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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
PMID18363841
show 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-beta (Abeta), 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.
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