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Biotech / Medical : Neuroscience -- Ignore unavailable to you. Want to Upgrade?


To: Jim Oravetz who wrote (229)10/28/2001 10:35:50 PM
From: Nikole Wollerstein  Respond to of 278
 
I think it will be make or brake day for NEOT:
IRVINE, Calif., Oct. 24 /PRNewswire/ -- NeoTherapeutics, Inc. (Nasdaq: NEOT - news) announced today that it will hold a conference call and webcast on Tuesday, October 30th at 10:30 a.m. (EST), 7:30 a.m. (PST), to provide an update on the Company's 521 patient pivotal study of Neotrofin in Alzheimer's disease. Alvin J. Glasky, Ph.D., Chairman and Chief Executive Officer, and Rajesh Shrotriya, M.D., President and Chief Operating Officer, will host the call.

To access the call please dial (888) 552-7850 approximately ten minutes prior to the scheduled start time. Slides used in the Company's presentation will be available on the Company's website at www.neotherapeutics.com.

A replay of the call will be available on our website at www.neotherapeutics.com.

NeoTherapeutics seeks to create value for stockholders through the discovery and development of central nervous system drugs, in-licensing and commercialization of anti-cancer drugs, and the licensing out of new drug targets discovered through genomics research. The Company has two drugs addressing major medical needs in pivotal/phase 3 stage of development: Neotrofin(TM) for Alzheimer's disease and Satraplatin for prostate cancer. Additional neurology and anti-cancer drugs such as AIT-034 and Neoquin(TM) are in phase 1 and 2 human clinical trials and the Company has a rich pipeline of pre-clinical drug candidates



To: Jim Oravetz who wrote (229)11/8/2001 7:36:47 AM
From: Jim Oravetz  Read Replies (1) | Respond to of 278
 
UCSD Researchers Suggest Naturally Occurring Molecules May Alleviate Build-Up Of Plaque In Parkinson's Patients
Source: University Of California - San Diego (http://www.ucsd.edu/)
Date: Posted 11/8/2001

Naturally occurring molecules called beta-synucleins (b-synucleins) may have the ability to halt the excessive build-up of plaque-like deposits, called Lewy bodies, that are found in the dying neuron cells of Parkinson’s disease patients, according to researchers in the University of California, San Diego (UCSD) School of Medicine.
In findings published recently in the journal Neuron, investigators in the lab of senior author Eliezer Masliah, M.D., professor of neurosciences and pathology, showed in mice that b-synuclein inhibits the Lewy body-producing activity of a cousin molecule called alpha-synuclein, which has been linked to abnormal accumulation of Lewy bodies characteristically seen in the brain’s of Parkinson’s patients.

Although the mechanism by which b-synuclein works to block a-synuclein Lewy body-formation is unknown, Masliah and his colleagues noted that an imbalance in the ratio of a- to b-synuclein might render a-synuclein more prone to the plaque-like development.

In test tube studies, the research team added b-synuclein to a-synuclein protein that had formed aggregates, the abnormal Lewy body deposits. When b-synuclein was added, the aggregates untangled.

In studies with mice, the researchers first developed one group with over-expressed a-synuclein and another group with large amounts of b-synuclein. The a-synuclein mice developed Lewy bodies while the b-synuclein group did not.

When the researchers developed mice bred with higher amounts of b-synuclein, compared to a-synuclein (such as in normal individuals), the b-synuclein ameliorated the motor deficits, neurodegenerative alteration, and neuronal a-synuclein accumulation of Lewy bodies that had been seen in the a-synuclein mice.

In addition to Masliah, the research team included first author Makoto Hashimoto, M.D.; Edward Rockenstein, B.S.; Michael Mante, B.S.; and Margaret Mallory, B.S., all in the UCSD Departments of Neurosciences and Pathology.

The research was supported by grants from the National Institute of Health and the Michael J. Fox Foundation for Parkinson’s Research.



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Note: This story has been adapted from a news release issued by University Of California - San Diego for journalists and other members of the public. If you wish to quote from any part of this story, please credit University Of California - San Diego as the original source. You may also wish to include the following link in any citation:

sciencedaily.com