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Olfactory Receptors: Location and Structure01:03

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The process of olfaction, also known as the sense of smell, is a sophisticated chemical response system. The specialized sensory neurons that facilitate this process, known as olfactory receptor neurons, are situated in an upper segment of the nasal cavity, known as the olfactory epithelium. Olfactory sensory neurons are bipolar, with their dendrites extending from the epithelium's apex into the mucus that lines the nasal cavity. Airborne molecules, when inhaled, traverse the olfactory...
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Humans detect odors with the help of specialized cells located in the upper part of the nasal cavity, called olfactory receptor neurons (ORNs). ORNs possess hair-like structures called cilia, which are receptive to sensations from the inhaled air. When an odorant molecule binds to a specific receptor on the cell of the cilia, it leads to a series of events that ultimately cause the ORN to send electrical signals to the olfactory bulb in the brain through the olfactory nerves.
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Updated: Sep 25, 2025

Olfactory Assays for Mouse Models of Neurodegenerative Disease
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Effect of olfactory bulb pathology on olfactory function in normal aging.

Cécilia Tremblay1, Geidy E Serrano1, Anthony J Intorcia1

  • 1Departement of Neuropathology, Banner Sun Health Research Institute, Sun City, Arizona, USA.

Brain Pathology (Zurich, Switzerland)
|April 29, 2022
PubMed
Summary

Olfactory decline in aging is common. While olfactory bulb tau pathology is frequent, it doesn't independently cause smell loss; widespread brain pathology, particularly alpha-synuclein, is linked to age-related olfactory impairment.

Keywords:
Alzheimer's diseaseLewy body diseaseagingamyloid βolfactory bulbtauα-synuclein

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Area of Science:

  • Neuroscience
  • Pathology
  • Aging Research

Background:

  • Olfactory dysfunction is a common sign of aging and neurodegenerative diseases.
  • The olfactory bulb (OB) is an early site affected in neurodegeneration.
  • Understanding OB pathology's role in age-related smell loss is crucial.

Discussion:

  • Tau pathology is highly prevalent (95%) in the OB of aging individuals.
  • Amyloid-beta (Aβ) and alpha-synuclein (αSyn) pathologies are less common in the OB.
  • OB tau pathology shows a weak correlation with olfactory performance, not significant after age correction.

Key Insights:

  • Neither OB tau, Aβ, nor αSyn pathology independently predict olfactory performance in non-demented aging individuals.
  • Whole brain tau and αSyn pathology loads correlate with olfactory function.
  • Only alpha-synuclein (αSyn) pathology load in the whole brain significantly predicts olfactory performance after accounting for age.

Outlook:

  • Age-related olfactory impairment may require pathology beyond the olfactory bulb.
  • Further research is needed to understand the complex interplay of brain pathologies and olfactory decline.
  • This study highlights the importance of considering widespread brain pathology in aging-related smell loss.