Structure of Human Fetal and Adult Olfactory Neuroepithelium

Abstract

\s=b\Human olfactory neuroepithelium and respiratory mucous membrane in fetal and adult whole-mount sections were studied. In the fetus, the olfactory neuroepithelium extends from the roof of the nasal cavity to the midportion of the nasal septum and onto the superior turbinate in a continuous fashion. In the adult, the zonal distribution of supporting, sensory receptor, and basal cells is frequently disrupted, and the supporting and sensory receptor cells are often depleted or degenerate. The degree of the degeneration of the adult olfactory neuroepithelium varies from case to case. The most striking feature in the adult is the replacement of large areas of olfactory neuroepithelium with respiratory epithelium. The extensive replacement of olfactory neuroepithelium with respiratory epithelium points out the sampling problem related to small, random biopsy specimens of the olfactory area.

Autologous mucosal transplant in chronic spinal cord injury: an Indian Pilot Study

“…23 Hence, participants, with spinal injury, less than 40 years of age only were included in our study. The same was the rationale for defining a smaller length of myelomalacia as inclusion criteria for participants aged between 35 and 40 years as opposed to participants less than 35 years of age.…”

Tests of human olfactory function: Principal components analysis suggests that most measure a common source of variance

“…Importantly, interindividual differences in test scores, which are essential to the production of correlations among test measures, may depend upon the relative degree of such damage. It is well established, for example, that the olfactory neuroepithelium, unlike more central olfactory centers, undergoes considerable deterioration throughout the normal life span (see Curcio, McNelly, & Hinds, 1985;Nakashima, Kimmelman, & Snow, 1984), being susceptible to insults from environmental agents (including viruses and airborne toxins), trauma, and a variety of disease processes (Deems et aI., 1991;Jafek, Eller, Esses, & Moran, 1989;Moran, Jafek, Rowley, & Eller, 1985;Trojanowski, Newman, Hill, & Lee, 1991).…”

The olfactory vector hypothesis of neurodegenerative disease: Is it viable?

“…The smell loss associated with the most salient of such risk factors, advanced age, is likely secondary to the aforementioned occlusion of the foramina of the cribriform plate by appositional bone growth and to cumulative damage to the olfactory neuroepithelium from bacteria, viruses, and other xenobiotic agents. 65 In potential accord with the "olfactory damage" hypothesis for AD is the finding that removal of the olfactory bulbs of both rats and mice leads to decreased performance on cognitive tasks not dependent on olfaction, 66 an effect attributed, in part, to degenerative disruption of interconnections with higher brain regions, such as those between the olfactory and septohippocampal systems. 67 Although olfactory bulbectomy is a severe insult to a rodent, inducing a wide range of behavioral, hormonal, neurochemical, and anatomic changes including the rewiring of synaptic assemblies and rebalancing of neurochemical systems, 68,69 a number of these changes mimic key elements of AD-related neuropathology.…”