@article{e6a5a99bfcb8414da6ceae1710c64ac5,
title = "Consistent immunohistochemical detection of intracellular β-amyloid42 in pyramidal neurons of Alzheimer's disease entorhinal cortex",
abstract = "We compared the effects of three pretreatment immunohistochemical techniques (no pretreatment, pepsin predigestion and heat pretreatment (HEAT)) for detecting intracellular β-amyloid42 (Aβ42) in pyramidal neurons of formalin-fixed Alzheimer's disease (AD) cortices (n=25). Although all three protocols immunostained Aβ42 in amyloid plaques using four commercially-obtained Aβ42 specific antibodies, only the HEAT protocol consistently detected prominent intracellular Aβ42 in pyramidal neurons. This suggests that the Aβ42 present in amyloid plaques may be structurally distinct from that located within the neurons perhaps due to differential binding proteins coupling or a consequence of formalin fixation. Detection of an abundant intracellular Aβ42 in neurons may provide alternate explanations for the origin of dense-core amyloid plaques in AD cortices other than the conventional chronic extracellular Aβ42 deposition hypothesis.",
author = "D'Andrea, {Michael R.} and Nagele, {Robert G.} and Wang, {Hoau Yan} and Lee, {Daniel H.S.}",
note = "Funding Information: Post-mortem brain tissues (entorhinal cortex) from patients clinically characterized with sporadic AD (n=25, age range=72–78, post mortem time, <18 h) were obtained from the Harvard Brain Tissue Resource Center (HBTRC, Belmont, MA), Analytical Biological Services, Inc. (Wilmington, DE) and the University of Florida Medical Coroners (Orlando and Miami Beach, FL) and were fixed in a 10% neutral buffered formalin solution under standard conditions for neuropathological diagnosis purposes. The HBTRC is supported in part by a Public Health Service grant #MH/NS 31862. Post-mortem pathological confirmation of AD was carried out for each AD brain specimen. Neuropathological changes presented in each of the brain sample were characterized by board certified neuropathologists. The diagnostic categorization of AD was based on published methods [17] and confirmed that all AD brain samples examined have extensive amyloid plaques and neurofibrillary tangles in the hippocampus and entorhinal cortex. All AD subjects included in the study can be classified as having a high likelihood that dementia is due to AD lesions according to NIA-Reagan criteria. Tissues were trimmed and processed for paraffin embedding according to conventional methods. Five-micron sections were serially cut and mounted onto SuperFrost Plus+ (Fisher Scientific, Pittsburgh, PA) microscopic slides and dried overnight. Copyright: Copyright 2008 Elsevier B.V., All rights reserved.",
year = "2002",
month = nov,
day = "29",
doi = "10.1016/S0304-3940(02)00875-3",
language = "English (US)",
volume = "333",
pages = "163--166",
journal = "Neuroscience Letters",
issn = "0304-3940",
publisher = "Elsevier Ireland Ltd",
number = "3",
}