Athena Neurosciences Inc. said Monday that it has formed acollaboration with doctors John Hardy and Alison Goate at St.Mary's Hospital Medical School of London to develop animal andcellular models for Alzheimer's disease.

The collaboration aims to develop models of Alzheimer's toidentify therapeutics that block or inhibit deposition ofamyloid plaque found in the brains of Alzheimer's patients. Theplaques are composed of an abnormal fragment of the largerbeta-amyloid precursor protein.

South San Francisco, Calif.-based Athena will have anexclusive option to commercialize both the London group'searlier discoveries and future technology arising from thecollaboration. No financial details were released.

In February, Hardy and Goate published in the journal Naturetheir discovery of a rare mutation of the human gene coding forbeta-amyloid precursor protein. The mutation is the cause ofAlzheimer's in some families suffering from the inheritedform of the disease.

Athena is looking for additional mutations that could causeAlzheimer's. "As we identify genes implicated in Alzheimer'sin other research, this group (Hardy and Goate) will be involvedin mapping those genes," said Ivan Lieberburg, vice presidentof Alzheimer's disease research at privately held Athena.

Although scientists are debating the extent to which thedisease is inherited, "a reasonable estimate would probably beon the order of 15 to 50 percent," Lieberburg said.

Athena hopes the mutation found by the Hardy team willaccelerate amyloid deposits in an animal model just as it doesin humans, said Lieberburg. People with the mutation get thedisease in their 40s.

Last month, groups from California Biotechnology and MilesResearch Center separately reported that they had developedtransgenic mice that express the human gene for beta amyloid.Cal Bio of Mountain View, Calif., inserted DNA coding for theprecursor protein. Miles of West Haven, Conn., used a geneconstruct of the beta amyloid protein itself.

Another model is being developed by Rachel Neve of thepsychobiology department at the University of California,Irvine. Neve 's mice contain a gene that encodes a fragment ofthe precursor protein that has been shown to be toxic to nervecells in lab cultures. Neve's mice, which are about 5 monthsold, also have amyloid deposits. Three companies areinterested in licensing the technology, Neve said.

-- Karen Bernstein BioWorld Staff

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