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Estrogen-Like Molecules

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By Report by the AD Educ & Referral Ctr • www.ProHealth.com • March 1, 1997


In addition to pursuing today's strongest prospects in their search for effective AD therapies, NIA's Drug Discovery Groups open new lines of inquiry and reexamine areas of research that others may assume are closed. Dr. James Simpkins, who directs a Drug Discovery Group at the University of Florida in Gainesville, says that the progress of his own career in AD research proves the value of exploring a range of theories--unpopular as well as popular. "My colleagues and I first became interested in estrogen in the mid-1980's. At that time, most researchers dismissed the idea that it had any role in AD. Today, estrogen has taken center stage."

Currently, Dr. Simpkins' team is working to transform the estrogen molecule into a safe and beneficial compound for people who have or are at risk for AD. Describing the group's efforts, he says, "Based on the substantial evidence that estrogen protects neurons, we set out to build models that explain how it works." Studying animals and tissue cultures, this team eventually linked estrogen's benefits to its anti-oxidant function. "With estrogen, we drastically reduced oxidation damage in tissue cultures and correlated that activity with less cell death," notes Dr. Simpkins. In addition, the group found that estrogen's neuron-protecting activities are not related to its "feminizing" properties, and that activating estrogen receptors is unnecessary to protect neurons. Receptors are proteins that recognize and bind to chemical messengers, such as neurotransmitters.

Building on these discoveries, Dr. Simpkins' team made a series of minor changes at various places in the structure of the estrogen molecule. The team sought to produce new substances that kept estrogen's anti-oxidant potential, but lost its feminizing qualities. They developed 10 molecules that may help protect neurons but do not act like sex hormones. Dr. Simpkins speculates that hundreds of similar, estrogen-like molecules may be found.

The University of Florida team also found that normal levels of estrogen help protect neurons. This finding suggests that estrogen-like therapies may be administered effectively at relatively low doses over many years. Dr. Simpkins notes that estrogen may help with other diseases of the central nervous system, including Parkinson's disease, and strokes.

In an agreement with a pharmaceutical company, Dr. Simpkins and his colleagues will further develop 3 of the 10 modified estrogen molecules prepared at the University of Florida. Paving the way for clinical trials, the drug company will test these substances in mice genetically engineered to produce abnormally high levels of APP. The company seeks to find out if the substances protect brain cells from the possibly toxic effects of amyloid.

Source: Connections Magazine [Volume 6(1), Spring 1997]

References

Aisen, P.S.; Davis, K.L. Inflammatory Mechanisms in Alzheimer's Disease: Implications for Therapy. American Journal of Psychiatry. 151(8): 1105-1113. August 1994.
Paganini-Hill, A.; Henderson, V.W. Estrogen Deficiency and Risk of Alzheimer's Disease in Women. American Journal of Epidemiology. 140(3): 256-261. August 1, 1994.
Rogers, J.; et al. Clinical Trial of Indomethacin in Alzheimer's Disease. Neurology. 43(8): 1609-1611. August 1993.
Simpkins, J.W.; Singh, M.; Bishop, J. The Potential Role for Estrogen Replacement Therapy in the Treatment of the Cognitive Decline and Neurodegeneration Associated With Alzheimer's Disease. Neurobiology of Aging. 15(Suppl 2): S195-S197. 1994.
Stewart, W.F.; et al. Risk of Alzheimer's Disease and Duration of NSAID Use. Neurology. 48(3): 626-632. March 1997.
Tang, M.X.; et al. Effect of Oestrogen During Menopause on Risk and Age at Onset of Alzheimer's Disease. The Lancet. 348(9025): 429-432. August 17, 1996.
Thal, L. Future Directions for Research in Alzheimer's Disease. Neurobiology of Aging. 15(Suppl 2): S71-S72. 1994.
Whitehouse, P.J. Cholinergic Therapy in Dementia. ACTA Neurology Scandinavia. Suppl 149: 42-45. 1993.



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