Cellular Aspects of the Inflammatory Response in Alzheimer's Disease

Kalaria, Rajesh N.; Cohen, D. L.; Premkumar, Daniel R.

doi:10.1006/neur.1996.0069

Cited by 36 publications

(15 citation statements)

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“…The phagocytic role of microglia has been well documented within plaques [32,61]. In fact, the characteristics of activated microglia resemble peripheral macrophages after injury in peripheral tissue, which is consistent with the shared developmental origin of these two cell types [25,32,33].…”

Section: Microglia As Phagocytessupporting

confidence: 57%

“…In fact, the characteristics of activated microglia resemble peripheral macrophages after injury in peripheral tissue, which is consistent with the shared developmental origin of these two cell types [25,32,33]. In vivo studies that include the direct injection of plaque cores into the rat cerebral cortex, result in phagocytosis, not deposition, of the beta-amyloid cores [24,51].…”

Section: Microglia As Phagocytesmentioning

confidence: 59%

“…In reference to plaque formation, the possibility that microglia could create any plaque type de novo is even more unlikely since they do not express detectable levels of amyloid precursor protein (APP) mRNA, implying that these cells are incapable of synthesizing or producing significant A␤ from endogenous APP [32,54]. Therefore, microglia cells are not necessary for the production of A␤ plaques.…”

Section: Introductionmentioning

confidence: 99%

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The microglial phagocytic role with specific plaque types in the Alzheimer disease brain

D’Andrea

Cole

Ard

2004

Neurobiology of Aging

193

129

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Alzheimer disease (AD) involves glial inflammation associated with amyloid plaques. The role of the microglial cells in the AD brain is controversial, as it remains unclear if the microglia form the amyloid fibrils of plaques or react to them in a macrophage-phagocytic role. Also, it is not known why microglia are preferentially associated with some amyloid plaque types. This review will provide substantial evidence to support the phagocytic role of microglia in the brain as well as explain why microglia are generally associated with specific plaque types that may be explained through their unique mechanisms of formation. In summary, the data presented suggests that plaque associated microglial activation is typically subsequent to specific amyloid plaque formations in the AD brain.

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Section: Microglia As Phagocytessupporting

confidence: 57%

Section: Microglia As Phagocytesmentioning

confidence: 59%

Section: Introductionmentioning

confidence: 99%

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The microglial phagocytic role with specific plaque types in the Alzheimer disease brain

D’Andrea

Cole

Ard

2004

Neurobiology of Aging

193

129

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“…Further supporting an inflammatory-driven process in AD are ex vivo and in vitro studies these showed that inflammatory factors are significantly elevated in AD brains [36]. These inflammatory elements include activated microglia and astrocytes, pro-inflammatory cytokines, complement components, acute-phase reactants such as ␣ 1 -antichymotrypsin (ACT), and cell surface molecules such as MHC II [37].…”

Section: Epidemiologymentioning

confidence: 94%

“…In addition to synthesizing inflammatory cytokines and complement factors, MP release other substances with the potential to induce damage [36]. These include proteases, NO [75], excess glutamate [76], superoxide anions [48], hydrogen peroxide [48], PAF [43], eicosanoids [44], and other toxins that act by way of N-methyl-D-aspartate (NMDA) receptors [77,78].…”

Section: Other Neurotoxinsmentioning

confidence: 99%

Insights into the neurodegenerative process of Alzheimer's disease: a role for mononuclear phagocyte-associated inflammation and neurotoxicity

Cotter

Burke

Thomas

et al. 1999

Journal of Leukocyte Biology

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Since the first description of Alzheimer's disease (AD) in 1907, significant progress was made into understanding disease pathophysiology. The enormous effort in AD research has translated into the discovery of genetic linkages for disease, into elucidating the structure and function of the etiologic ␤-amyloid protein, and into unraveling the seemingly complex neuroimmunological cascade that affects neuronal dysfunction. Although effective therapies do not currently exist, many are being developed. We propose that the neuropathogenesis of AD, in measure, revolves around the immunological activation of glial cells, which in turn leads to alterations in inflammatory neurotoxin production, and ultimately to neuronal injury and death. Elucidating the mechanisms involved in such glial cell immune activation should provide valuable insights into understanding the disease process and in providing effective therapeutics to prevent and/or retard the devastating neurodegeneration that afflicts so many of our elderly. J. Leukoc. Biol. 65: 416-427; 1999.

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Effect of Anti-inflammatory Medications on Neuropathological Findings in Alzheimer Disease

Halliday¹,

Shepherd²,

McCann³

et al. 2000

Arch Neurol

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Cellular Aspects of the Inflammatory Response in Alzheimer's Disease

Cited by 36 publications

References 0 publications

The microglial phagocytic role with specific plaque types in the Alzheimer disease brain

The microglial phagocytic role with specific plaque types in the Alzheimer disease brain

Insights into the neurodegenerative process of Alzheimer's disease: a role for mononuclear phagocyte-associated inflammation and neurotoxicity

Effect of Anti-inflammatory Medications on Neuropathological Findings in Alzheimer Disease

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