Possible biochemical mechanism underlying long-term memories identified

There are already multiple known molecular mechanisms for long-term memories though.

One of the simplest is spike-timing-dependent plasticity [1], which is caused by the behavior of NMDA receptors shortly before and after depolarization. (This is why ethanol, an NMDA antagonist, can produce a "blackout" in high doses, where no memories are formed.)

In general, neurons have a lot of mutable long-term state. The graph of how neurons are connected can change, the strength of those connections can change, the internal chemistry of the neurons can change through gene expression factors, and, apparently, levels of long-lived prions can change.

This is not to say that the whole mechanism of long-term memory is understood, but that this discovery is just one of a class of mechanisms that may all be working in parallel or even independently.

[1] https://en.wikipedia.org/wiki/Spike-timing-dependent_plastic...

They are claiming that amyloids are used for long term memory (ie getting rid of amyloid-beta may be a bad for Alzheimer's patients), but don't really make the connection. The amyloid-beta is protective/compensatory idea has been around for while. "Long term memory" here is a fly not trying to mate 48 hours after being rejected though:

>"In this paradigm, male flies learn to suppress their courtship behavior upon repeated exposure to an unreceptive female. The 201Y-Gal4:UAS-CG4612RNAi flies developed normally, and when tested, they did not display a deficit in shortterm memory or memory up to a day. However, when tested 48 hr after training, there was significant impairment in learned suppression of male courtship"