The more we learn, the more we learn what we don’t know

As we considered in Beating the Dementia Monster, beta amyloid may be a red herring in the search for an actual cure for Alzheimer’s disease.  The amyloid plaques appear as the disease progresses, and removing them seems to improve memory.  But are they a fundamental part of the disease mechanism?  Or are they perhaps something separate, such as a mechanism the body uses to fight a pathogen causing the disease?  Perhaps their effect on memory is simply a secondary phenomenon unrelated to their purpose or origin.  Or maybe they don’t affect memory at all. 

There’s an interesting new study (again, with mice) from the University of New South Wales in Australia that suggests the plaques may not even be implicated in memory loss.  Instead, memory loss results from a breakdown in regulation of the synapses, the tiny spaces between brain cells.  Memories are held in these spaces, and there are special proteins that regulate this activity.  What if there’s a problem with these proteins? 

The research was published in the journal Molecular Neurodegeneration. Recall that RNA plays an important role in the generation of proteins.  RNA editing (which I’d never heard of before) is a process by which the RNA and its resultant proteins are sometimes modified.  This might be a good thing, but it can apparently go wrong.  The research suggested that inappropriately edited RNA generated proteins that did not regulate the synapses correctly.  Our memories live in the synapses, and this apparently destroys them. 

What’s exciting here is that the researchers seem to have found a way to control the errant editing process.  One researcher, Bryce Vissel explained, "RNA editing can be used as a 'molecular switch.'  By flicking the switch in the mice models we use in our research we were able to stop the brain cell connections from breaking down."  This improved memory performance in the mice. 

Can the process they used be adapted to humans?  Will it actually stop the degeneration of brain cells?  More research is required.  (Which is why I support funding research for Alzheimer’s disease.)