Alzheimer's reversed in mice
.
Alzheimer's Donation
Donate Online Now
.
Giving mice with Alzheimer's disease a certain enzyme seems to restore memory, U.S. researchers said Thursday.
The enzyme is called ubiquitin C-terminal hydrolase L1 (Uch-L1), said the team at Columbia University Medical Center in New York.
The research was led by Ottavio Arancio and Michael Shelanski, who noted that, when the mice were given supplemental Uch-L1, their ability to form new memories returned.
"What makes this newly discovered enzyme exciting as a potentially effective therapy is that it restores memory without destroying amyloid beta proteins," Arancio said.
Because amyloid beta proteins play important roles in the rest of the body in both mice and humans, the researchers said it was not possible to eliminate them to slow Alzheimer's.
Shelanski added that, although their discovery was promising, it was currently useful only in animals and it would take some time before it could lead to therapies in humans. "We continue to work towards that crucial goal," he said.
Uch-L1 is part of a biochemical network that controls the CREB molecule, which is necessary for normal memory in mice. CREB is inhibited by the amyloid beta proteins that are produced in the brains of mice and humans with Alzheimer's disease and cause the memory impairment and brain damage typical of the disorder.
The enzyme is called ubiquitin C-terminal hydrolase L1 (Uch-L1), said the team at Columbia University Medical Center in New York.
The research was led by Ottavio Arancio and Michael Shelanski, who noted that, when the mice were given supplemental Uch-L1, their ability to form new memories returned.
"What makes this newly discovered enzyme exciting as a potentially effective therapy is that it restores memory without destroying amyloid beta proteins," Arancio said.
Because amyloid beta proteins play important roles in the rest of the body in both mice and humans, the researchers said it was not possible to eliminate them to slow Alzheimer's.
Shelanski added that, although their discovery was promising, it was currently useful only in animals and it would take some time before it could lead to therapies in humans. "We continue to work towards that crucial goal," he said.
Uch-L1 is part of a biochemical network that controls the CREB molecule, which is necessary for normal memory in mice. CREB is inhibited by the amyloid beta proteins that are produced in the brains of mice and humans with Alzheimer's disease and cause the memory impairment and brain damage typical of the disorder.
0 Comments:
Post a Comment
Subscribe to Post Comments [Atom]
<< Home