Inflammatory cytokines, cognition, neuronal regeneration or neurodegeneration

[Guest guest]

This is in response to Sharon's post earlier..

Inflammation and Cognition, Neurogenesis/Neurodegeneration and dysregulation

J Am Geriatr Soc. 2002 Dec;50(12):2041-56.

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

CJ, Finch CE, Cohen HJ.

St. Institute on Aging, St. Hospitals and Health

Services, Indianapolis, Indiana 46260, USA. cjwilson@...

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.

Publication Types:

* Review

PMID: 12473019 [PubMed - indexed for MEDLINE]

Semin Clin Neuropsychiatry. 2001 Oct;6(4):229-40.

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Interactions between the nervous and immune systems.

Fehder WP, SD.

MCP Hahnemann University, College of Nursing and Health

Professions, Philadelphia, PA, USA.

Substantial morphologic and functional evidence exists that

supports the reciprocal interactions that occur between the nervous

and immune systems. The nervous and immune systems have been

increasingly found to use a common chemical language in the form of

neuropeptides, cytokines, and hormones. Sophisticated immunologic

techniques such as the identification and detection of immune cell

surface markers enable researchers to determine the origin and

activity of diverse cells in the blood and central nervous system.

These techniques have elucidated the activity of immune cells in the

central nervous system (CNS) that was previously thought to be

privileged from immune surveillance in the presence of an intact blood

brain barrier. Immune cells in the CNS play a central role in several

degenerative diseases such as Alzheimer's disease, Huntington's

disease, Multiple sclerosis, AIDS dementia complex, and nerve

destruction associated with trauma. Immune cells also play a role in

demyelinating peripheral nerve disorders. Cytokines and neuropeptides

secreted by peripheral immune cells have profound effects on behavior

that is mediated by the CNS. The close integration between immune and

nervous system responses is being increasingly recognized in

physiologic and pathologic conditions. Copyright 2001 by W.B. Saunders

Company

Publication Types:

* Review

PMID: 11607919 [PubMed - indexed for MEDLINE]

J Mol Med. 2006 Jul;84(7):532-43. Epub 2006 Jun 14.

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Antigen presentation in autoimmunity and CNS inflammation: how T

lymphocytes recognize the brain.

Becher B, Bechmann I, Greter M.

Neurology Department, Division for Neuroimmunology, University of

Zurich, Winterthurerstrasse 190, CH-8057 Zurich, Switzerland.

burkhard.becher@...

The central nervous system (CNS) is traditionally viewed as an

immune privileged site in which overzealous immune cells are prevented

from doing irreparable damage. It was believed that immune responses

occurring within the CNS could potentially do more damage than the

initial pathogenic insult itself. However, virtually every aspect of

CNS tissue damage, including degeneration, tumors, infection, and of

course autoimmunity, involves a significant cellular inflammatory

component. While the blood-brain barrier (BBB) inhibits diffusion of

hydrophilic (immune) molecules across brain capillaries, activated

lymphocytes readily pass the endothelial layer of postcapillary

venules without difficulty. In classic neuro-immune diseases such as

multiple sclerosis or acute disseminated encephalomyelitis, it is

thought that neuroantigen-reactive lymphocytes, which have escaped

immune tolerance, now invade the CNS and are responsible for tissue

damage, demyelination, and axonal degeneration. The developed animal

model for these disorders, experimental autoimmune encephalomyelitis

(EAE), reflects many aspects of the human conditions. Studies in EAE

proved that auto-reactive encephalitogenic T helper (Th) cells are

responsible for the onset of the disease. Th cells recognize their

cognate antigen (Ag) only when presented by professional Ag-presenting

cells in the context of major histocompatibility complex class II

molecules. The apparent target structures of EAE immunity are

myelinating oligodendrocytes, which are not capable of presenting Ag

to invading encephalitogenic T cells. A compulsory third party is thus

required to mediate between the attacking T cells and the

myelin-expressing target. This review will discuss the recent advances

in this field of research and we will discuss the journey of an

auto-reactive T cell from its site of activation into perivascular

spaces and further into the target tissue.

Publication Types:

* Review

PMID: 16773356 [PubMed - indexed for MEDLINE]