Page

14

Location

England

Related Subject Headings

  • Neurology & Neurosurgery
  • 3209 Neurosciences
  • 3101 Biochemistry and cell biology
  • 1109 Neurosciences
  • 1103 Clinical Sciences
  • 0604 Genetics
 

Citation

APA
Chicago
ICMJE
MLA
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Webber, K. M., Stocco, D. M., Casadesus, G., Bowen, R. L., Atwood, C. S., Previll, L. A., … Smith, M. A. (2006). Steroidogenic acute regulatory protein (StAR): evidence of gonadotropin-induced steroidogenesis in Alzheimer disease. Mol Neurodegener, 1, 14. https://doi.org/10.1186/1750-1326-1-14
Webber, Kate M., Douglas M. Stocco, Gemma Casadesus, Richard L. Bowen, Craig S. Atwood, Laura A. Previll, Peggy L. R. Harris, Xiongwei Zhu, George Perry, and Mark A. Smith. “Steroidogenic acute regulatory protein (StAR): evidence of gonadotropin-induced steroidogenesis in Alzheimer disease.Mol Neurodegener 1 (October 3, 2006): 14. https://doi.org/10.1186/1750-1326-1-14.
Webber KM, Stocco DM, Casadesus G, Bowen RL, Atwood CS, Previll LA, et al. Steroidogenic acute regulatory protein (StAR): evidence of gonadotropin-induced steroidogenesis in Alzheimer disease. Mol Neurodegener. 2006 Oct 3;1:14.
Webber, Kate M., et al. “Steroidogenic acute regulatory protein (StAR): evidence of gonadotropin-induced steroidogenesis in Alzheimer disease.Mol Neurodegener, vol. 1, Oct. 2006, p. 14. Pubmed, doi:10.1186/1750-1326-1-14.
Webber KM, Stocco DM, Casadesus G, Bowen RL, Atwood CS, Previll LA, Harris PLR, Zhu X, Perry G, Smith MA. Steroidogenic acute regulatory protein (StAR): evidence of gonadotropin-induced steroidogenesis in Alzheimer disease. Mol Neurodegener. 2006 Oct 3;1:14.
Journal cover image

Published In

Mol Neurodegener

DOI

EISSN

1750-1326

Publication Date

October 3, 2006

Volume

1

Start / End Page

14

Location

England

Related Subject Headings

  • Neurology & Neurosurgery
  • 3209 Neurosciences
  • 3101 Biochemistry and cell biology
  • 1109 Neurosciences
  • 1103 Clinical Sciences
  • 0604 Genetics