New Potential Cause of Alzheimer's Disease Detected
BusinessWeek
2010-06-11
Researchers have discovered that the mutation of a gene associated with early onset Alzheimer's may block a key recycling process necessary for brain cell survival -- a finding that points the way to possible treatment for the disease.
When it's working properly, this gene -- called presenilin 1 (PS1) -- performs a crucial house-cleaning service by helping brain cells digest unwanted, damaged and potentially toxic proteins. But in its mutated form, the gene fails to help cells recycle these potential toxins, suggesting an explanation for the damage to the brain characteristic of Alzheimer's disease.
"We believe we have identified the principal mechanism by which mutations of PS1 cause the most common genetic form of Alzheimer's disease," study co-author Dr. Ralph A. Nixon, professor in the departments of psychiatry and cell biology as well as director of NYU's Center of Excellence on Brain Aging and the Silberstein Alzheimer's Institute, said in a university news release.
"Presently, no effective treatment exists to either slow or prevent the progression of Alzheimer's disease," added Nixon, also director of the Center for Dementia Research at the Nathan S. Kline Institute for Psychiatric Research in New York City. "This discovery has the potential of identifying such a treatment."
Mutations of the PS1 gene have previously been thought to increase production of the toxic beta amyloid protein that appears to collect in the brains of Alzheimer's patients. In turn, scientists have theorized that by preventing amyloid deposits from accumulating, they might be able to slow or prevent Alzheimer's progression.
However, the current investigation into PS1 behavior side-steps this potential scenario -- without questioning its validity -- by focusing on the possibility that abnormal PS1 function may cause cell death unconnected to beta amyloid buildup. PS1 mutations and other factors could, therefore, promote Alzheimer's in entirely different ways, the team said.
BusinessWeek
2010-06-11
Researchers have discovered that the mutation of a gene associated with early onset Alzheimer's may block a key recycling process necessary for brain cell survival -- a finding that points the way to possible treatment for the disease.
When it's working properly, this gene -- called presenilin 1 (PS1) -- performs a crucial house-cleaning service by helping brain cells digest unwanted, damaged and potentially toxic proteins. But in its mutated form, the gene fails to help cells recycle these potential toxins, suggesting an explanation for the damage to the brain characteristic of Alzheimer's disease.
"We believe we have identified the principal mechanism by which mutations of PS1 cause the most common genetic form of Alzheimer's disease," study co-author Dr. Ralph A. Nixon, professor in the departments of psychiatry and cell biology as well as director of NYU's Center of Excellence on Brain Aging and the Silberstein Alzheimer's Institute, said in a university news release.
"Presently, no effective treatment exists to either slow or prevent the progression of Alzheimer's disease," added Nixon, also director of the Center for Dementia Research at the Nathan S. Kline Institute for Psychiatric Research in New York City. "This discovery has the potential of identifying such a treatment."
Mutations of the PS1 gene have previously been thought to increase production of the toxic beta amyloid protein that appears to collect in the brains of Alzheimer's patients. In turn, scientists have theorized that by preventing amyloid deposits from accumulating, they might be able to slow or prevent Alzheimer's progression.
However, the current investigation into PS1 behavior side-steps this potential scenario -- without questioning its validity -- by focusing on the possibility that abnormal PS1 function may cause cell death unconnected to beta amyloid buildup. PS1 mutations and other factors could, therefore, promote Alzheimer's in entirely different ways, the team said.
