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Striatal function in normal aging: implications for Parkinson's disease.

G V Sawle1, J G Colebatch, A Shah

  • 1MRC Cyclotron Unit, Hammersmith Hospital, London, UK.

Annals of Neurology
|December 1, 1990
PubMed
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This study found no age-related decline in the nigrostriatal dopaminergic system in healthy individuals using L-6-[18F] fluoro-Dopa positron emission tomography. This suggests Parkinson's disease pathology may arise later in life.

Area of Science:

  • Neuroscience
  • Gerontology
  • Radiochemistry

Background:

  • Current Parkinson's disease (PD) theories often assume nigrostriatal dopaminergic system degeneration occurs with normal aging.
  • Postmortem neurochemical studies have historically supported this aging-dopamine hypothesis.

Purpose of the Study:

  • To investigate age-related changes in the nigrostriatal dopaminergic system in healthy adults.
  • To assess striatal and frontal cortical tracer uptake using L-6-[18F] fluoro-Dopa and positron emission tomography (PET).

Main Methods:

  • Utilized L-6-[18F] fluoro-Dopa and PET in 26 healthy volunteers (ages 27-76).
  • Employed a graphical approach to calculate the influx constant (Ki) for tracer uptake in the caudate, putamen, and medial frontal cortex.
  • Conducted physiological measurements on older subjects to assess age-related changes.

Related Experiment Videos

Main Results:

  • No significant decline in L-6-[18F] fluoro-Dopa influx constant (Ki) with age was observed in the caudate, putamen, or medial frontal cortex.
  • Few significant age-related physiological changes were detected in the older subjects.
  • PET findings indicated preservation of nigrostriatal dopaminergic function throughout the studied age range.

Conclusions:

  • Normal aging does not appear to involve a significant degeneration of the nigrostriatal dopaminergic system.
  • The pathological processes underlying Parkinson's disease may initiate closer to clinical presentation than previously hypothesized.
  • This challenges the long-held view of age-related dopaminergic decline as a primary factor in PD etiology.