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Chemosensory Disorders and Nutrition
Published in Alan R. Hirsch, Nutrition and Sensation, 2023
Carl M. Wahlstrom, Alan R. Hirsch, Bradley W. Whitman
Many possible mechanisms have been postulated for age-induced olfactory defects (Doty 1991). One theory posits that degenerative processes caused by toxins and viruses produce a cumulative effect on the olfactory epithelium. A second theory suggests that age-related immunocompromise predisposes people to upper respiratory infections, which may be followed by postviral upper respiratory infection-induced anosmia. The premise of a third hypothesis suggests that in the elderly, the central neural pathway degenerates with concomitant reduction in noradrenergic chemosensory projections. A fourth theory postulates ossification of the foramina of the cribriform plate with secondary occlusion and compression of the olfactory fila. These hypotheses are not mutually exclusive.
Abnormalities of Smell
Published in R James A England, Eamon Shamil, Rajeev Mathew, Manohar Bance, Pavol Surda, Jemy Jose, Omar Hilmi, Adam J Donne, Scott-Brown's Essential Otorhinolaryngology, 2022
Richard L. Doty, Steven M. Bromley
In some circumstances, both can be involved. Chronic rhinosinusitis, for example, can produce damage to the olfactory membrane in addition to blocking airflow, and altered membrane function can, over time, lead to degeneration within the olfactory bulb, which is a central structure. Although many causes of olfactory disturbance due to conductive factors or inflammation of the olfactory epithelium can be treated, most olfactory disorders due to sensorineural factors remain untreatable.
Cranial Neuropathies I, V, and VII–XII
Published in Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw, Hankey's Clinical Neurology, 2020
Damage to olfactory epithelium: Upper respiratory infections.Exposure to chemicals and toxins: herbicides, pesticides, solvents, and heavy metals (cadmium, chromium, nickel, and manganese).
Analyses on the influence of normal nasal morphological variations on odorant transport to the olfactory cleft
Published in Inhalation Toxicology, 2022
Ryan M. Sicard, Reanna Shah, Dennis O. Frank-Ito
According to Hahn et al. (1993) and Keyhani et al. (1995), approximately 10% of inhaled air reaches the olfactory cleft during a normal resting breath, while Zhao and Jiang (2014) reported about 6%±4% of flow volume passing through the olfactory cleft. Additionally, variations in nasal morphology have been traditionally understood to play a critical role in olfactory function (Van Valkenburgh et al. 2014) as it influences airflow (Craven et al. 2010; Eiting et al. 2014; Keeler et al. 2016; Patki and Frank-Ito 2016; Ramprasad and Frank-Ito 2016; Rygg et al. 2017; Inthavong et al. 2019) and odorant transport in the nasal cavity (Lawson et al. 2012; Rygg et al. 2017). Morphological profiles that have been postulated to be associated with improved olfaction include the dorsal conduit, which delivers inhaled odorant-laden air to the olfactory cleft through enhanced olfactory airflow, and an enlarged olfactory cleft at the posterior end of the nasal cavity (Craven et al. 2007; Eiting et al. 2014, 2015). It has also been reported that anatomical changes in the olfactory cleft or the nasal valve region alter odorant transport to the olfactory epithelium (Zhao et al. 2004). Subsequently, as the nasal vestibule lies exactly posterior to the nostrils and is the primary point of contact between odorant-laden air and nasal mucosa, it is essential to explore the impacts of morphological variations in the nasal vestibule on airflow and odorant concentration in the olfactory regions.
Whole-body inhalation exposure to 2-ethyltoluene for two weeks produced nasal lesions in rats and mice
Published in Inhalation Toxicology, 2021
Madelyn C. Huang, Cynthia J. Willson, Sridhar Jaligama, Gregory L. Baker, Alan W. Singer, Yu Cao, Jessica Pierfelice, Esra Mutlu, Brian Burback, Guanhua Xie, David E. Malarkey, Barney Sparrow, Kristen Ryan, Matthew Stout, Georgia K. Roberts
Atrophy of the olfactory epithelium and olfactory nerves after only 2 weeks of exposure may have implications for longer studies of 2-ET. As many animals rely on odors to locate and discriminate food (Aimé et al. 2007), impaired olfaction in rodents could potentially lead to reduced feed consumption and subsequently lower body weight. On the other hand, the olfactory epithelium can have regenerative capacity even during exposures to toxicants as long as enough regenerating cells remain unharmed (Hurtt et al. 1988; Upadhyay and Holbrook 2004). Furthermore, rodents exhibit normal olfactory-mediated behaviors even with large reductions in olfactory nerves and epithelium. For instance, social interactions and maternal behaviors were maintained in unilaterally bulbectomized rodents (Devor and Murphy 1973; Fleming and Rosenblatt 1974) and food-finding behavior was unaffected in mice with only 10% of normal receptor cells in the olfactory epithelium (Harding et al. 1978). Thus, the implications of these nasal lesions for feed consumption and other aspects of animal behavior after chronic exposures to 2-ET will depend on the balance of toxicant damage and regenerative capacity of the olfactory epithelium and nerves.
Repurposing ibuprofen-loaded microemulsion for the management of Alzheimer’s disease: evidence of potential intranasal brain targeting
Published in Drug Delivery, 2021
Ming Ming Wen, Noha Ismail Khamis Ismail, Maha M. A. Nasra, Amal Hassan El-Kamel
To overcome the limited blood-brain barrier (BBB) penetration, intranasal administration through olfactory delivery provides a rationale for a noninvasive alternative on the clinical ground to target the brain for direct drug delivery and offers benefit to avoid the side effects often associated with oral dosage forms of NSAIDs, such as gastrointestinal disturbances, gastric irritation, and increased risk of ulcer formation (Laine, 2003). In recent years, the olfactory mucosa has also been proposed as a potential target for an early marker of neurodegenerative conditions, such as schizophrenia, AD, multiple sclerosis, and Parkinson’s disease (Rey et al., 2018; Bhattamisra et al., 2020). Although olfactory epithelium is presented in only 3% of the nasal cavity, this route is short and direct because the olfactory sensory neurons do not have a synapse between the two-element sensory receptors (Wen, 2011). Ibuprofen has known limited ability to cross the BBB (Mandal et al., 2018); therefore, a novel formulation that can deliver ibuprofen through an intranasal route for brain targeting is vitally needed.