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Olfaction in neurodegenerative disorder.

Christopher Hawkes1

  • 1Essex Centre for Neuroscience, Oldchurch Hospital, Romford, UK.

Advances in Oto-Rhino-Laryngology
|May 31, 2006
PubMed
Summary
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Olfactory dysfunction, or a reduced sense of smell, is an early and common symptom in both idiopathic Parkinson's disease (IPD) and Alzheimer's disease (AD). This smell impairment often precedes motor or cognitive symptoms, highlighting its potential as an early diagnostic marker.

Area of Science:

  • Neuroscience
  • Gerontology
  • Neurology

Background:

  • Olfactory dysfunction, particularly anosmia (loss of smell), is increasingly recognized as a common feature of neurodegenerative diseases.
  • The link between olfactory impairment and conditions like idiopathic Parkinson's disease (IPD) and Alzheimer's disease (AD) suggests smell changes may be early indicators.
  • Understanding the role of smell dysfunction across various neurological disorders is crucial for early diagnosis and management.

Purpose of the Study:

  • To review the prevalence and significance of olfactory dysfunction in aging and various neurological conditions.
  • To assess the diagnostic value of smell testing in idiopathic Parkinson's disease, Alzheimer's disease, and other parkinsonian syndromes.
  • To explore the relationship between olfactory impairment, genetic factors (ApoE4), and neurodegenerative disease risk.

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Main Methods:

  • Review of existing literature on olfactory function in aging, idiopathic Parkinson's disease (IPD), Alzheimer's disease (AD), parkinsonian syndromes, motor neuron disease (MND), Huntington's chorea (HC), and inherited ataxia.
  • Analysis of observations regarding the onset, severity, and patterns of olfactory dysfunction in these conditions.
  • Consideration of diagnostic implications and potential clinical utility of smell testing and olfactory neuron biopsy.

Main Results:

  • Olfactory senescence begins around age 36, accelerating with age and preferentially affecting pleasant odors.
  • Olfactory dysfunction is nearly universal, early, and often severe in IPD and AD, preceding motor or cognitive deficits.
  • Normal smell identification in IPD is rare (except in females with tremor-dominant disease); atypical anosmia in progressive supranuclear palsy and corticobasal degeneration warrants diagnostic review. Hyposmia with one ApoE4 allele increases AD risk fivefold. Smell testing has limited clinical value in HC and MND, and olfactory neuron biopsy shows non-specific changes in IPD and AD.

Conclusions:

  • Olfactory dysfunction is a significant early marker for idiopathic Parkinson's disease and Alzheimer's disease.
  • Smell testing can aid in the diagnosis of IPD and AD, and prompt re-evaluation when findings are atypical for other parkinsonian syndromes.
  • While olfactory impairment is linked to increased risk in some neurodegenerative conditions, its clinical utility varies, and current biopsy methods are not diagnostic.