"Our findings of early reversible neurophysiological and cognitive deficits occurring prior to neuronal loss open new avenues in the prion field," they wrote. "To date, prion infection in mice has conventionally been diagnosed when motor deficits reflect advanced neurodegeneration. Now the identification of earlier dysfunction helps direct the study of mechanisms of neurotoxicity and therapies to earlier stages of disease, when rescue is still possible.
"Eventually it may also enable preclinical testing of therapeutic strategies through cognitive endpoints. These data now lead to the hope that early intervention in human prion disease will not only halt clinical progression but allow reversal of early behavioral and cognitive abnormalities," wrote the scientists.
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Source:Cell Press