A red dye derived¹ from lichens²（地衣） that has been used for centuries to color fabrics³ and food appears to reduce the abundance of small toxic⁴ protein aggregates⁵ in Alzheimer's disease. The dye, a compound called orcein（地衣红） , and a related substance, called O4, bind⁶ preferentially to small amyloid（淀粉体） aggregates that are considered to be toxic and cause neuronal dysfunction and memory impairment in Alzheimer's disease. O4 binding⁷ to small aggregates promotes their conversion⁸ into large, mature plaques⁹（斑块） which researchers assume to be largely non-toxic for neuronal cells. Further research with animal models is needed to determine whether this new approach by Dr. Jan Bieschke (Max Delbrück Center for Molecular¹⁰ Medicine, MDC, Berlin-Buch), Dr. Martin Herbst (Charité -- Universitätsmedizin Berlin) and Professor Erich Wanker (MDC) in Berlin, Germany, will be useful for therapy development.

Protein misfolding is considered to be the cause of Alzheimer's, Parkinson's and also Huntington's disease. In a multistep process, proteins misfold and accumulate into large extra- or intracellular（细胞内的） plaques. Researchers assume that small misfolded protein aggregates that are precursors¹¹ of mature plaques are toxic for nerve cells and are the reason why they are eventually destroyed.

Dye from the Canary Islands

The dye orcein is isolated¹² from lichens that grow on the Canary Islands, among other places. Lichens have been used for centuries to color fabrics and food. Eight years ago Professor Wanker screened hundreds of natural compounds to find potential candidate drug molecules¹³ for the treatment of neurodegenerative（神经变性的） diseases. Among those substances he found orcein, a compound made up of about 14 small molecules. As these molecules might have different biological effects, the researchers in Berlin began to search for pure chemicals with similar properties. They identified the substance O4, a blue dye, which is structurally¹⁴ very similar to one of the 14 molecules. Moreover, they showed that O4 stimulates¹⁵ the formation of large, non-toxic protein plaques from small toxic protein assemblies.