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(7)
Astrocyte
Environmental Risk
Genetics
Head Injury
Immune Response
Normal Aging
Amyloid Precursor Protein
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Glia and their cytokines in progression of neurodegeneration
Glia and their cytokines in progression of neurodegeneration,10.1016/j.neurobiolaging.2004.05.010,Neurobiology of Aging,Robert E. Mrak,W. Sue T. Griff
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Glia and their cytokines in progression of neurodegeneration
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Citations: 140
)
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Robert E. Mrak
,
W. Sue T. Griffin
A glia-mediated, inflammatory
immune response
is an important component of the neuropathophysiology of Alzheimer's disease, of the midlife neurodegeneration of Down's syndrome, and of other age-related neurodegenerative conditions. All of these conditions are associated with early and often dramatic activation of, and cytokine overexpression in, microglia and astrocytes, sometimes decades before pathological changes consistent with a diagnosis of Alzheimer's disease are apparent, as in patients with Down's syndrome or head injury. Brains of normal elderly individuals also often show Alzheimer-type neuropathological changes, although to a lesser degree than those seen in Alzheimer's disease itself. These normal age-related glial changes, likely a response to the normal wear and tear of the aging process, raise the threshold of glial activation and thus may explain the fact that even genetically determined Alzheimer's disease, resulting from genetic mutations such as those in β-amyloid precursor protein and presenilins or from genetic duplication such as of chromosome 21, only shows the full manifestation of the disease decades after birth. In the more common sporadic form of Alzheimer's disease, age-related increases in glial activation and expression of cytokines may act in synergy with other genetic and acquired environmental risks to culminate in the development of disease.
Journal:
Neurobiology of Aging - NEUROBIOL AGING
, vol. 26, no. 3, pp. 349-354, 2005
DOI:
10.1016/j.neurobiolaging.2004.05.010
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Citation Context
(24)
...Besides, studies had reported activation of astrocytes and microglia often initiates a neuroinflammatory cascade, which contributes to the neuronal damage after TBI (Somera-Molina et al. 2007;
Mrak and Griffin 2005
)...
...Activation of astrocytes and microglia often initiates a neuroinflammatory cascade, which contributes to the neuronal damage after TBI (Somera-Molina et al. 2007;
Mrak and Griffin 2005
)...
Zhiqiang LiuDonglin
,
et al.
Increased expression of transcription initiation factor IIB after rat ...
...Fractalkine-activated microglia could form a first line of defense in the CNS injury through their capacity to migrate, proliferate and secrete inflammatory and neurotrophic factors, phagocytase damaged cells and debris as well as present antigens [
51
]...
Joaquin Merino
,
et al.
Gut-Brain Chemokine Changes in Portal Hypertensive Rats
...However, clinical studies and preclinical animal models have implicated dysregulation and overproduction of proinflammatory cytokines from activated microglia in the CNS as a contributor to pathophysiology progression in both chronic neurodegenerative disorders such as Alzheimer’ sd isease (AD), Parkinson’ sd isease, and multiple sclerosis, as well as acute neurodegenerative conditions such as traumatic brain injury and stroke [
11-13
]...
...It should be emphasized that microglia responses to stimuli can be neuroprotective and assist with phagocytosis or protein aggregate clearance, or can be detrimental and contribute to a progression of pathology [
13
,49-51]...
Adam D Bachstetter
,
et al.
Microglial p38α MAPK is a key regulator of proinflammatory cytokine up...
...microglial activation) as underlying the continuing neuronal damage [2, 35, 36, 48, 66,
70
, 123]...
Delphine Boche
,
et al.
Neuropathology after active Aβ42 immunotherapy: implications for Alzhe...
...Microglial cells, the major immunocompetent cells in the brain, are known to contribute to the development and progression of a variety of neuropathologic disorders in humans (Dheen et al. 2007;
Mrak and Griffin 2005
)...
Birgit Kraus
,
et al.
Hyperforin is a modulator of inducible nitric oxide synthase and phago...
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