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Cytokine/neurotrophin interaction in the aged central nervous system

Published online by Cambridge University Press:  06 February 2001

NANCY J. MACDONALD
Affiliation:
Department of Anatomy and Neuroscience and Marine Biomedical Institute, University of Texas Medical Branch at Galveston, Texas, USA
FRANCESCO DECORTI
Affiliation:
Department of Anatomy and Neuroscience and Marine Biomedical Institute, University of Texas Medical Branch at Galveston, Texas, USA
TODD C. PAPPAS
Affiliation:
Division of Infectious Disease, University of Texas Medical Branch at Galveston, Texas, USA
GIULIO TAGLIALATELA
Affiliation:
Department of Anatomy and Neuroscience and Marine Biomedical Institute, University of Texas Medical Branch at Galveston, Texas, USA
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Abstract

Age-associated neurodegenerative diseases such as Alzheimer's disease are characterised by neuronal impairment that leads to cognitive deficits. As certain affected neurons depend on trophic factors such as neurotrophins (NTs), impairment in NT function has been suggested to be a component of neuronal damage associated with such disorders. Age-related neurodegenerative diseases are also characterised by high levels of proinflammatory cytokines such as tumour necrosis factor alpha (TNFα) in the CNS. Because TNFα receptors and certain NT receptors share a high degree of homology and are capable of activating similar signalling pathways, one possibility is that altered cytokine levels may affect NT function in the aged or diseased CNS. Here we wish briefly to review the evidence suggesting a role for cytokine and NT in the onset of age-associated neurodegenerative diseases. We propose that cytokine/NT interactions may alter neuronal homeostasis, thus possibly contributing to some of the neuronal degeneration occurring during such age-associated CNS diseases.

Type
Review
Copyright
© Anatomical Society of Great Britain and Ireland 2000

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