Insulin-like growth factor-1 receptors in human spinal cord: changes in amyotrophic lateral sclerosis

A. Adem, J. Ekblom, P. G. Gillberg, S. S. Jossan, A. Höög, B. Winblad, S. M. Aquilonius, L. H. Wang, V. Sara

Research output: Contribution to journalArticlepeer-review

49 Scopus citations


Neurotrophic factors are important for neuronal survival and maintenance in the adult nervous system. The regional distribution of insulin-like growth factor-1 (IGF-1) receptors in human spinal cords from controls and amyotrophic lateral sclerosis (ALS) patients was studied by immunohistochemistry and quantitative autoradiography. When comparing125I-IGF-1 binding in the different spinal levels of normal spinal cord the same distribution pattern was found in which the binding was highest in the central canal > dorsal horn > ventral horn > white matter. In the ALS cases although a general upregulation of IGF-1 receptors was observed throughout the spinal cord, significant increases were observed in the cervical and sacral segments compared to controls. IGF-1 receptor immunoreactivity showed a similar pattern to that for125I-IGF-1 binding, with immunoreactivity being found in the gray matter of the spinal cord and enhanced immunoreactivity occuring in ALS patients compared to controls. In agreement with the distribution of IGF-1 receptors, IGF-1 immunoreactivity was found within the gray matter of the spinal cord. The cartography of IGF-1 receptors in the normal spinal cord as well as the change of these receptors in diseased spinal cord may be of importance in future treatment strategies of ALS.

Original languageBritish English
Pages (from-to)73-84
Number of pages12
JournalJournal of Neural Transmission
Issue number1
StatePublished - Feb 1994


  • Amyotrophic lateral sclerosis
  • human
  • insulin-like growth factor receptors
  • insulin-like growth factors
  • motor neurons
  • receptor autoradiography
  • spinal cord


Dive into the research topics of 'Insulin-like growth factor-1 receptors in human spinal cord: changes in amyotrophic lateral sclerosis'. Together they form a unique fingerprint.

Cite this