The National Institutes of Health has given a UCSB chemistry professor nearly $2 million in funding to study a new approach to Alzheimer’s disease.

Professor Michael Bowers of the Chemistry and Biochemistry Dept. spent four years developing the project, which studies a particular protein as a potential cause for the disease. Along with UCLA neurology professor David Teplow, Bowers has isolated what he believes to be the main toxic agent causing the disease.

After Bowers’ team demonstrated that its research would contribute to a cure, the NIH provided a five-year, $9 million grant for the project, which will be carried out at four research universities, including UCSB. Bowers’ team will receive $1.3 million in grant money, as well as $500,000 worth of biological samples provided by Teplow.

Alzheimer’s is a neurodegenerative disease characterized by increasing problems with memory and decline in quality of everyday life. It is the most common type of dementia and affects an estimated 4.5 million Americans, with the number increasing as the baby boomer generation ages.

Bowers, who spent most of his career as a physical chemist, said he became interested in the study of neurological diseases by accident while reading a trade publication.

“Biological molecules are much more complex, so the methods of physical chemistry don’t always directly transfer,” Bowers said. “[But I realized that] some of the methods I developed for completely other purposes in the material sciences might be useful here.”

Recent research on Alzheimer’s disease has mostly focused on amyloid plaques, a buildup of proteins, and neurofibrillary tangles, or knots of brain tissue filaments, which are clearly visible in autopsied brains of Alzheimer’s patients as the cause of the disease, according to a UCSB press release. This new research, however, views the deposits as merely a marker, and will study rare proteins to see how they disrupt neurons and cause Alzheimer’s.

Professor Joan-Emma Shea of the Chemistry and Biochemistry Dept., and head of theoretical modeling for the project, said it is difficult to develop an Alzheimer’s drug because scientists don’t know exactly what the toxic agents are.

“The hypothesis is that very small aggregates are the toxic agents, but we don’t know what they look like,” Shea said. “The computational work that the Shea group is doing aims at providing a structure for these toxic oligomers – [short, single-stranded DNA fragments]. Once you know the structure, you can design inhibitor molecules that bind to the clusters and get rid of them. They stop growth of the oligomers but they also seem to disable them.”

Bowers described the research as a search for a compound that will prove harmless to human tissue, but at the same time destroy the molecules that cause Alzheimer’s.

“I think we can fairly quickly find agents,” Bowers said. “The most difficult thing will be finding molecules that are not humanly toxic that can be delivered to the brain [to stop the progression of the disease].”

In addition to UCLA’s professor Teplow, a main collaborator on the project, researchers at Boston University and Massachusetts Institute of Technology have signed onto the project, which could potentially provide the key for early detection of Alzheimer’s disease and aid scientists in the search for a nontoxic drug to slow down or stop the process before a patient has suffered too much brain damage. The potential drug could not repair already damaged tissue, said a UCSB press release.

Shea said that although the research is still in a preliminary stage, she is optimistic that the results will provide a break in the fight against Alzheimer’s.

“Our preliminary results are going in the right direction,” Shea said. “We hope that in the near future we can prove, in a cell culture at least, that these molecules reduce toxicity.”

Shea said any prescription drug to treat or prevent the disease, however, will not be available for many years because of strict Food and Drug Administration regulations which require rigorous and repeated testing before a drug is made available to the public.

Bowers said he is optimistic the research will bear fruit in time to benefit the current generation of college students.

“It’s not that easy, [but] we’re actively starting on it,” Bowers said. “I never dreamed that we would get this far in only three years.”

In addition to Alzheimer’s disease, Bowers is researching several other neurological diseases. He has promising early data on the protein responsible for Parkinson’s disease and is also working on a project, funded by the British government, to develop a pre-mortem test for mad cow disease.