Abstract
The Lewy body variant of Alzheimer disease (LBV) occupies a messy middle ground between Alzheimer disease (AD) on the one hand, and pure Lewy body diseases (Parkinson’s disease or diffuse Lewy body disease), on the other. In addition to brainstem and neocortical Lewy bodies, LBV brains have enough neocortical neuritic plaques to meet diagnostic criteria for AD. However, neurofibrillary pathology in LBV is modest, since tangle densities in LBV are typically intermediate between AD and age-matched controls or pure Lewy body disease brains. Apolipoprotein E-4 is overrepresented in LBV, as it is in AD but is not in PD or diffuse Lewy body disease (DLBD). Neurologically, LBV patients often display sufficient parkinsonian signs to separate them from AD, but these findings are usually too subtle to warrant clinical diagnoses of Parkinson’s disease (PD). Neuropsychological deficits in LBV include a subcortical dementia pattern similar to DLBD, and more severe global cognitive impairment reminiscent of AD.