For at least the earlier stages of some forms of dementia it has been shown that lost memories are still there, just inaccessible. The storage is not destroyed, but rather the process of retrieval is impacted. Here researchers demonstrate that they can block and restore interaction with memory in rats, but it isn't yet clear that the restoration portion of their work can be applied to age-related loss of memory. The underlying cellular mechanisms look similar, but may or may not turn out to be similar enough, and there is also the case that the actual demonstration is quite specific to one portion of the nervous system. So a confirmation of utility for human medicine is something to look for in the years ahead:
Scientists optically stimulated a group of nerves in a rat's brain that had been genetically modified to make them sensitive to light, and simultaneously delivered an electrical shock to the animal's foot. The rats soon learned to associate the optical nerve stimulation with pain and displayed fear behaviors when these nerves were stimulated. Analyses showed chemical changes within the optically stimulated nerve synapses, indicative of synaptic strengthening.
In the next stage of the experiment, the research team demonstrated the ability to weaken this circuitry by stimulating the same nerves with a memory-erasing, low-frequency train of optical pulses. These rats subsequently no longer responded to the original nerve stimulation with fear, suggesting the pain-association memory had been erased. In what may be the study's most startlingly discovery, scientists found they could re-activate the lost memory by re-stimulating the same nerves with a memory-forming, high-frequency train of optical pulses. These re-conditioned rats once again responded to the original stimulation with fear, even though they had not had their feet re-shocked.
In terms of potential clinical applications [researchers] noted that the beta amyloid peptide that accumulates in the brains of people with Alzheimer's disease weakens synaptic connections in much the same way that low-frequency stimulation erased memories in the rats. "Since our work shows we can reverse the processes that weaken synapses, we could potentially counteract some of the beta amyloid's effects in Alzheimer's patients."