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Brain enzyme treatment relieves memory lapse in Alzheimer's mice

tone, suggesting variation among brain regions in the role of Uch-L1.

In mice with symptoms that mimic those found in patients with Alzheimer's disease, treatments that raised Uch-L1 greatly increased their freezing time compared to their transgenic littermates when contextual learning was assessed over time, the researchers found. Improvements in the treated animals' ability to establish a memory for fear did not depend on changes in Aß levels.

The findings provide a new window into the Alzheimer's brain that could lead to new therapies, the researchers said.

"The rapid fall in Uch-L1 activity in response to Aß raises the possibility that, in the Alzheimer's brain, Aß initiates a signaling cascade that results in the partial inhibition of proteasome activity more rapidly than is likely as the result of the accumulation of misfolded or undigestable proteins."

"Our data suggest that Uch-L1 could be an attractive target for the development of new therapeutic approaches to Alzheimer's disease, either alone or in combination with therapies that alter Aß levels."


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Source:Cell Press


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