Ever since Dr. Coleman's first publication on Alzheimer's disease that indicated continuing neuronal plasticity in the aging human brain and loss of this plasticity in Alzheimer's disease (Science, 1979) his work has focused on differentiating changes in the brain in Alzheimer's disease from changes related to normal, non-demented ageing. His initial studies in this area were based on quantitative Golgi studies of dendritic extent in human and rodent brains. Feeling a need to be able to competently expand into studies using molecular biology, he spent much of two summers at Cold Spring Harbor Laboratories learning molecular biology and molecular biology methods. One of these summers resulted in the first publication (with Jim Eberwine in PNAS) of a method of profiling gene expression in single identified neurons. Most recently, Dr. Coleman’s work has expanded into the realm of epigenetics. This work is successfully demonstrating that reduced transport of epigenetic molecules from the cytoplasm into the cell nucleus is an early key event in the cellular pathology of Alzheimer's disease. This inability of epigenetic molecules to translocate to the nucleus, where they should be, has consequences for chromatin structure and consequently, the massive changes in gene expression seen in the AD brain. In addition, the aberrant cytoplasmic localization of epigenetic molecules leads to interactions with transport mechanisms in axons and dendrites, to interactions with mitochondria and to other interactions leading to the pathophysiology of Alzheimer's disease.