Larry D. Reid, Dylan Z Taylor, Alicia A. Walf


Epidemiological research has identified loss of olfactory perception as a salient risk-factor

associated with the slowly developing, but insidious, cognitive decline characteristic of late onset

Alzheimer’s disease (LOAD). Evidence supports the conclusion that the first appearance of neural loss

associated with LOAD occurs in the periphery of the olfactory brain. These two well-supported

conclusions focus attention on the nasal cavity’s olfactory mucosa which contains the dendrites of

the olfactory nerves whose axons ascend through the foramina of the cribriform plate to the olfactory

bulb. Consequently, this review begins with a description of the physiology of the olfactory mucosal

tissue, the barrier between contaminants in breathed air and the olfactory bulb. The functionality of the mucosa’s innate immune system(IIS) regularly protects the olfactory bulb from infectious threats in breathed air. Therefore, any event hindering the efficiency of the IIS of the olfactory mucosa, in turn, enhances the likelihood of disease of the olfactory bulb which is where LOAD begins. Given the known of the physiology of the olfactory mucosa, an event likely disrupting the efficiency of the IIS is the wide-spread use of drugs to treat the symptoms of the common cold and insomnia. A prudent resolution to decreasing the risk of LOAD is ultimately a cognitive, behavioral issue of avoiding the use of these drugs which may seem utilitarian, but probably is not, and whose use is risky.



Alzheimer’s disease; olfaction; over-the-counter drugs; sleep-aids, histamine; innate immune system(IIS); psychoneuroimmunology

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