Migraine is a collection of neurological symptoms that include recurring, intense, throbbing headache pain thatcan last from 4 to 72 hours and affects millions of people. The discovery of the triptan drugs was a majorbreakthrough for the treatment of debilitating pain for many migraine sufferers. Unfortunately, repeated orprolonged use of triptans and other analgesic drugs (e.g. opioids, ergotamines) often results in production of aserious, disabling adverse effect known as medication overuse headache (MOH).

Alcohol consumption impairs motor coordination, attentional efforts and memory function. Alcohol-impaireddriving accounted in 2013 for ~31% of all traffic accidents resulting in 10,076 fatalities and $59 billion crash-related cost. We propose to study the mechanisms how ethanol affects brain state-dependent neuralsignaling. Brain state-dependent signaling comprises adjustments in cellular and circuit activity to optimizehow the brain processes information in a distinct behavioral context.

Migraine is a collection of neurological symptoms that include recurring, intense, throbbing headache pain thatcan last from 4 to 72 hours and affects millions of people. The discovery of the triptan drugs was a majorbreakthrough for the treatment of debilitating pain for many migraine sufferers. Unfortunately, repeated orprolonged use of triptans and other analgesic drugs (e.g. opioids, ergotamines) often results in production of aserious, disabling adverse effect known as medication overuse headache (MOH).

Alzheimer's disease (AD) is a profoundly debilitating neurodegenerative disorder without effective treatment or determinative antemortem diagnostics. Improvements in diagnostic and treatment options will require a better understanding of the biological processes that drive AD onset and progression. The prevailing model to explain AD pathogenesis holds that neuronal degeneration and clinical demise are precipitated by the gradual accumulation, in brain centers controlling memory and cognition, of amyloid-? (A?) peptide, a catabolite of the transmembrane Amyloid Precursor Protein (APP).

Alzheimer's disease (AD) is a profoundly debilitating neurodegenerative disorder without effective treatment or determinative antemortem diagnostics. Improvements in diagnostic and treatment options will require a better understanding of the biological processes that drive AD onset and progression. The prevailing model to explain AD pathogenesis holds that neuronal degeneration and clinical demise are precipitated by the gradual accumulation, in brain centers controlling memory and cognition, of amyloid-? (A?) peptide, a catabolite of the transmembrane Amyloid Precursor Protein (APP).