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Microglia: The Working Class Cell of the Brain | OMICS International
ISSN: 2161-0460
Journal of Alzheimers Disease & Parkinsonism

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Microglia: The Working Class Cell of the Brain

Livio Luongo* and Sabatino Maione

Department of Experimental Medicine, Division of Pharmacology, The Second University of Naples, Italy

Corresponding Author:
Livio Luongo
Department of Experimental Medicine
Division of Pharmacology
The Second University of Naples, Italy
Tel: +02 29520311
E-mail: [email protected]

Received Date: May 27, 2016; Accepted Date: June 01, 2016; Published Date: June 08, 2016

Citation: Luongo L, Maione S (2016) Microglia: The “Working Class” Cell of the Brain. J Alzheimers Dis Parkinsonism 6:242. doi: 10.4172/2161-0460.1000242

Copyright: © 2016 Luongo L, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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The concept of microglia has been introduced by Pio del Rio- Hortega in the 1932.

Microglias are the resident immune cells of the central nervous system (CNS). Their origin has been debated for a long time. At the beginning they were thought to become from neuroectoderm, whereas nowadays it is generally believed that they own peripheral origins and migrate into all regions of the CNS during the development and acquire a characteristic ramified shape called “resting microglia” (Figure 1) [1]. Unlike CNS macrophages found in the meninges, choroid plexus, and perivascular space, microglia derive from stem produced by primitive hematopoiesis in the yolk sac [2].

alzheimers-disease-parkinsonism-Resting-microglia

Figure 1: Resting microglia cells in the ventral horn of spinal cord. Picture performed and elaborated by Dr. Livio Luongo.

In the last decade several reports have shown the key role played by microglia cells in the brain diseases. Interestingly, these non-neuronal cells can acquire different phenotypes and perform various tasks in the brain. In particular, during the post-natal brain development microglia are in charge with the synaptic pruning necessary for the correct brain functions [3]. Thus, resting microglia is not “sleeping” cells. Indeed, it has recently become clear that microglias constantly patrol the brain environment and contact synapses. Activated microglia are able to remove damaged cells as well as dysfunctional synapses, a process defined “synaptic stripping” [4]. Therefore, it is now recognized that these cells are involved in the maintenance of CNS homeostasis.

The majority of the studies on microglia have been focused mainly on their functions in the injured brain or in neurological diseases associated with neuroinflammation including Alzheimer Disease, Parkinson Disease, neuropathic pain and others [5].

In particular, microglia can shift from a resting state to an activated pro-inflammatory (also called M1) phenotype in certain conditions. The activation process is triggered by several mediators released by other cells such as neurons, astrocytes and other in response to a peripheral or central insult. Indeed, it is possible to find the activation of microglia in several brain areas not only during CNS inflammatory conditions [5], but also in peripheral lesions or inflammatory/pathological conditions such as in the spinal cord of various form of neuropathic pain [6-9], in nucleus of solitary tract in the capsaicin-induced airway over-responsiveness [10] and in several brain areas of rodents with the myocardial infarction [11,12]. Beside this “dark side” of the microglia, that have been defined as “bad guys” in several pathological conditions [13], emerging evidence suggests also a second phenotype named alternatively activated (also called M2) microglia [14]. Interestingly, molecule that facilitates the phenotypic shift of microglia from M1 to M2 might represent potential pharmacological tools to treat chronic/ degenerative diseases. New theories highlight also the role of a third phenotype the so called “dystrophic/senescent” microglia. Intriguingly, the latest phenotype seems to be the major responsible for the neuronal damage in several pathological conditions such as Alzheimer Disease in human [15]. Recent reports also identified the presence of the dystrophic microglia in a transgenic mouse model of increased glutamatergic tone [16]. Therefore, microglia cells play several functions in the CNS in all the existing phenotypes. Indeed, several “nicknames” have been attributed to microglia such as scavengers, scapegoat, saboteur and gardeners. All these tasks justified the new appellation that we are going to attribute to microglia in this commentary: the working class cell of the brain.

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