Expression of iron transport proteins and excessive iron accumulation in the brain in neurodegenerative disorders

Brain Res Brain Res Rev. 1998 Aug;27(3):257-67. doi: 10.1016/s0165-0173(98)00012-5.


New findings on the role of LfR (lactotransferrin receptor), MTf (melanotransferrin), CP (ceruloplasmin) and DCT1 (Divalent Cation Transporter) in brain iron transport, obtained during the past 3 years, are important advances in the fields of physiology and pathophysiology of brain iron metabolism. According to these findings, disruption in the expression of these proteins in the brain is probably one of the important causes of the altered brain iron metabolism in age-related neurodegenerative diseases, including Parkinson's Disease, Alzheimer's disease, Huntington's disease and amyotrophic lateral sclerosis. Further studies on the involvement of LfR, MTf and DCT1 in iron uptake by and CP in iron egress from different types of brain cells as well as control mechanisms of expression of these proteins in the brain are critical for elucidating the causes of excessive accumulation of iron in the brain and neuronal death in neurodegenerative diseases.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Antigens, Neoplasm
  • Brain / metabolism*
  • Carrier Proteins / biosynthesis*
  • Ceruloplasmin / biosynthesis
  • Humans
  • Iron / metabolism
  • Iron / pharmacokinetics*
  • Melanoma-Specific Antigens
  • Neoplasm Proteins / biosynthesis
  • Nerve Tissue Proteins / biosynthesis*
  • Neurodegenerative Diseases / metabolism*
  • Receptors, Cell Surface / biosynthesis


  • Antigens, Neoplasm
  • Carrier Proteins
  • Melanoma-Specific Antigens
  • Neoplasm Proteins
  • Nerve Tissue Proteins
  • Receptors, Cell Surface
  • lactoferrin receptors
  • Iron
  • Ceruloplasmin