Monday, June 18, 2012

Memories Blocked..but Recall Restored

HDAC2 ( histone deacetylase 2 ) regulates the expression of genes involved in learning and memory. MIT scientists led by Li-Huei Tsai,PhD blocked the buildup of HDAC2 in a mouse model of Alzheimer's disease and it restored structural and synaptic plasticity allowing mice with symptoms of AD to restore and access memory. This experiment suggests that memories of things learned may still be stored in the brain but overproduction of HDAC2 blocks access to those memories. This finding has already been experimentally replicated.
In another epigenetic part of their study, these researchers found that glucocorticoid receptor 1normally turned on by stress was in fact switched on/activated from the accumulation of Abeta amyloid causing an increase in HDAC2 and chronic blockage of the genes necessary for memory.
For alzheimer's patients , these MIT researchers have developed a potent HDCA2 inhibitor and are preparing to submit papers to the FDA to begin experimental testing.
NATURE 2012 ; 483 (7388):222-226
Also see Science 2012;335(6075):1513-1516 "Generation of a synthetic memory trace"

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