新的療法可望預防老年癡呆（阿爾茨海默病）

Last March, researchers at UCLA reported the development of a molecular compound called CLR01 that prevented toxic proteins associated with Parkinson's disease from binding together and killing the brain's neurons. Building on those findings, they have turned their attention to Alzheimer's disease, which is thought to be caused by a similar toxic aggregation or clumping, but with different proteins, especially amyloid-beta and tau.

Using the same compound, which they've dubbed a "molecular tweezer," in a living mouse model of Alzheimer's, the researchers demonstrated for the first time that the compound CLR01 safely crossed the blood–brain barrier, cleared the existing amyloid-beta and tau aggregates, and also proved to be protective to the neurons' synapses.

Molecular tweezers are complex compounds capable of binding to other proteins. Shaped like the letter "C," they wrap around chains of lysine, a basic amino acid that is a constituent of most proteins. In collaboration with scientists at the Università Cattolica in Rome, the researchers, working first in cell cultures, found that CLR01 effectively inhibited a process called synaptotoxicity, in which clumps of toxic amyloid damage or destroy a neuron's synapses. Even though synapses in transgenic mice with Alzheimer's may shut down and the mice may lose their memory, upon treatment, they form new synapses and regain their learning and memory abilities.

Study authors stress that application of the findings to humans is uncertain, because in humans with Alzheimer’s disease the neurons gradually die. But the research could lead to prophylactic treatment for people at risk of Alzheimer’s. The report appears in the online edition of the journal Brain. Read the study abstract.