We investigated the expression of P-glycoprotein (P-gp) in brain samples of Alzheimer disease (AD) and normative brains (NM). Superior temporal cortex hippocampal and brainstem samples from 15 AD and NM brains were selected from comparable sites. P-gp positive capillaries and β-amyloid (Aβ) senile plaques (SP) were counted. Statistical analysis of the data was performed using nonparametric data analysis with Mann-Whitney, Kruskal-Wallis, and Spearman’s tests. There were no significant differences in P-gp expression between superior temporal and hippocampus samples. However, there were significant differences in P-gp expression, when comparing brainstem with both hippocampal and superior temporal samples in both conditions ( ; in NM cases and ; in AD cases); the brainstem has greater P-gp expression in each case and condition. In addition, there was a notable inverse negative correlation ( ) between P-gp expression and the presence of SPs in the AD condition superior temporal cortex. The results of this study suggest that there were significant site-dependent differences in the expression of P-gp. There may be an increased protective role for P-gp expression against amyloid deposition in the brainstem and in the superior temporal cortex of AD brains. 1. Introduction Alzheimer’s disease, which is largely a sporadic disease, increases in prevalence with age. In addition, in individual cases, the neuropathologic burden of Alzheimer disease, that is, neuronal neurofibrillary tangle and related dysfunction as well as beta amyloid (Aβ) senile plaques [SPs] increases progressively with time [1–3]. The hallmark lesions for AD are neurofibrillary tangles (NFTs) and senile plaques (SPs) [4]. A striking characteristic of these lesions is that they develop in particularly predictable areas of the brain and are completely or mostly absent in other areas [5, 6]. Neurofibrillary tangles, as they progressively populate neuronal populations of brain tissue, progress from the earliest lesion in the entorhinal cortex to involve neighbouring limbic cortex and then progressively through neocortex [7]. However, neurofibrillary tangles are typically and frequently found in key selected subcortical structures, chiefly, hippocampus, the nucleus basalis of Meynert, and the pontine locus ceruleus [8–11]. SPs develop as a result of a pathologic accumulation of Aβ proteins in the cerebral interstitium as well as within the walls of capillaries and larger cerebral vessels [12]. Senile plaques also have a characteristic distribution which is chiefly neocortical and limbic cortex [13].
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