作者: D. Selkoe , C. Joachim , D. Frenkel , P. Ward , D. Games
DOI:
关键词: Immunohistochemistry 、 Alzheimer's disease 、 Neurite 、 Biology 、 Amyloid beta 、 Amyloid 、 Beta (finance) 、 Pathology 、 Senile plaques 、 Epitope
摘要: A central unresolved issue in Alzheimer's disease is the origin of extracellular amyloid beta protein (A P) found senile plaques and its relationship to dystrophic neurites that intimately surround it. Here presence distribution within various epitopes beta-amyloid precursor (APP) are compared with P itself markers for plaque neurites. Several principal findings emerge: 1) antibodies regions APP outside ('APP antibodies') recognize only a subgroup plaques; 2) these plaques, label discrete globular granular structures morphologically resembling neurites; 3) virtually all labeled by also contain reactive tau; 4) double labeling anti-tau an antibody shows neuritelike profiles stained always closely associated tau-positive same minority appear be both antibodies; 5) different throughout suggesting full-length precursor. The authors conclude immunostained Because many P-containing neocortex, cerebellum, striatum were devoid any labeling, as vascular deposits, it unlikely principally derived from immunodetection apparently APP, axonally transported protein, selected provides yet another marker neuritic dystrophy, possibly indicative aberrant regenerative response.