In the present study, we expanded on these observations by using tyrosine hydroxylase (TH) immunohistochemistry and unbiased stereology to investigate the extent of noradrenergic LC neuron loss in postmortem samples obtained from subjects who received an antemortem clinical diagnosis of no cognitive impairment (NCI), amnestic MCI (aMCI; the MCI subtype most likely to convert to frank AD [96, 121, 122]), or mild/moderate AD. The gene discussed is TH; the disease is Alzheimer disease.