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New Drug Delivery Systems

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By Report by the AD Educ & Referral Ctr • www.ProHealth.com • March 21, 1997


Perhaps as important as the University of Florida Drug Discovery Group's development of new compounds is its work to find better ways to deliver drugs to the brain. The expensive and fierce competition in commercial drug development often means that if a drug does not yield immediate results, it is abandoned quickly, even when ineffective delivery is the reason.

Nicholas Bodor, a chemist with the University of Florida Drug Discovery Group, is working to develop effective chemical delivery systems. These systems combine substances with drugs to assist entry into the brain. The University of Florida group has developed a chemical delivery system that consists of cholesterol and several other proteins. This system seems to disguise the appearance of a neuropeptide called thyrotropin releasing hormone (TRH) so that it can pass through the blood-brain barrier. Once TRH enters the brain, enzymes break down the chemical delivery system in a way that locks TRH in the brain, thereby strengthening its effects.

"Enhancing the effects of drugs in the brain with chemical delivery systems may lead to new treatments for AD and increase the effectiveness of some drugs as much as 50 times," says Dr. Simpkins. He believes that delivery systems could significantly enhance cholinergic therapy.

Drugs like tacrine increase the availability of acetylcholine to neurons by inhibiting cholinesterase, an enzyme that breaks down acetylcholine. Cholinergic therapy also includes drugs called cholinergic agonists that act in place of acetylcholine. Cholinergic agonists directly stimulate neuron receptors. Because high doses can damage vital organs such as the heart and liver, both types of cholinergic drugs must be used sparingly. But, the right chemical delivery system may raise the effectiveness of safe doses of cholinergic therapy.

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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