Increased numbers of beta APP-immunoreactive neurones in the entorhinal cortex after head injury

Abstract

In a previous publication we hypothesized that Alzheimer's disease (AD) can be induced by the age-related increase in expression of beta-amyloid precursor protein (beta APP) in the medial temporal lobe. Head injury has also been identified as a risk factor for AD and as such, similarities should exist between the pathology found after head injury and the earliest stages of pathology in AD. In this study, we have quantified the number of beta APP-immunoreactive neurones in the medial temporal cortex (pre-alpha cells, layer II) of 13 head injured and 17 control patients. Significantly more beta APP immunoreactive neurones were observed in head injury cases (mean 18.4 per cluster) compared with controls (mean 13.4 per cluster, p < 0.05). These data provide a mechanism to explain how an environmental event such as head injury can generate the same molecular pathology (increased neuronal beta APP) as is found in the earliest stages of AD.