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Drug Rescues Memory Lost To Alzheimer's Disease

Date:
July 27, 2009
Source:
University of California - Irvine
Summary:
A drug similar to one used in clinical trials for treatment of rheumatoid arthritis and psoriasis has been found to rescue memory in mice exhibiting Alzheimer's symptoms.

Andrea Tenner and colleagues identified a drug that reduces damaging inflamed immune cells (red, background) and Alzheimer's lesions called amyloid plaques (green, background) from gathering in brains of mice, preventing the loss of cognitive abilities.
Credit: Photo by Daniel A. Anderson / University Communications

A drug similar to one used in clinical trials for treatment of rheumatoid arthritis and psoriasis has been found to rescue memory in mice exhibiting Alzheimer's symptoms.

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The discovery by UC Irvine scientists offers hope that a new treatment may be on the horizon for people in the early stages of Alzheimer's, the leading cause of elderly dementia afflicting more than 5 million people in the U.S. and for which no cure exists.

The drug, called PMX205, prevented inflamed immune cells from gathering in brain regions with Alzheimer's lesions called amyloid plaques. Cell inflammation in these areas accelerates neuron damage, exacerbating the disease.

"We used a multidisciplinary approach combining an understanding of immunology and neurobiology to uncover a completely different target than other therapies," said Andrea Tenner, lead author of the study that led to the findings and a molecular biology & biochemistry professor at UCI.

Study results are reported in the July 15 edition of the Journal of Immunology.

For 12 weeks, Tenner and colleagues added PMX205 to the drinking water of mice genetically altered to develop age-related Alzheimer's-like symptoms. The treatment occurred at an age when plaques were accumulating in their brains.

Scientists gave the treated mice learning and memory tests and then examined their brains for evidence of the disease. Alzheimer's mice that were not given the drug performed significantly worse on the test than normal mice. But – in all but one case – the treated Alzheimer's mice performed almost as well as the normal mice. Those with the rescued cognitive ability had more than 50 percent fewer Alzheimer's lesions and inflammatory immune cells than the untreated diseased mice.

PMX53, a similar drug that can be taken orally, passed Phase 1 human clinical trials for safety with no major problems reported. Possible side effects include an increased susceptibility to some infections. PMX205 is a modified version that may be more potent for treatment of brain disorders.

"This approach may work even better if combined with treatments targeting other problems in the Alzheimer's brain," said Tenner, also a professor of pathology and neurobiology & behavior, as well as a member of UCI's Institute for Immunology and Institute for Memory Impairments and Neurological Disorders, or UCI MIND.

In addition to Tenner, UCI graduate student Rahasson Ager and senior researcher Marisa Fonseca worked on this study. They collaborated with Australian scientists Trent Woodruff and Steve Taylor, who demonstrated the drug's effectiveness in rat models of other diseases.

The research was supported by the National Institutes of Health and the National Health and Medical Research Council of Australia.


Story Source:

The above story is based on materials provided by University of California - Irvine. Note: Materials may be edited for content and length.


Cite This Page:

University of California - Irvine. "Drug Rescues Memory Lost To Alzheimer's Disease." ScienceDaily. ScienceDaily, 27 July 2009. <www.sciencedaily.com/releases/2009/07/090714125000.htm>.
University of California - Irvine. (2009, July 27). Drug Rescues Memory Lost To Alzheimer's Disease. ScienceDaily. Retrieved January 30, 2015 from www.sciencedaily.com/releases/2009/07/090714125000.htm
University of California - Irvine. "Drug Rescues Memory Lost To Alzheimer's Disease." ScienceDaily. www.sciencedaily.com/releases/2009/07/090714125000.htm (accessed January 30, 2015).

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