Relationship between apolipoprotein E and the amyloid deposits and dystrophic neurites of Alzheimer's disease

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Abstract
T. C. Dickson, H. L. Saunders and J. C. Vickers (1997) Neuropathology and Applied Neurobiology, 23, 483–491Relationship between apolipoprotein E and the amyloid deposits and dystrophic neurites of Alzheimer's diseaseAlthough the inheritance of certain apolipoprotein E (ApoE) alleles has been recognized as a genetic risk factor for Alzheimer's disease, the role of ApoE in the pathology underlying this disease is unclear. Several reports have emphasized the association of ApoE with either β‐amyloid plaque formation or the development of neurofibrillary pathology. Utilization of multiple label immunohistochemical methods enabled us to examine directly the localization of ApoE immunoreactivity relative to β‐ amyloid plaques, dystrophic neurites and neurofibrillary tangles. In Alzheimer's disease cases, β‐amyloid plaques showing high ApoE immunoreactivity were localized to layers II, III and V of the neocortex. In layer I, β‐amyloid plaques were unlabelled for ApoE relative to β‐amyloid. Dense core plaques labelled for β‐amyloid often had only the central portions labelled for ApoE. Conversely, ApoE labelled spherical structures within some plaques were not immunoreactive for β‐amyloid or dystrophic neurite markers. Unlike β‐amyloid labelled plaques, all ApoE immunoreactive plaques were associated with dystrophic neurites. In preclinical Alzheimer's disease cases, most plaques were double labelled for β‐amyloid and ApoE. ApoE did not label dystrophic neurites or the early stages of neurofibrillary tangle formation, indicating that ApoE may not be directly involved in neurofibrillary pathology. The specific presence of ApoE in plaques associated with dystrophic neurites in demented patients suggests that ApoE may contribute toward a higher degree of β‐ amyloid fibrillogenesis, enhancing the ability of certain plaques to cause damage to surrounding axons.