Effect of Huntington's and Alzheimer's diseases on the transport of nicotinic acid or nicotinamide across the human blood-brain barrier

Adv Exp Med Biol. 1991:294:675-8. doi: 10.1007/978-1-4684-5952-4_91.

Abstract

The cerebral uptake of 11C-nicotinic acid (11C-NAC) and 11C-nicotinamide (11C-NAM) was quantified by the use of PET. Based on the amount of activity injected, the PET images showed a low cerebral uptake of 11C-NAC, while 11C-NAM was clearly visualized in the cortical areas. This discrepancy was found to be the result of the binding of 11C-NAC to the red blood cells by a factor of 5 to 20 above that for 11C-NAM. 11C-NAM was better extracted by the cerebrum than 11C-NAC, as shown by the mean values of the cortical tissue/plasma ratio of 1.9 for 11C-NAC and 5 for 11C-NAM at 30 min. post-injection. An analysis of Patlak-Gjedde plot curves revealed a metabolic compartment for 11C-NAC and 11C-NAM with similar values of about 0.02 l/min for the accumulation constant K3. This was indicative of a slower transport rate for 11C-NAC. A significant finding of the study was the increasing ratio of activity concentrations in red blood cells versus the concentrations in plasma (over time). There were no significant differences between the data from normal volunteers and patients with Huntington's or Alzheimer's disease.

MeSH terms

  • Alzheimer Disease / diagnostic imaging
  • Alzheimer Disease / metabolism*
  • Blood-Brain Barrier*
  • Brain / diagnostic imaging
  • Brain / metabolism
  • Humans
  • Huntington Disease / diagnostic imaging
  • Huntington Disease / metabolism*
  • Niacin / pharmacokinetics*
  • Niacinamide / pharmacokinetics*
  • Tomography, Emission-Computed

Substances

  • Niacinamide
  • Niacin