メディエイゴ

A Northwestern University-led(1) research team reports that insulin(2), by shielding(3) memory-forming(4) synapses(5) from harm, may slow or prevent the damage and memory loss(6) caused by toxic(7) proteins(8) in Alzheimer’s disease(9).

The findings, which provide additional new evidence that Alzheimer’s could be due to a novel third form of diabetes(10), will be published online(11) the week of Feb. 2 by the Proceedings of the National Academy of Sciences(12) (PNAS).

In a study of neurons(13) taken from the hippocampus(14), one of the brain(15)’s crucial(16) memory centers(17), the scientists treated(18) cells(19) with insulin and the insulin-sensitizing drug(20) rosiglitazone(21), which has been used to treat type 2 diabetes(22). (Isolated(23) hippocampal cells(24) are used by scientists to study memory chemistry(25); the cells are susceptible to(26) damage caused by ADDLs(27), toxic proteins that build up(28) in persons with Alzheimer’s disease.)

The researchers discovered that damage to neurons exposed to(29) ADDLs was blocked by(30) insulin, which kept(31) ADDLs from attaching to the cells. They also found that protection by low levels of insulin was enhanced(32) by rosiglitazone.

ADDLs (short for(33) “amyloid beta-derived diffusible ligands”) were discovered at Northwestern and are known to attack memory-forming synapses. After ADDL binding(34), synapses lose their capacity to respond to incoming(35) information, resulting in memory loss.

The protective(36) mechanism of insulin works through a series of steps by ultimately(37) reducing the actual number of ADDL binding sites(38), which in turn(39) results in a marked reduction of ADDL attachment(40) to synapses, the researchers(41) report.