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Cytokines and cognition--the case for a head-to-toe inflammatory paradigm.

Publication ,  Journal Article
Wilson, CJ; Finch, CE; Cohen, HJ
Published in: J Am Geriatr Soc
December 2002

The brain is not only immunologically active of its own accord, but also has complex peripheral immune interactions. Given the central role of cytokines in neuroimmmunoendocrine processes, it is hypothesized that these molecules influence cognition via diverse mechanisms. Peripheral cytokines penetrate the blood-brain barrier directly via active transport mechanisms or indirectly via vagal nerve stimulation. Peripheral administration of certain cytokines as biological response modifiers produces adverse cognitive effects in animals and humans. There is abundant evidence that inflammatory mechanisms within the central nervous system (CNS) contribute to cognitive impairment via cytokine-mediated interactions between neurons and glial cells. Cytokines mediate cellular mechanisms subserving cognition (e.g., cholinergic and dopaminergic pathways) and can modulate neuronal and glial cell function to facilitate neuronal regeneration or neurodegeneration. As such, there is a growing appreciation of the role of cytokine-mediated inflammatory processes in neurodegenerative diseases such as Alzheimer's disease and vascular dementia. Consistent with their involvement as mediators of bidirectional communication between the CNS and the peripheral immune system, cytokines play a key role in the hypothalamic-pituitary-adrenal axis activation seen in stress and depression. In addition, complex cognitive systems such as those that underlie religious beliefs, can modulate the effects of stress on the immune system. Indirect means by which peripheral or central cytokine dysregulation could affect cognition include impaired sleep regulation, micronutrient deficiency induced by appetite suppression, and an array of endocrine interactions. Given the multiple levels at which cytokines are capable of influencing cognition it is plausible that peripheral cytokine dysregulation with advancing age interacts with cognitive aging.

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Published In

J Am Geriatr Soc

DOI

ISSN

0002-8614

Publication Date

December 2002

Volume

50

Issue

12

Start / End Page

2041 / 2056

Location

United States

Related Subject Headings

  • Stress, Psychological
  • Inflammation
  • Humans
  • Geriatrics
  • Dementia, Vascular
  • Cytokines
  • Cognition
  • Central Nervous System
  • Alzheimer Disease
  • Aging
 

Citation

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ICMJE
MLA
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Wilson, C. J., Finch, C. E., & Cohen, H. J. (2002). Cytokines and cognition--the case for a head-to-toe inflammatory paradigm. J Am Geriatr Soc, 50(12), 2041–2056. https://doi.org/10.1046/j.1532-5415.2002.50619.x
Wilson, Craig J., Caleb E. Finch, and Harvey J. Cohen. “Cytokines and cognition--the case for a head-to-toe inflammatory paradigm.J Am Geriatr Soc 50, no. 12 (December 2002): 2041–56. https://doi.org/10.1046/j.1532-5415.2002.50619.x.
Wilson CJ, Finch CE, Cohen HJ. Cytokines and cognition--the case for a head-to-toe inflammatory paradigm. J Am Geriatr Soc. 2002 Dec;50(12):2041–56.
Wilson, Craig J., et al. “Cytokines and cognition--the case for a head-to-toe inflammatory paradigm.J Am Geriatr Soc, vol. 50, no. 12, Dec. 2002, pp. 2041–56. Pubmed, doi:10.1046/j.1532-5415.2002.50619.x.
Wilson CJ, Finch CE, Cohen HJ. Cytokines and cognition--the case for a head-to-toe inflammatory paradigm. J Am Geriatr Soc. 2002 Dec;50(12):2041–2056.
Journal cover image

Published In

J Am Geriatr Soc

DOI

ISSN

0002-8614

Publication Date

December 2002

Volume

50

Issue

12

Start / End Page

2041 / 2056

Location

United States

Related Subject Headings

  • Stress, Psychological
  • Inflammation
  • Humans
  • Geriatrics
  • Dementia, Vascular
  • Cytokines
  • Cognition
  • Central Nervous System
  • Alzheimer Disease
  • Aging