Neuroplasticity in Alzheimer's disease

J Neurosci Res. 2002 Nov 1;70(3):402-37. doi: 10.1002/jnr.10441.

Abstract

Ramon y Cajal proclaimed in 1928 that "once development was ended, the founts of growth and regeneration of the axons and dendrites dried up irrevocably. In the adult centers the nerve paths are something fixed, ended and immutable. Everything must die, nothing may be regenerated. It is for the science of the future to change, if possible, this harsh decree." (Ramon y Cajal, 1928). In large part, despite the extensive knowledge gained since then, the latter directive has not yet been achieved by 'modern' science. Although we know now that Ramon y Cajal's observation on CNS plasticity is largely true (for lower brain and primary cortical structures), there are mechanisms for recovery from CNS injury. These mechanisms, however, may contribute to the vulnerability to neurodegenerative disease. They may also be exploited therapeutically to help alleviate the suffering from neurodegenerative conditions.

Publication types

  • Review

MeSH terms

  • Alzheimer Disease / metabolism*
  • Alzheimer Disease / pathology
  • Alzheimer Disease / physiopathology
  • Amyloid beta-Peptides / genetics
  • Amyloid beta-Peptides / metabolism
  • Animals
  • Apolipoproteins E / genetics
  • Apolipoproteins E / metabolism
  • Brain / growth & development
  • Brain / metabolism*
  • Brain / physiopathology
  • Estrogens / metabolism
  • Growth Cones / metabolism*
  • Growth Cones / pathology
  • Humans
  • Neural Pathways / growth & development
  • Neural Pathways / metabolism
  • Neural Pathways / physiopathology
  • Neuronal Plasticity / physiology*
  • tau Proteins / genetics
  • tau Proteins / metabolism

Substances

  • Amyloid beta-Peptides
  • Apolipoproteins E
  • Estrogens
  • tau Proteins