Microglia are a type of glial cell that acts as the first and main form of active immune defense in the central nervous system (CNS).
Microglia constitute 20% of the total glial cell population within the brain. Unlike astrocytes, individual microglia are distributed in large non-overlapping regions throughout the brain and spinal cord.[1] Microglia are constantly moving and analyzing the CNS for damaged neurons, plaques, and infectious agents.[2] The brain and spinal cord are considered “immune privileged” organs in that they are separated from the rest of the body by a series of endothelial cells known as the blood-brain barrier, which prevents most infections from reaching the vulnerable nervous tissue. In the case where infectious agents are directly introduced to the brain or cross the blood-brain barrier, microglial cells must react quickly to increase inflammation and destroy the infectious agents before they damage the sensitive neural tissue. Due to the unavailability of antibodies from the rest of the body
(antibodies are too large to cross the blood-brain barrier),

microglia must be able to recognize foreign bodies, swallow them, and act as antigen-presenting cells activating T-cells. Since this process must be done quickly to prevent potentially fatal damage, microglia are extremely sensitive to even small pathological changes in the CNS.[3] They achieve this sensitivity in part by having unique potassium channels that respond to even small changes in extracellular potassium.[2]

http://www.answers.com/topic/microgl...80.99s_disease

Parkinson’s disease
Parkinson’s disease is a movement disorder in which the dopamine producing neurons in the brain, don’t work properly.[18] The area of the brain affected by Parkinson’s is called the substantia nigra. It is here that the neurons either become impaired or die.[18] The substantia nigra has one of the highest concentrations of microglia in the brain.[14]

Activated microglial cells have been found around extraneuronal neuromelanin released from impaired dopaminergic neurons in the substantia nigra of patients with Parkinson’s disease.[19] A study by Henrik Wilms discovered that neuromelanin acts as a chemoattractant for microglial cells and induces morphological transformation of microglia cells to an activated state.[19] Neuromelanin also induces synthesis of proinflammatory microglial molecules.[19] All of the inflammatory compounds that are up-regulated in Parkinson’s disease can be produced by microglia, especially activated microglia.[14]

Another study conducted by Wei Zhang stated, “…We have shown for the first time aggregated α-synuclein, the major components of Lewy bodies in patients with Parkinson's disease or dementia with Lewy bodies, activated microglia leading to enhanced dopaminergic neurotoxicity.”[20]

External links
Microglia home page at
microglia.net
http://www.microglia.net/
The Role of Microglia in the Central Nervous System - Clinical Microbiology Reviews October 2004, p. 942-964, Vol. 17, No. 4
Creeping into your Head - A Brief Introduction to Microglia - A Review from the Science Creative Quarterly
"Immune Scavengers Target Alzheimer’s Plaques". Retrieved on 2007-05-09. - from Harvard University

The Microglia Home Page

Manuel B. Graeber





For today's neuropathologist it must be hard to believe that microglia were once considered an endangered species. Yet, a few years ago, it was suggested that the existence of the microglia is in doubt and that their name should be abandoned (1). What can be regarded a gross scientific error by today's standards (2,3) has a long and complicated history. Discovered independently by Nissl (4) and Robertson (5), microglia were first studied in detail by del Rio-Hortega (6). He also deserves the credit for establishing valuable knowledge on the role of microglia in CNS pathology. However, in the following years, and mainly due to a lack of cell type-specific markers, controversy arose around microglial embryonic development and their 'nature' as well as their cellular 'identity'. Thus, in the mid-1980s, microglia were "rediscovered" with the advent of immunocytochemistry and lectin markers. Meanwhile, the esoteric debate that surrounded microglia for decades had given way to research activity involving a broad circle of scientists. As a result, more than 1,000* papers have been published on microglia over the last few years. The biology and function of microglia is central to many issues in modern neuropathology. Microglia and brain macrophages have been recognized to play crucial roles in important diseases such as viral infections, autoimmunity and neurodegenerative disorders. HIV encephalitis, multiple sclerosis and Alzheimer's disease are examples where understanding the role of microglia promises to hold essential information concerning disease pathogenesis. In addition, it is becoming increasingly clear that certain molecules expressed by microglia have the potential of serving as diagnostic "sensors" in day-to-day neuropathological practice. These markers point to subtle tissue pathology that may otherwise go undetected
(7-9).

The text was taken from Graeber MB, Kreutzberg GW (1994) Brain Pathology 4: 337-9 where the references can be found. *>7,000 today
Copyright 1995-2004, published under the ICDNS general public license

Proceed -
http://www.microglia.net

British Medical Bulletin 65:121-131 (2003)
© 2003 The British Council


Neuropathological imaging: in vivo detection of glial activation as a measure of disease and adaptive change in the brain
Richard B Banati
Molecular Neuropsychiatry, Departments of Neuropathology and Psychiatry, Charing Cross Hospital, Imperial College School of Medicine, and MRC Clinical Sciences Centre (PET Neurology), Hammersmith Hospital, London, UK

http://bmb.oxfordjournals.org/cgi/content/full/65/1/121

An interesting paper on microglial brain inflammation, aspirin and Parkinson's.
Ashley

http://www.neurology.org/cgi/content...act/69/19/1836
Objective: Markers of neuroinflammation, including activated microglia and increased levels of circulating proinflammatory cytokines, have been observed in the brains and CSF of patients with Parkinson disease (PD). Yet the link between anti-inflammatory agents and PD in humans remains uncertain, despite indications that neuroinflammation may contribute to cell death in the PD brain and experimental evidence of anti-inflammatory agents such as nonsteroidal anti-inflammatory drugs (NSAIDs) exerting neuroprotective effects in animal models. Methods: Using a population-based approach, we studied NSAID use among 293 incident idiopathic PD cases and 286 age-, race-, and gender-matched controls from three rural California counties.
Results: Our data suggested a decreased risk of PD among regular (2 pills/week for at least 1 month) aspirin NSAID users (OR, 0.80; 95% CI, 0.56 to 1.15). A stronger protective effect was observed for regular nonaspirin NSAID users (OR, 0.52; 95% CI, 0.35 to 0.79), particularly those who reported 2 or more years of use (OR, 0.44; 95% CI, 0.26 to 0.74). The aspirin effect estimates differed by gender, showing a protective effect only in women, especially among long term (24 months) regular users (OR, 0.51; 95% CI, 0.26 to 1.02).
Conclusion: Our study contributes to the growing body of literature suggesting a protective role for nonsteroidal anti-inflammatory drugs (NSAIDs) in Parkinson disease (PD). Given our results and the biologic plausibility of a neuroprotective function for NSAIDs there is a pressing need for further studies elucidating the protective role such drugs may play in PD.

Another study conducted by Wei Zhang stated, “…We have shown for the first time aggregated α-synuclein, the major components of Lewy bodies in patients with Parkinson's disease or dementia with Lewy bodies, activated microglia leading to enhanced dopaminergic neurotoxicity.”[20]



I believed all along that my mom was wrongly diagnosed...Schizophrenia/Alzheimers/Dementa...Now I KNOW what she has! She has LBD. Lewy Body Dementia....very close to the same but now I know why she didn't do well on the meds! They are actually extremely Bad for her so Dr. will now re-do everything. Not a better diagnosis, but a correct one. Now atleast we can treat her properly!
Your Quote has me a lillte confused..can you explain the last sentence in EXTREME laymens terms? lol...Thanks!