There are already multiple known molecular mechanisms for long-term memories though.<p>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 &quot;blackout&quot; in high doses, where no memories are formed.)<p>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.<p>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.<p>[1] <a href="https:&#x2F;&#x2F;en.wikipedia.org&#x2F;wiki&#x2F;Spike-timing-dependent_plasticity" rel="nofollow">https:&#x2F;&#x2F;en.wikipedia.org&#x2F;wiki&#x2F;Spike-timing-dependent_plastic...</a>