U.S. study: insulin possible new treatment for Alzheimer's disease

WASHINGTON, Feb. 2 (Chinese media) -- A Northwestern

University-led research team reports that insulin, by shielding memory-forming

synapses from harm, may slow or prevent the damage and memory loss caused by

toxic proteins in Alzheimer's disease.

The findings, which provide additional new evidence

that Alzheimer's could be due to a novel third form of diabetes, was published

Monday in the online edition of the Proceedings of the National Academy of

Sciences.

In a study of neurons taken from the hippocampus, one

of the brain's crucial memory centers, the scientists treated cells with insulin

and the insulin-sensitizing drug rosiglitazone, which has been used to treat

type 2 diabetes. (Isolated hippocampal cells are used by scientists to study

memory chemistry; the cells are susceptible to damage caused by ADDLs, toxic

proteins that build up in persons with Alzheimer's disease.)

The researchers discovered that damage to neurons

exposed to ADDLs was blocked by insulin, which kept ADDLs from attaching to the

cells. They also found that protection by low levels of insulin was enhanced by

rosiglitazone.

ADDLs, short for "amyloid beta-derived diffusible

ligands," are known to attack memory-forming synapses. After ADDL binding,

synapses lose their capacity to respond to incoming information, resulting in

memory loss.

The protective mechanism of insulin works through a

series of steps by ultimately reducing the actual number of ADDL binding sites,

which in turn results in a marked reduction of ADDL attachment to synapses, the

researchers report.

"Therapeutics designed to increase insulin

sensitivity in the brain could provide new avenues for treating Alzheimer's

disease," said senior author William L. Klein, a researcher in North western's

Cognitive Neurology and Alzheimer's Disease Center." Sensitivity to insulin can

decline with aging, which presents a novel risk factor for Alzheimer's disease.

Our results demonstrate that bolstering insulin signaling can protect neurons

from harm."