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Sex Hormones and Memory

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And I thought it was cortisol....bet you did too. I'll be posting some of my other finds under this topic...tee hee



Here are some web links of interest:


Neurendocrinology Briefings Number 6

Sex,Hormones, Mood, Mental State, and Memory



Women under stress

The role of estrogen in memory and learning



UCSF Study Links Estrogen and Memory:



ABCs Of Aging, Alzheimer's, Estrogen & Memory



What Are the Effects on Mental Functioning with Estrogen Depletion?




Hormone Replacement Therapy for Men? Testosterone & Male Menopause




Should Men With "Male Menopause" Symptoms Take Hormone Replacement Therapy?



Testosterone boosts verbal, spatial memory in small trial.

Author/s: Andrew Bowser

Urology Times Issue: Oct 1, 1998



Alzheimer's Protein Increases When Testosterone Drops


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Well, it was about memory...

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If you haven't figured it out yet, I will start with estrogen first, then will switch to testosterone.


Here is the first study that I found interesting. Let me know if you want the full text:


Vol. 8, No. 3, pp. 121-133, May/June 2001


Cellular and Molecular Mechanisms of Estrogen Regulation of Memory Function and Neuroprotection Against Alzheimer's Disease: Recent Insights and Remaining Challenges

Roberta Diaz Brinton

Department of Molecular Pharmacology and Toxicology and the Program in Neuroscience, University of Southern California, Pharmaceutical Sciences Center, Los Angeles, California 90033, USA


This review focuses on recent advances in our knowledge of estrogen action in the brain. The greatest amount of attention was devoted to those studies that impact our understanding of estrogen regulation of memory function and prevention of degenerative diseases associated with memory systems, such as Alzheimer's disease. A review of recent advances in our understanding of estrogen receptors, both nuclear and membrane, is also presented. Finally, these data are considered in regard to their relevancy to the use of estrogen replacement therapy for cognitive health throughout menopause and the development of an estrogen replacement therapy designed for the unique requirements of the brain.

LEARNING & MEMORY 8:121-133 ? 2001 by Cold Spring Harbor Laboratory Press ISSN1072-0502/01 $5.00

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Here is a second study of interest:


Published online before print February 6, 2001, 10.1073/pnas.041483198;

Proc. Natl. Acad. Sci. USA, Vol. 98, Issue 4, 1952-1957, February 13, 2001


Estrogen receptor , not , is a critical link in estradiol-

mediated protection against brain injury

Dena B. Dubal*, Hong Zhu, Jin Yu,, Shane W. Rau*, Paul J. Shughrue?,?, Istvan Merchenthaler?, Mark S. Kindy,, and Phyllis M. Wise*,

Departments of * Physiology and  Biochemistry, and  Stroke Program of Sanders-Brown Center on Aging, University of Kentucky College of Medicine, Lexington, KY 40536; and ? Women's Health Research Institute, Wyeth Ayerst Research, Radnor, PA 19087


Edited by William H. Daughaday, University of California, Irvine, CA, and approved December 15, 2000 (received for review October 11, 2000)


Estradiol protects against brain injury, neurodegeneration, and cognitive decline. Our previous work demonstrates that physiological levels of estradiol protect against stroke injury and that this protection may be mediated through receptor-dependent alterations of gene expression. In this report, we tested the hypothesis that estrogen receptors play a pivotal role in mediating neuroprotective actions of estradiol and dissected the potential biological roles of each estrogen receptor (ER) subtype, ER and ER, in the injured brain. To investigate and delineate these mechanisms, we used ER-knockout (ERKO) and ER-knockout (ERKO) mice in an animal model of stroke. We performed our studies by using a controlled endocrine paradigm, because endogenous levels of estradiol differ dramatically among ERKO, ERKO, and wild-type mice. We ovariectomized ERKO, ERKO, and the respective wild-type mice and implanted them with capsules filled with oil (vehicle) or a dose of 17-estradiol that produces physiological hormone levels in serum. One week later, mice underwent ischemia. Our results demonstrate that deletion of ER completely abolishes the protective actions of estradiol in all regions of the brain; whereas the ability of estradiol to protect against brain injury is totally preserved in the absence of ER. Thus, our results clearly establish that the ER subtype is a critical mechanistic link in mediating the protective effects of physiological levels of estradiol in brain injury. Our discovery that ER mediates protection of the brain carries far-reaching implications for the selective targeting of ERs in the treatment and prevention of neural dysfunction associated with normal aging or brain injury.

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