Refining HDAC inhibition to restore memory

Nevit Dilmen [creativecommons license] via Wikimedia Commons

Alzheimer disease is a progressive neurodegenerative disorder that impairs memory and mental function. It is the most common form of dementia, accounting for 60–70% of cases, and its prevalence is increasing worldwide, a trend that is expected to continue for the next few decades. Memory loss in Alzheimer disease is driven by the loss of synapses. Previous research has shown that memory can be partially restored in animal models of Alzheimer disease by inhibiting a family of enzymes called histone deacetylases (HDACs), which are involved in transcriptional control of gene expression. HDACs have many roles in the body, however, and manipulating them to improve memory might have unwanted effects on other systems. To minimize these off-target effects, some neuroscientists have suggested refining HDAC inhibition to focus on specific HDAC isoforms. But it is not known which isoforms have the greatest potential to affect memory nor how selective HDAC inhibition might affect synapse formation or function.

Lab Anim. (NY) 44, 194 (2015).
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