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10.1111/j.1582-4934.2008.00314.x http://scihub22266oqcxt.onion/10.1111/j.1582-4934.2008.00314.x C4401126!4401126!18363841     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Cell+Mol+Med 2008 ; 12 (3): 762-80 Nephropedia Template TP {{tp|p=18363841|t=2008. Neuroprotective and neurotoxic properties of glial cells in the pathogenesis of Alzheimer s disease |pdf=|usr=}}{{18363841}} gab.com Text Neuroprotective and neurotoxic properties of glial cells in the pathogenesis of Alzheimer s disease JO: J Cell Mol Med http://www.kidney.de/pget.php?&tw=1&pmid=18363841 #FOAvip Alzheimer's disease (AD) affects more than 18 million people worldwide and is characterized by progressive memory deficits, cognitive impairment and personality changes. The main cause of AD is generally attributed to the increased production and accumulation of amyloid-? (A?), in association with neurofibrillary tangle (NFT) formation. Increased levels of pro-inflammatory factors such as cytokines and chemokines, and the activation of the complement cascade occurs in the brains of AD patients and contributes to the local inflammatory response triggered by senile plaque. The existence of an inflammatory component in AD is now well known on the basis of epidemiological findings showing a reduced prevalence of the disease upon long-term medication with anti-inflammatory drugs, and evidence from studies of clinical materials that shows an accumulation of activated glial cells, particularly microglia and astrocytes, in the same areas as amyloid plaques. Glial cells maintain brain plasticity and protect the brain for functional recovery from injuries. Dysfunction of glial cells may promote neurodegeneration and, eventually, the retraction of neuronal synapses, which leads to cognitive deficits. The focus of this review is on glial cells and their diversity properties in AD. Twit Text FOAVip Neuroprotective and neurotoxic properties of glial cells in the pathogenesis of Alzheimer s disease ????J Cell Mol Med http://www.kidney.de/pget.php?&tw=1&pmid=18363841 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=18363841 #FOAvip English Wikipedia <ref>{{Cite pmid|18363841}}</ref> Neuroprotective and neurotoxic properties of glial cells in the pathogenesis of Alzheimer s disease #MMPMID18363841 Farfara D; Lifshitz V; Frenkel D J Cell Mol Med 2008[Jun]; 12 (3): 762-80 PMID18363841show ga Alzheimer's disease (AD) affects more than 18 million people worldwide and is characterized by progressive memory deficits, cognitive impairment and personality changes. The main cause of AD is generally attributed to the increased production and accumulation of amyloid-? (A?), in association with neurofibrillary tangle (NFT) formation. Increased levels of pro-inflammatory factors such as cytokines and chemokines, and the activation of the complement cascade occurs in the brains of AD patients and contributes to the local inflammatory response triggered by senile plaque. The existence of an inflammatory component in AD is now well known on the basis of epidemiological findings showing a reduced prevalence of the disease upon long-term medication with anti-inflammatory drugs, and evidence from studies of clinical materials that shows an accumulation of activated glial cells, particularly microglia and astrocytes, in the same areas as amyloid plaques. Glial cells maintain brain plasticity and protect the brain for functional recovery from injuries. Dysfunction of glial cells may promote neurodegeneration and, eventually, the retraction of neuronal synapses, which leads to cognitive deficits. The focus of this review is on glial cells and their diversity properties in AD. äNeuroprotective and neurotoxic properties of glial cells in the pathog(epmc).pdf DeepDyve Pubget Overpricing