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Neuroinflammation has come to denote CNS-specific inflammation-like glial responses that may engender neurodegenerative events; including plaque formation, dystrophic neurite growth, and excessive tau phosphorylation. The discipline of pathology makes a fundamental distinction between acute and chronic neuroinflammation and, therefore, these are addressed separately in the following sections.

Sino Biological offers a comprehensive set of tools for research on neuroinflammation, including recombinant proteins, antibodies (rabbit mAbs, mouse mAbs, rabbit pAbs), ELISA kits, and ORF cDNA clones.

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신경염증 Background

Neuroinflammation has come to denote CNS-specific inflammation-like glial responses that may engender neurodegenerative events; including plaque formation, dystrophic neurite growth, and excessive tau phosphorylation. The discipline of pathology makes a fundamental distinction between acute and chronic neuroinflammation and, therefore, these are addressed separately in the following sections.

Acute neuroinflammation

In limited, acute reactions to injury, in the absence of blood-brain barrier breakdown, there is the subtler response of the brain's own immune system, composed largely of rapid activation of glial cells. Limited neuronal insults trigger glial cell activation without breakdown of the blood brain barrier and without concomitant leukocytic infiltration.

Chronic neuroinflammation

Although such specific responses might, in a strict sense, be included in the term "neuroinflammation," neuroinflammation as generally used and understood applies to more chronic, sustained cycles of injury and response, in which the cumulative ill effects of immunological microglial and astrocytic activation contribute to and expand the initial neurodestructive effects, thus maintaining and worsening the disease process through their actions. The concept of chronic inflammation (as opposed to acute inflammation) is more relevant in the context of understanding CNS disease.

Chronic multiple sclerosis is, of course, an unequivocal and long-recognized example of an inflammatory brain disease. The persistent injurious stimulus that accounts for neuroinflammation in multiple sclerosis is a myelin-related protein that has escaped self-tolerance and become an autoimmunogen. Consistent with the chronic persistence of this autoimmunogen is a persistent accumulation of blood-derived mononuclear leukocytes in the CNS parenchyma, a phenomenon that is similar to what is found in other autoimmune diseases such as rheumatoid arthritis or polymyositis.

Today, the most important example of a chronic brain infection is human immunodeficiency virus (HIV). Chronic HIV encephalitis is characterized by the same nodules of activated microglia that Babes described in rabies. HIV enters and persists in the CNS via myelomonocytic cells: monocytes, perivascular cells, and microglia.

신경염증 References

    1. Vargas DL, et al. (2005) Neuroglial activation and neuroinflammation in the brain of patients with autism. Ann Neurol. 57(1): 67-81.
    2. Streit WJ, et al. (2004) Microglia and neuroinflammation: a pathological perspective. J Neuroinflammation. 1(1): 14.
    3. Eikelenboom P, et al. (2002) Neuroinflammation in Alzheimer's disease and prion disease. Glia. 40(2): 232-9.
    4. Mennicken F, et al. (1999) Chemokines and chemokine receptors in the CNS: a possible role in neuroinflammation and patterning. Trends Pharmacol Sci. 20(2): 73-8.