Michael Kelberman
Post-Doctoral Fellow

Throughout my undergraduate and graduate careers, I've been interested in understanding the locus coeruleus norepinephrine system's influences over diverse sets of behaviors, and how these normal processes go awry in disease. Specifically, my current work with Dr. David Weinshenker seeks to describe how hyperphosphorylated tau affects locus coeruleus function in the context of Alzheimer's disease. Although dysregulation of the locus coeruleus has long been implicated in Alzheimer's disease, it has only been recently identified as one of the first sites to accumulate hyperphosphorylated tau, a precursor to neurofibrillary tangles. Despite this early pathology, the locus coeruleus does not degenerate until mid to late stages of Alzheimer's disease, suggesting that any detrimental effects of this pathology could persist for decades. The early accumulation of hyperphosphorylated tau in the locus coeruleus also provides a potential therapeutic target, prior to substantial cognitive impairment or brain atrophy when interventions may be more effective. To explore these questions, we employ a multifaceted approach including behavioral assays, electrophysiology, optogenetics, and functional magnetic resonance imaging in rodent models of Alzheimer's disease.