Neuroplasticity in Alzheimer's disease.
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.
Teter
Bruce
B
Department of Medicine, University of California Los Angeles, California and Veteran's Affairs-Greater Los Angeles Healthcare System, Sepulveda, California 91343, USA.
Ashford
J Wesson
JW
D000544:Alzheimer Disease / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D016229:Amyloid beta-Peptides / Q000235:genetics / Q000378:metabolism; D000818:Animals; D001057:Apolipoproteins E / Q000235:genetics / Q000378:metabolism; D001921:Brain / Q000254:growth & development / Q000378:metabolism* / Q000503:physiopathology; D004967:Estrogens / Q000378:metabolism; D020439:Growth Cones / Q000378:metabolism* / Q000473:pathology; D006801:Humans; D009434:Neural Pathways / Q000254:growth & development / Q000378:metabolism / Q000503:physiopathology; D009473:Neuronal Plasticity / Q000502:physiology*; D016875:tau Proteins / Q000235:genetics / Q000378:metabolism
D016229:Amyloid beta-Peptides; D001057:Apolipoproteins E; D004967:Estrogens; D016875:tau Proteins