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Human olfactory epithelium in normal aging, alzheimer's disease, and other neurodegenerative disorders
Author(s) -
Trojanowski John Q.,
Newman Paul D.,
Hill William D.,
Lee Virginia M.Y.
Publication year - 1991
Publication title -
journal of comparative neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.855
H-Index - 209
eISSN - 1096-9861
pISSN - 0021-9967
DOI - 10.1002/cne.903100307
Subject(s) - neurite , peripherin , biology , neurofilament , olfactory epithelium , olfactory mucosa , synaptophysin , neuroscience , olfactory bulb , olfactory ensheathing glia , microbiology and biotechnology , olfactory system , olfactory nerve , intermediate filament , olfactory marker protein , pathology , central nervous system , cytoskeleton , immunohistochemistry , immunology , cell , medicine , in vitro , genetics , gene
By use of immunohistochemistry, we characterized the molecular phenotype of human olfactory epithelial (OE) cells and assessed the nature of the dystrophic olfactory neurites described initially in Alzheimer's disease (AD). Keratin 8 was present in all classes of OE cells. Sustentacular cells lacked other cell type specific polypeptides and were distinguished from neurons and basal cells because the latter two classes of OE cells expressed neural cell adhesion molecules (N‐CAMs) and microtubule associated proteins (MAPs), i.e., MAP5. Basal cells expressed nerve growth factor receptors (NGFRs), which distinguished them from olfactory neurons. Unlike their perikarya, olfactory axons expressed vimentin and GAP‐43, but not peripherin or neurofilament (NF) proteins. Olfactory nerves were distinguished from other axons because the latter were positive for all three NF subunits and peripherin, in addition to vimentin and GAP‐43. Dystrophic neurites in the OE were GAP‐43 positive, but they also expressed proteins that were not detected in normal olfactory nerves (i.e., synaptophysin, MAP2, tau, peripherin, NF proteins). Further, rare NF positive olfactory neurons gave rise to NF positive dystrophic neurites. These neurites were present in all 11 AD cases, 11 of 14 subjects with other neurodegenerative diseases, and 6 of 8 neurologically normal adult controls, but no dystrophic neurites were seen in 9 fetal and neonatal case. We conclude that the molecular phenotype of different human OE cells is distinct and that dystrophic olfactory neurites occur very frequently in neurologically normal adults. The relevance of these neurites to aging or specific disease processes remains speculativ.