Alzheimer's disease (AD) is a progressive neurological disorder that slowly attacks and purloins the minds of its victims. It is the most common of all neurodegenerative disorders, with approximately 25 million people worldwide suffering from this devastating disease. One of the main risk factors of AD is increased age. As life expectancies continue to rise, AD is becoming tragically common. It is estimated that the number of people afflicted with AD will triple by the year 2050 and cause a huge economical and emotional burden to our societies. Despite intensive studies, effective therapies still await discovery. Several studies have suggested that regulation of histones, and thus chromatin structure, is an important step in modulating transcription and facilitating long term changes in neuronal physiology. Indeed, the studies Tsai et al. have provided convincing proof-of-principle evidence that agents, called histone deacetylase inhibitors, that can modulate chromatin structure and augment gene expression can improve memory capabilities in a genetically engineered Alzheimer's mouse model. The results implicate HDAC inhibitors as a potential therapeutics with novel mechanisms for AD and other cognitive and neurodegenerative diseases Our previous work has demonstrated that mercaptoacetamide-based HDACIs are able to protect cortical neurons in culture from oxidative stress-induced death; a major underlying contributor to Alzheimer's disease pathology. More importantly, some of the mercaptoacetamide-based HDAC inhibitors are fully neuroprotective over a wide range of concentrations. These studies argue that this HDAC inhibitor design strategy may lead to ideal therapeutics for the treatment of neurodegenerative diseases including those associated with neuronal, learning and memory loss, such as Alzheimer's disease.