ERROR 1
ERROR 1
ERROR 2
ERROR 2
ERROR 2
ERROR 2
ERROR 2
Password and Confirm password must match.
If you have an ACS member number, please enter it here so we can link this account to your membership. (optional)
ERROR 2
ACS values your privacy. By submitting your information, you are gaining access to C&EN and subscribing to our weekly newsletter. We use the information you provide to make your reading experience better, and we will never sell your data to third party members.
An experimental Alzheimer’s treatment that targets and traps amyloid-β oligomers improves cognitive performance in mice used as a model for the disease, according to a study (ACS Chem. Neurosci., DOI: 10.1021/cn100057j). Dieter Willbold of Heinrich Heine University Düsseldorf and the Jülich Research Center, in Germany, and colleagues believe the findings support the increasingly popular theory that soluble amyloid-β oligomers, rather than insoluble fibrils and plaques, are the neurotoxic species that cause the brain disease. The researchers showed that the treatment, a peptide known as D3, binds to amyloid-β oligomers, altering their conformation and inducing them to coalesce into huge, nontoxic clumps. D3 is much less capable of binding amyloid-β monomers, Willbold says, so the treatment won’t interfere with the monomers’ normal functions, which are still unclear. Cell culture and animal assays to date have shown no toxicity for the compound, he adds. The researchers have patented the peptide in Europe and are negotiating with pharmaceutical companies interested in developing it further.
Join the conversation
Contact the reporter
Submit a Letter to the Editor for publication
Engage with us on X