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Mechanisms Underlying Inflammation in Neurodegeneration

Mechanisms Underlying Inflammation in Neurodegeneration,10.1016/j.cell.2010.02.016,Cell,Christopher K. Glass,Kaoru Saijo,Beate Winner,Maria Carolina M

Mechanisms Underlying Inflammation in Neurodegeneration   (Citations: 89)
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Journal: Cell , vol. 140, no. 6, pp. 918-934, 2010
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    • ...and, interestingly, these disorders have often been found as being associated with inflammation of pathogenic relevance ...

    Chi Wang Ipet al. Neuroinflammation by Cytotoxic T-Lymphocytes Impairs Retrograde Axonal...

    • ...control) in inflammatory markers, evaluating anti-inflammatory interventions, or delineating the molecular basis of inflammation (Blasko et al, 2004; Glass, Saijo, Winner, Marchetto, & Gage, 2010; Gorelick, 2010; McGeer & McGeer, 1995; Wyss-Coray & Mucke, 2002), but instead will be directed towards elucidating cognitive and neurobehavioral associations with inflammatory burden in neurodegenerative diseases...

    Brianne Magouirk Bettcheret al. Inflammation and clinical presentation in neurodegenerative disease: a...

    • ...In the presence of IL-6 and TGFβ, T cells will express retinoic acid receptor-related orphan receptor γt and differentiate into Th17 cells that secrete IL-17 and TNFα to produce damage to myelin (Glass et al. 2010)...

    Nicole A. Northrupet al. Neuroimmune Pharmacology from a Neuroscience Perspective

    • ...Collectively, the neurodegenerative diseases such as Alzheimer’s disease (AD), Parkinson’s disease (PD), amyotrophic lateral sclerosis (ALS), and Huntington’s disease are clinically disparate in etiology, but all share a common trait in their pathogenesis: Sustained activation of CNS inflammatory processes (Gendelman and Ikezu, 2008, Glass et al., 2010; Ch 39)...
    • ...Two key pathologies are observed in AD are extracellular plaques composed of cleaved fragments of amyloid precursor protein (APP), Aβ1-42 or Aβ1-40, and intracellular neurofibrillary tangles composed of hyperphosphorylated microtubule binding tau protein (Gendelman and Ikezu, 2008, Glass et al., 2010)...
    • ...AD brain, both cell types appear in their activated state, see “Microglia role in CNS inflammation” and “Astrocytes activation in CNS inflammation” sections, respectively, surrounding the Aβ plaques (Glass et al., 2010)...
    • ...Further, microglia are elaborating pro-inflammatory cytokines IL- 1β, TNF-α, IL-6, and have upregulated MHC-II expression, all markers of activated microglia, as well increased production of ROS/RNS and astrocyte activation (Glass et al., 2010)...
    • ...Activation of microglia by Aβ plaques is thought to occur through interactions with either TLR receptors and/or scavenger receptor for advanced glycosolation end-products receptors (Glass et al., 2010)...
    • ...It is thought that the proinflammatory factors and ROS/RNS are neurotoxic, particularly to the cholinergic neurons in the basal forebrain involved in short- to long-term memory conversion being the most sensitive, which in turn further activates microglia through the release of ATP and interactions with the P2X7 receptor, see “Purinergic receptors” section (Glass et al., 2010)...
    • ...One of the strongest genetic associations with AD is apolipoprotien E (apoE4), a protein involved in very low-density-lipoprotein clearance (Glass et al., 2010)...
    • ...In addition, overproduction of microglia, through sustained stimulation by macrophage-colony stimulating factor (m-CSF) injections over a 4-month period increased both the number of microglia and clearance of Aβ plaque and conveyed neuroprotection, see “Alzheimer’ sd isease and neuroinflammation” section for lab exercise (Glass et al., 2010)...
    • ...PD is the second most common neurodegenerative disease and most common movement disorder in the US (Glass et al., 2010)...
    • ...PD is characterized by bradykinesia (slow to initiate movements), “pill-rolling” tremor, rigidity, and postural instability (Glass et al., 2010)...
    • ...Damage seems to focus in the dopaminergic neurons of the substantia nigra (SN) and is the hallmark pathology is the presence of Lewy bodies, aggregates of misfolded α-synuclein protein in neurons (Glass et al., 2010)...
    • ...The etiological cause of PD is unclear, but inflammatory process appears to play a role in the pathogenesis of PD (Glass et al., 2010)...
    • ...Activated microglia, ROS and increased levels of pro-inflammatory cytokines (TNF-α and IL-1β) are observed in the SN of PD patients (Glass et al., 2010)...
    • ...Whether neuronal cell death leading to release of misfolded α-synuclein or extra cellular aggregation of misfolded α-synuclein play a role in initiating the immune response in PD is unclear (Glass et al., 2010)...
    • ...One thing is clear, once initiated, inflammation seems to exacerbate the damage through further production of ROS, which is already increased as a result of increased dopamine synthesis, making the remaining neurons highly susceptible to further cell death from oxidative stresses, see “Parkinson’s disease and neuroinflammation” section (Glass et al., 2010)...
    • ...ALS, or Lou Gehrig’s disease, is a fatal neurodegenerative disease affecting both upper motor (motor cortex) and lower motor (anterior horn of spinal segments) neurons (Glass et al., 2010)...
    • ...ALS patients suffer from fasciculations, muscle wasting and weakness, increased spasticity and hyper-reflexia (Glass et al., 2010)...
    • ...Inflammation is prominent component of ALS and activated microglia and astrocytes are observed in all regions affected by ALS, see “ALS and neuroinflammation” section for lab exercise (Glass et al., 2010)...

    Robert W. Freilichet al. Neuroimmune Pharmacology as a Subdiscipline of Medical Neuroscience in...

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