CHICAGO (Reuters) - Restoring levels of a nerve-protecting enzyme offers a new approach to developing treatments for Alzheimer’s disease, U.S. researchers said on Wednesday.
They said the enzyme SIRT1 may help prevent the formation of a toxic form of the protein tau that kills brain cells in people with Alzheimer’s disease.
“This is definitely the first step toward finding new strategies to reduce tau,” Li Gan at the Gladstone Institute of Neurological Disease in San Francisco, whose study appears in the journal Neuron, said in a telephone interview.
She said people with Alzheimer’s tend to have low levels of SIRT1, and drugs that boost these levels may keep this toxic form of tau from forming, they said.
The team studied the link between SIRT1 and a form of tau that is strongly linked with Alzheimer’s disease. called p-tau.
They found that mice genetically engineered to lack the SIRT1 gene were more likely to make the toxic form of tau.
When they tested a chemical that restores levels of SIRT1, it curbed the formation if p-tau.
The finding offers a new approach to reducing levels of tau in people with Alzheimer’s.
“We think by modulating this pathway, we will be able to lower the pathogenic form of tau,” Gan said.
Many companies, including GlaxoSmithKline, have been working on drugs that activate SIRT1, which is thought to control many age-related diseases.
Alzheimer’s is a progressive and fatal form of dementia that kills brain cells, causing steady declines in memory and thinking until people lose the ability to care for themselves.
Current drugs can treat symptoms, but none can close the progression of the disease, which affects 26 million people globally.
On Tuesday Alzheimer’s Disease International projected the worldwide costs of dementia would reach $604 billion in 2010, more than one percent of global GDP output.
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