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The Inflammatory Component of Neurodegenerative Diseases

  • Reference work entry
Handbook of Neurochemistry and Molecular Neurobiology

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Abstract:

Inflammation is a key component in the immunological defense of the organism against health-threatening pathogens. On the other hand, a dysregulated inflammatory response can lead to tissue damage and disease. In the central nervous system (CNS), the inflammatory response obeys different rules than the periphery. The presence of a selective blood–brain barrier, the lack of dendritic cells, the chronic downregulation of costimulatory molecules, and a bias towards an immunosuppressive environment are mainly responsible for the characteristic features of the inflammatory response in the CNS. Until recently, with the exception of multiple sclerosis, the inflammatory component present in major chronic neurodegenerative diseases has been regarded as a logical consequence of cell death with no major functional relevance but to remove cellular debris. However, inflammation is now known to have toxic and protective effects in chronic neurodegenerative diseases such as Parkinson's, Alzheimer's, and prion diseases. Microglial activation appears as a common feature to all these pathologies. However, microglial cells do not seem to be activated to an end-stage, proinflammatory phenotype during chronic neurodegeneration. Instead, they appear to be in a “primed” state where major proinflammatory cytokine production is tightly controlled. These observations are in agreement with the noninflammatory nature of apoptotic cell death. In addition, evidence is accumulating to favour the hypothesis that these “primed” microglial cells will produce an exacerbated amount of proinflammatory cytokines if a proinflammatory stimulus hits them in this state. The resulting exacerbated inflammatory response can lead to a toxic effect on the degenerating cells, exacerbating disease and aggravating symptoms.

These observations are seminal to understand the pathophysiology of neurodegenerative diseases and prevent putative disease exacerbation by inflammation.

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Abbreviations

APP:

amyloid precursor protein

CJD:

Creutzfeld-Jacob diseases

CNS:

central nervous system

GSS:

Gertsmann-Straussler-Scheinker syndrome

IFN-γ:

interferon-γ

IL-1α:

interleukin 1α

IL-1β:

interleukin 1β

IL-4:

interleukin-4

IL-6:

interleukin-6

IL-8:

interleukin-8

IL-10:

interleukin-10

LPS:

bacterial lipopolysaccharide

MPTP:

1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine

PS1:

presenilin 1

PS2:

presenilin 2

6-OHDA:

6-hydroxydopamine

SN:

substantia nigra

TNFα:

tumor necrosis factor-α

TSEs:

transmissible spongiform encephalopathies

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Authors
  1. C. C. Ferrari
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  2. F. J. Pitossi
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Editors and Affiliations

  1. Center for Neurochemistry, Nathan S. Kline Institute for Psychiatric Research, 140 Old Orangeburg Road, 10962, New York, Orangeburg, USA

    Abel Lajtha (Director) (Director)

  2. The Buniatian Institute of Biochemistry the National Academy of Sciences, 5/1 Sevag str., 375014, Yerevan, Republic of Armenia

    Armen Galoyan

  3. Dept. Immunophysiology Medical Faculty, Inst. of Normal and Pathological Physiology, Deutschhausstrase 2, D–35037, Marburg, Germany

    Hugo O. Besedovsky

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Ferrari, C.C., Pitossi, F.J. (2008). The Inflammatory Component of Neurodegenerative Diseases. In: Lajtha, A., Galoyan, A., Besedovsky, H.O. (eds) Handbook of Neurochemistry and Molecular Neurobiology. Springer, Boston, MA. https://doi.org/10.1007/978-0-387-30398-7_18

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