Blocking a memory protein eases PTSD-like symptoms in mice
Spanish scientists dampened the protein that locks in long-term memories. The mice still learned normally, but their fear responses faded faster. It's an early proof of concept.
There is no drug designed specifically for post-traumatic stress disorder: existing treatments ease symptoms without tackling their root. A team at Spain’s Cajal Neuroscience Centre (CSIC), led by Mariano Carrión-Vázquez, has taken a first step towards one.
They targeted CPEB3, a brain protein that works like a memory switch, forming very stable structures after learning so that memories stick. To dampen it they used QBP1, a small engineered protein.
Mice producing QBP1 learned normally and had good short-term memory, but struggled to consolidate long-term memories. In a PTSD-like protocol, their fear responses faded faster over the following days and they showed less anhedonia – the inability to feel pleasure. No unwanted health effects were detected.
This is a proof of concept in genetically modified mice, still far from patients. Next, the team will test whether a nasal dose given soon after a traumatic experience is enough to stop symptoms becoming chronic. The study is published in Advanced Science.
