Senior author Rudolph Tanzi of Harvard said Alzheimer's disease brains have two types of lesions -- beta-amyloid plaques outside neurons, and neurofibrillary tangles within them. The known Alzheimer's disease genes implicate plaques but Alzheimer's disease symptoms correlate more closely with tangles, comprised of "tau" protein, normally adhered to microtubules.
Tanzi said zinc stabilizes many protein complexes, including microtubules, polymers of tubulin, which regulate synapses and play recently revealed key roles in memory encoding in neurons.
Tanzi and colleagues at Boston University, The University of Alberta, The University of Arizona and The Chopra Foundation identified specific zinc-tubulin binding sites promoting side-to-side tubulin interactions.
"It looks like beta-amyloid plaques -- linked to Alzheimer's disease's -- themselves aren't destructive directly but lead to lower zinc levels within neurons. This in turn disrupts microtubules and tau, causing tangles and memory loss," Tanzi said in a statement. "Protecting microtubules and their association with tau may be the best treatment approach in Alzheimer's disease."
The findings published in the journal PLoS One might lead to different therapies.
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