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n3:pmcid
PMC0
bibo:doi
10.1186%2F1750-1326-4-47
n6:contains
_:vb6412154 _:vb6412157 _:vb6412146
Subject Item
_:vb6412146
rdf:type
n6:Section
dc:title
overview
n6:contains
_:vb6412152 _:vb6412153 _:vb6412148 _:vb6412149 _:vb6412150 _:vb6412151 _:vb6412147
Subject Item
_:vb6412147
rdf:type
n3:Context
rdf:value
brain barrier (BBB), it is now clear that while peripheral immune access to the central nervous system (CNS) is restricted and tightly controlled, the CNS is capable of dynamic immune and inflammatory responses to a variety of insults [>>1<<]. Infections, trauma, stroke, toxins and other stimuli are capable of producing an immediate and short lived activation of the innate immune system within the CNS [2,3].
n3:mentions
n2:19461673
Subject Item
_:vb6412148
rdf:type
n3:Context
rdf:value
Infections, trauma, stroke, toxins and other stimuli are capable of producing an immediate and short lived activation of the innate immune system within the CNS [>>2<<,3]. This acute neuroinflammatory response includes activation of the resident immune cells (microglia) resulting in a phagocytic phenotype and the release of inflammatory mediators such as cytokines and chemokines [4]. While an acute
n3:mentions
n2:18040798
Subject Item
_:vb6412149
rdf:type
n3:Context
rdf:value
Infections, trauma, stroke, toxins and other stimuli are capable of producing an immediate and short lived activation of the innate immune system within the CNS [2,>>3<<]. This acute neuroinflammatory response includes activation of the resident immune cells (microglia) resulting in a phagocytic phenotype and the release of inflammatory mediators such as cytokines and chemokines [4]. While an acute insult
n3:mentions
n2:18490917
Subject Item
_:vb6412150
rdf:type
n3:Context
rdf:value
This acute neuroinflammatory response includes activation of the resident immune cells (microglia) resulting in a phagocytic phenotype and the release of inflammatory mediators such as cytokines and chemokines [>>4<<]. While an acute insult may trigger oxidative and nitrosative stress, it is typically short-lived and unlikely to be detrimental to long-term neuronal survival. Therefore, it is believed that an acute neuroinflammatory response is
n3:mentions
n2:17720159
Subject Item
_:vb6412151
rdf:type
n3:Context
rdf:value
Chronic neuroinflammation includes not only long-standing activation of microglia and subsequent sustained release of inflammatory mediators, but also results in increased oxidative and nitrosative stress [>>4<<]. The sustained release of inflammatory mediators works to perpetuate the inflammatory cycle, activating additional microglia, promoting their proliferation, and resulting in further release of inflammatory factors. Owing to the chronic
n3:mentions
n2:17720159
Subject Item
_:vb6412152
rdf:type
n3:Context
rdf:value
Owing to the chronic and sustained nature of the inflammation, there is often compromise of the BBB which increases infiltration of peripheral macrophages into the brain parenchyma to further perpetuate the inflammation [>>1<<]. Rather than serving a protective role as does acute neuroinflammation, chronic neuroinflammation is most often detrimental and damaging to nervous tissue. Thus, whether neuroinflammation has beneficial or harmful outcomes in the brain
n3:mentions
n2:19461673
Subject Item
_:vb6412153
rdf:type
n3:Context
rdf:value
Parkinson's disease (PD), Huntington's disease (HD), amyotrophic lateral sclerosis (ALS), tauopathies, and age-related macular degeneration (ARMD), are associated with chronic neuroinflammation and elevated levels of several cytokines [>>5<<-8]. Neuropathological and neuroradiological studies indicate that neuroinflammatory responses may begin prior to significant loss of neuronal populations in the progression of these diseases.
n3:mentions
n2:16823625 n2:17850169 n2:16081203 n2:15639313
Subject Item
_:vb6412154
rdf:type
n6:Section
dc:title
microglia activation: convergence point for diverse stimuli that compromise neuronal survival
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_:vb6412156 _:vb6412155
Subject Item
_:vb6412155
rdf:type
n3:Context
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In the presence of an activating stimulus, microglial cell-surface receptor expression is modified and the cells change from a monitoring role to one of protection and repair (reviewed in [>>4<<,9]). In addition to up-regulation of the key surface receptors mentioned above, there is up-regulation of proteins such as CD1, lymphocyte function-associated antigen 1 (LFA-1), intercellular adhesion molecule 1 (ICAM-1 or CD54), and
n3:mentions
n2:17720159
Subject Item
_:vb6412156
rdf:type
n3:Context
rdf:value
Persistent activation of brain-resident microglia may increase the permeability of the BBB and promote increased infiltration of peripheral macrophages, the phenotype of which is critically determined by the CNS environment [>>10<<].
n3:mentions
n2:19393017
Subject Item
_:vb6412157
rdf:type
n6:Section
dc:title
evidence of neuroinflammation and cytokine involvement in neurodegenerative diseases
n6:contains
_:vb6412158 _:vb6412159 _:vb6412176 _:vb6412177 _:vb6412178 _:vb6412179 _:vb6412180 _:vb6412181 _:vb6412182 _:vb6412183 _:vb6412184 _:vb6412185 _:vb6412186 _:vb6412187 _:vb6412188 _:vb6412189 _:vb6412190 _:vb6412191 _:vb6412160 _:vb6412161 _:vb6412162 _:vb6412163 _:vb6412164 _:vb6412165 _:vb6412166 _:vb6412167 _:vb6412168 _:vb6412169 _:vb6412170 _:vb6412171 _:vb6412172 _:vb6412173 _:vb6412174 _:vb6412175 _:vb6412208 _:vb6412209 _:vb6412210 _:vb6412211 _:vb6412212 _:vb6412213 _:vb6412214 _:vb6412215 _:vb6412216 _:vb6412217 _:vb6412218 _:vb6412219 _:vb6412220 _:vb6412221 _:vb6412222 _:vb6412223 _:vb6412192 _:vb6412193 _:vb6412194 _:vb6412195 _:vb6412196 _:vb6412197 _:vb6412198 _:vb6412199 _:vb6412200 _:vb6412201 _:vb6412202 _:vb6412203 _:vb6412204 _:vb6412205 _:vb6412206 _:vb6412207 _:vb6412240 _:vb6412241 _:vb6412242 _:vb6412243 _:vb6412244 _:vb6412245 _:vb6412246 _:vb6412247 _:vb6412248 _:vb6412249 _:vb6412250 _:vb6412251 _:vb6412252 _:vb6412253 _:vb6412254 _:vb6412255 _:vb6412224 _:vb6412225 _:vb6412226 _:vb6412227 _:vb6412228 _:vb6412229 _:vb6412230 _:vb6412231 _:vb6412232 _:vb6412233 _:vb6412234 _:vb6412235 _:vb6412236 _:vb6412237 _:vb6412238 _:vb6412239 _:vb6412256 _:vb6412257 _:vb6412258 _:vb6412259 _:vb6412260 _:vb6412261 _:vb6412262 _:vb6412263 _:vb6412264 _:vb6412265 _:vb6412266 _:vb6412267 _:vb6412268 _:vb6412269 _:vb6412270 _:vb6412271
Subject Item
_:vb6412158
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n3:Context
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AD in humans is unknown, mutations in Amyloid Precursor Protein (APP) or components of its processing machinery (β-secretase and γ-secretase) result in overproduction of Aβ1-40 and 1-42 peptides and are sufficient to cause disease [>>11<<-17]. Over 20 years ago, microglia were reported to localize to amyloid plaques in AD brain [18] and since then, the association between neuroinflammation and AD has been extensively investigated [7,19-24] and reviewed [19,25].
n3:mentions
n2:8837617 n2:16242634 n2:1671712 n2:9052708 n2:1465129 n2:6600923 n2:8424174
Subject Item
_:vb6412159
rdf:type
n3:Context
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Over 20 years ago, microglia were reported to localize to amyloid plaques in AD brain [>>18<<] and since then, the association between neuroinflammation and AD has been extensively investigated [7,19-24] and reviewed [19,25].
n3:mentions
n2:3670729
Subject Item
_:vb6412160
rdf:type
n3:Context
rdf:value
Over 20 years ago, microglia were reported to localize to amyloid plaques in AD brain [18] and since then, the association between neuroinflammation and AD has been extensively investigated [>>7<<,19-24] and reviewed [19,25].
n3:mentions
n2:15639313
Subject Item
_:vb6412161
rdf:type
n3:Context
rdf:value
Over 20 years ago, microglia were reported to localize to amyloid plaques in AD brain [18] and since then, the association between neuroinflammation and AD has been extensively investigated [7,>>19<<-24] and reviewed [19,25].
n3:mentions
n2:12165466 n2:12921904 n2:16384684 n2:17036175 n2:10858586 n2:16470015
Subject Item
_:vb6412162
rdf:type
n3:Context
rdf:value
Over 20 years ago, microglia were reported to localize to amyloid plaques in AD brain [18] and since then, the association between neuroinflammation and AD has been extensively investigated [7,19-24] and reviewed [>>19<<,25]. Human microglia display an activated phenotype when they surround plaques [23] that includes upregulation of Human Leukocyte Antigen-DR (HLA-DR) [18]. In addition to producing cytokines and other pro-inflammatory mediators [19,26],
n3:mentions
n2:10858586
Subject Item
_:vb6412163
rdf:type
n3:Context
rdf:value
Over 20 years ago, microglia were reported to localize to amyloid plaques in AD brain [18] and since then, the association between neuroinflammation and AD has been extensively investigated [7,19-24] and reviewed [19,>>25<<]. Human microglia display an activated phenotype when they surround plaques [23] that includes upregulation of Human Leukocyte Antigen-DR (HLA-DR) [18]. In addition to producing cytokines and other pro-inflammatory mediators [19,26],
n3:mentions
n2:19320056
Subject Item
_:vb6412164
rdf:type
n3:Context
rdf:value
Human microglia display an activated phenotype when they surround plaques [>>23<<] that includes upregulation of Human Leukocyte Antigen-DR (HLA-DR) [18].
n3:mentions
n2:12921904
Subject Item
_:vb6412165
rdf:type
n3:Context
rdf:value
Human microglia display an activated phenotype when they surround plaques [23] that includes upregulation of Human Leukocyte Antigen-DR (HLA-DR) [>>18<<]. In addition to producing cytokines and other pro-inflammatory mediators [19,26], microglia have also been reported to exert toxicity on neurons that have been pre-exposed to low concentrations of Aβ42 via a CD14-dependent process [27].
n3:mentions
n2:3670729
Subject Item
_:vb6412166
rdf:type
n3:Context
rdf:value
In addition to producing cytokines and other pro-inflammatory mediators [>>19<<,26], microglia have also been reported to exert toxicity on neurons that have been pre-exposed to low concentrations of Aβ42 via a CD14-dependent process [27].
n3:mentions
n2:10858586
Subject Item
_:vb6412167
rdf:type
n3:Context
rdf:value
In addition to producing cytokines and other pro-inflammatory mediators [19,>>26<<], microglia have also been reported to exert toxicity on neurons that have been pre-exposed to low concentrations of Aβ42 via a CD14-dependent process [27].
n3:mentions
n2:12379910
Subject Item
_:vb6412168
rdf:type
n3:Context
rdf:value
In addition to producing cytokines and other pro-inflammatory mediators [19,26], microglia have also been reported to exert toxicity on neurons that have been pre-exposed to low concentrations of Aβ42 via a CD14-dependent process [>>27<<]. Although it is clear that not all microglia activation is injurious to neurons, it is becoming widely accepted that a type of neurotoxic microglia phenotype has a central role in the pathophysiology of AD.
n3:mentions
n2:15194867
Subject Item
_:vb6412169
rdf:type
n3:Context
rdf:value
While microglia can become activated after exposure to fibrillary Aβ in vitro and are capable of phagocytosing it in vitro [>>28<<-30], it has been reported that in the presence of inflammatory cytokines or certain extracellular matrix proteins, microglia cannot phagocytize Aβ [31].
n3:mentions
n2:9798938 n2:8820967 n2:8532106
Subject Item
_:vb6412170
rdf:type
n3:Context
rdf:value
exposure to fibrillary Aβ in vitro and are capable of phagocytosing it in vitro [28-30], it has been reported that in the presence of inflammatory cytokines or certain extracellular matrix proteins, microglia cannot phagocytize Aβ [>>31<<]. This observation has been used to support the idea that the persistence and accumulation of amyloid plaques in vivo may be a direct result of this inhibitory behavior exerted by neuroinflammation.
n3:mentions
n2:16148231
Subject Item
_:vb6412171
rdf:type
n3:Context
rdf:value
Moreover, numbers of IL-1α positive (i.e., pro-inflammatory) microglia are increased in the cortical layers affected by plaque pathology in AD patients [>>32<<]. Since microglia are found in large numbers around neuritic amyloid plaques, but not diffuse in human AD patients, and in mice transgenic for mutant APP [33], it has been postulated that microglia play a role in the conversion of diffuse
n3:mentions
n2:9775393
Subject Item
_:vb6412172
rdf:type
n3:Context
rdf:value
Since microglia are found in large numbers around neuritic amyloid plaques, but not diffuse in human AD patients, and in mice transgenic for mutant APP [>>33<<], it has been postulated that microglia play a role in the conversion of diffuse to neuritic senile plaques but not in the origin of diffuse plaques [34].
n3:mentions
n2:9422548
Subject Item
_:vb6412173
rdf:type
n3:Context
rdf:value
but not diffuse in human AD patients, and in mice transgenic for mutant APP [33], it has been postulated that microglia play a role in the conversion of diffuse to neuritic senile plaques but not in the origin of diffuse plaques [>>34<<]. Specifically, post-mortem analyses of microglia density in the neocortex of three groups of nondemented individuals at different stages of senile plaque formation versus AD patients revealed that the mean density of microglia was
n3:mentions
n2:8532113
Subject Item
_:vb6412174
rdf:type
n3:Context
rdf:value
effect of Aβ deposition in brain has been recapitulated in aged mice transgenic for a familial AD mutation of APP, in which astrocytes and microglia expressing Il-1β, IL-6 and TNF have been found surrounding amyloid plaques [>>35<<]. The bacterial endotoxin lipopolysaccharide (LPS), a powerful inducer of inflammatory responses [36], exacerbates the appearance and severity of AD pathology in the APPV717F transgenic mouse [37], the APPswe transgenic mouse [38], and
n3:mentions
n2:10674423
Subject Item
_:vb6412175
rdf:type
n3:Context
rdf:value
The bacterial endotoxin lipopolysaccharide (LPS), a powerful inducer of inflammatory responses [>>36<<], exacerbates the appearance and severity of AD pathology in the APPV717F transgenic mouse [37], the APPswe transgenic mouse [38], and the triple-transgenic (3xTgAD) mouse [39].
n3:mentions
n2:3527951
Subject Item
_:vb6412176
rdf:type
n3:Context
rdf:value
The bacterial endotoxin lipopolysaccharide (LPS), a powerful inducer of inflammatory responses [36], exacerbates the appearance and severity of AD pathology in the APPV717F transgenic mouse [>>37<<], the APPswe transgenic mouse [38], and the triple-transgenic (3xTgAD) mouse [39].
n3:mentions
n2:11553297
Subject Item
_:vb6412177
rdf:type
n3:Context
rdf:value
The bacterial endotoxin lipopolysaccharide (LPS), a powerful inducer of inflammatory responses [36], exacerbates the appearance and severity of AD pathology in the APPV717F transgenic mouse [37], the APPswe transgenic mouse [>>38<<], and the triple-transgenic (3xTgAD) mouse [39].
n3:mentions
n2:13678674
Subject Item
_:vb6412178
rdf:type
n3:Context
rdf:value
(LPS), a powerful inducer of inflammatory responses [36], exacerbates the appearance and severity of AD pathology in the APPV717F transgenic mouse [37], the APPswe transgenic mouse [38], and the triple-transgenic (3xTgAD) mouse [>>39<<]. In addition, the Transforming Growth Factor-β (TGF-β) cytokine family increases Aβ accumulation in the cerebral blood vessels of mice transgenic for human APP and is upregulated in blood vessels of human patients with Cerebral Amyloid
n3:mentions
n2:16192374
Subject Item
_:vb6412179
rdf:type
n3:Context
rdf:value
Transforming Growth Factor-β (TGF-β) cytokine family increases Aβ accumulation in the cerebral blood vessels of mice transgenic for human APP and is upregulated in blood vessels of human patients with Cerebral Amyloid Angiopathy (CAA) [>>40<<]. Co-addition of TGF-β1, 2 and 3 isoforms with Aβ causes increased Aβ accumulation in organotypic hippocampal slices [41].
n3:mentions
n2:9335500
Subject Item
_:vb6412180
rdf:type
n3:Context
rdf:value
Co-addition of TGF-β1, 2 and 3 isoforms with Aβ causes increased Aβ accumulation in organotypic hippocampal slices [>>41<<]. Together, these findings demonstrate the close association between microglia and plaque deposition and the ability of certain chronic inflammatory stimuli to exacerbate and accelerate amyloid-associated pathology. The emerging idea is
n3:mentions
n2:9852574
Subject Item
_:vb6412181
rdf:type
n3:Context
rdf:value
Cyclooxygenase 2 (COX2), a pro-inflammatory protein that is one of the targets of non-steroidal anti-inflammatory drugs (NSAIDs), and its homolog COX-1 [>>42<<], are elevated in AD brains [43].
n3:mentions
n2:9920782
Subject Item
_:vb6412182
rdf:type
n3:Context
rdf:value
Cyclooxygenase 2 (COX2), a pro-inflammatory protein that is one of the targets of non-steroidal anti-inflammatory drugs (NSAIDs), and its homolog COX-1 [42], are elevated in AD brains [>>43<<]. Serum levels of the acute phase protein α1-antichymotrypsin, which is upregulated by injury, trauma and infection, are also significantly higher in AD patients than healthy controls [44]. And clinically, a proteomic study of plasma from
n3:mentions
n2:11059791
Subject Item
_:vb6412183
rdf:type
n3:Context
rdf:value
Serum levels of the acute phase protein α1-antichymotrypsin, which is upregulated by injury, trauma and infection, are also significantly higher in AD patients than healthy controls [>>44<<]. And clinically, a proteomic study of plasma from control subjects, patients with Mild Cognitive Impairment (MCI) and patients with AD suggested that dysregulated systemic immune responses are present in patients who progress from MCI
n3:mentions
n2:8532107
Subject Item
_:vb6412184
rdf:type
n3:Context
rdf:value
systemic immune responses are present in patients who progress from MCI and go on to develop AD, raising the interesting possibility that this inflammation "communicome" may serve as signature for early detection of the disease [>>45<<].
n3:mentions
n2:17934472
Subject Item
_:vb6412185
rdf:type
n3:Context
rdf:value
Not only is neuroinflammation believed to be one of the earliest consequences of Aβ deposition, it has been shown to accelerate neurodegeneration and contribute to progression of pathology [>>46<<]. Epidemiological studies suggest a link between chronic use of non-steroidal anti-inflammatory drugs (NSAIDs) and reduced risk for AD.
n3:mentions
n2:16369931
Subject Item
_:vb6412186
rdf:type
n3:Context
rdf:value
In a study of siblings who all eventually developed AD, regular use of NSAIDs delayed the onset of AD and reduced the risk of AD with each year of use [>>47<<]. Participants in the Baltimore Longitudinal Aging Study also exhibited a reduced risk for AD with the use of NSAIDs, with those patients who had taken NSAIDs for more than 2 years showing the most reduction in AD risk [48]. Comparison of
n3:mentions
n2:8544901
Subject Item
_:vb6412187
rdf:type
n3:Context
rdf:value
Participants in the Baltimore Longitudinal Aging Study also exhibited a reduced risk for AD with the use of NSAIDs, with those patients who had taken NSAIDs for more than 2 years showing the most reduction in AD risk [>>48<<]. Comparison of brains of aged but cognitively normal patients who used NSAIDs chronically with that of cognitively normal patients who did not use NSAIDs revealed no changes in the appearance of senile plaques, but a 3-fold decrease in
n3:mentions
n2:9065537
Subject Item
_:vb6412188
rdf:type
n3:Context
rdf:value
NSAIDs chronically with that of cognitively normal patients who did not use NSAIDs revealed no changes in the appearance of senile plaques, but a 3-fold decrease in the number of activated microglia in the brains of chronic NSAID users [>>49<<]. Most recently in what is the largest and longest duration epidemiological study to date, long-term (> 5 yrs) NSAID use, in particular ibuprofen, was shown to be protective against development of AD [50].
n3:mentions
n2:9566383
Subject Item
_:vb6412189
rdf:type
n3:Context
rdf:value
Most recently in what is the largest and longest duration epidemiological study to date, long-term (> 5 yrs) NSAID use, in particular ibuprofen, was shown to be protective against development of AD [>>50<<]. These findings suggest that the protection afforded by chronic NSAID use in the studies of AD patients may in part be derived by attenuation of microglia activation. Consistent with the epidemiological findings on ibuprofen, chronic
n3:mentions
n2:18458226
Subject Item
_:vb6412190
rdf:type
n3:Context
rdf:value
Consistent with the epidemiological findings on ibuprofen, chronic ibuprofen administration in aged transgenic mice reduced the number and area of amyloid plaques, as well as the numbers of activated microglia [>>51<<], and administration of R-flurbiprofen rescued deficits in hippocampal and medial temporal lobe-dependent memory and learning [52].
n3:mentions
n2:10908610
Subject Item
_:vb6412191
rdf:type
n3:Context
rdf:value
mice reduced the number and area of amyloid plaques, as well as the numbers of activated microglia [51], and administration of R-flurbiprofen rescued deficits in hippocampal and medial temporal lobe-dependent memory and learning [>>52<<]. However, thus far, clinical trials using systemic administration of NSAIDs have yielded mixed or inconclusive results [53-55], reflecting the need to identify and target the key inflammatory mediators that promote amyloid-associated
n3:mentions
n2:17650315
Subject Item
_:vb6412192
rdf:type
n3:Context
rdf:value
However, thus far, clinical trials using systemic administration of NSAIDs have yielded mixed or inconclusive results [>>53<<-55], reflecting the need to identify and target the key inflammatory mediators that promote amyloid-associated neuropathology.
n3:mentions
n2:12883918 n2:16697488 n2:12662122
Subject Item
_:vb6412193
rdf:type
n3:Context
rdf:value
For example, the activation of complement factor C3, the central component of the complement system and a key inflammatory protein may be necessary for plaque clearance by microglia in the AD-afflicted brain [>>56<<,57]. In addition, an important component of any inflammatory response is the activation of anti-inflammatory loops that serve to limit and resolve the initial inflammatory response. The Peroxisome Proliferator-Activated Receptor-γ
n3:mentions
n2:18562603
Subject Item
_:vb6412194
rdf:type
n3:Context
rdf:value
For example, the activation of complement factor C3, the central component of the complement system and a key inflammatory protein may be necessary for plaque clearance by microglia in the AD-afflicted brain [56,>>57<<]. In addition, an important component of any inflammatory response is the activation of anti-inflammatory loops that serve to limit and resolve the initial inflammatory response. The Peroxisome Proliferator-Activated Receptor-γ (PPARγ), a
n3:mentions
n2:12119423
Subject Item
_:vb6412195
rdf:type
n3:Context
rdf:value
Peroxisome Proliferator-Activated Receptor-γ (PPARγ), a nuclear receptor which is activated by metabolites of prostaglandins generated by the COX enzymes and by certain NSAIDs, is upregulated in concert with the COX enzymes in AD brain [>>42<<]. As such, PPARγ activation exerts an anti-inflammatory effect, and PPARγ agonists have been shown to inhibit the production of cytokines and pro-inflammatory mediators in response to Aβ [58].
n3:mentions
n2:9920782
Subject Item
_:vb6412196
rdf:type
n3:Context
rdf:value
As such, PPARγ activation exerts an anti-inflammatory effect, and PPARγ agonists have been shown to inhibit the production of cytokines and pro-inflammatory mediators in response to Aβ [>>58<<]. In addition, there appears to be a feedback signaling loop between Aβ and IL-1β: Aβ can induce the production of IL-1β [7], and the presence of IL-1β greatly increases the secretion of cytokines IL-6 and IL-8 in response to Aβ by
n3:mentions
n2:10632585
Subject Item
_:vb6412197
rdf:type
n3:Context
rdf:value
In addition, there appears to be a feedback signaling loop between Aβ and IL-1β: Aβ can induce the production of IL-1β [>>7<<], and the presence of IL-1β greatly increases the secretion of cytokines IL-6 and IL-8 in response to Aβ by astrocytes; in the other direction, IL-1α and IL-1β both upregulate the expression of APP, thus probably upregulating the
n3:mentions
n2:15639313
Subject Item
_:vb6412198
rdf:type
n3:Context
rdf:value
of IL-1β greatly increases the secretion of cytokines IL-6 and IL-8 in response to Aβ by astrocytes; in the other direction, IL-1α and IL-1β both upregulate the expression of APP, thus probably upregulating the production of Aβ [>>59<<]. The ratio of the pro-inflammatory cytokine IL-1β to the anti-inflammatory cytokine IL-10 is drastically elevated in the serum of AD patients, giving these patients a definite pro-inflammatory profile [60].
n3:mentions
n2:8892349
Subject Item
_:vb6412199
rdf:type
n3:Context
rdf:value
The ratio of the pro-inflammatory cytokine IL-1β to the anti-inflammatory cytokine IL-10 is drastically elevated in the serum of AD patients, giving these patients a definite pro-inflammatory profile [>>60<<]. Increases in levels of IL-1β have been correlated with decreases in LTP in the hippocampus, showing that the cytokine itself may impair memory [61]. Other evidence, however, suggests that IL-1β may not be driving AD pathogenic processes.
n3:mentions
n2:11162920
Subject Item
_:vb6412200
rdf:type
n3:Context
rdf:value
Increases in levels of IL-1β have been correlated with decreases in LTP in the hippocampus, showing that the cytokine itself may impair memory [>>61<<]. Other evidence, however, suggests that IL-1β may not be driving AD pathogenic processes. For example, functional inhibition of IL-1β signaling in mice by genetic ablation of the IL1 receptor [62] or by infusion of IL-1ra did not
n3:mentions
n2:9775404
Subject Item
_:vb6412201
rdf:type
n3:Context
rdf:value
For example, functional inhibition of IL-1β signaling in mice by genetic ablation of the IL1 receptor [>>62<<] or by infusion of IL-1ra did not modulate Aβ deposition.
n3:mentions
n2:16872492
Subject Item
_:vb6412202
rdf:type
n3:Context
rdf:value
In addition, IL-1β was recently shown to upregulate the α-secretase TACE, thus increasing non-amyloidogenic cleavage of APP and decreasing Aβ production [>>63<<]. Therefore, while it may participate in neuroinflammatory responses in AD brain by activating microglia to secrete other inflammatory mediators, IL-1β is not required to drive Aβ deposition and may in fact activate non-amyloidogenic
n3:mentions
n2:18021299
Subject Item
_:vb6412203
rdf:type
n3:Context
rdf:value
Immunizing PDAPP mice with Aβ42 prevented or reduced the progression of AD pathology in these mice, depending on whether the immunization took place before or after the development of plaque pathology [>>64<<]. Vaccination with Aβ peptides also ameliorated cognitive deficits in mice transgenic for a familial AD (FAD) mutation in APP and an FAD mutation in PS1 [65]. As an alternative delivery route, intranasal administration of Aβ peptides
n3:mentions
n2:10408445
Subject Item
_:vb6412204
rdf:type
n3:Context
rdf:value
Vaccination with Aβ peptides also ameliorated cognitive deficits in mice transgenic for a familial AD (FAD) mutation in APP and an FAD mutation in PS1 [>>65<<]. As an alternative delivery route, intranasal administration of Aβ peptides reduced amyloid deposition in AD mouse models [66,67]. Aβ vaccinations were also found successful in reducing Aβ levels in two non-human primates, the rhesus
n3:mentions
n2:11140686
Subject Item
_:vb6412205
rdf:type
n3:Context
rdf:value
As an alternative delivery route, intranasal administration of Aβ peptides reduced amyloid deposition in AD mouse models [>>66<<,67]. Aβ vaccinations were also found successful in reducing Aβ levels in two non-human primates, the rhesus monkey [68] and the Caribbean vervet [69]. A clinical trial of Aβ42 vaccinations was undertaken by Elan Pharmaceuticals in AD
n3:mentions
n2:11788048
Subject Item
_:vb6412206
rdf:type
n3:Context
rdf:value
As an alternative delivery route, intranasal administration of Aβ peptides reduced amyloid deposition in AD mouse models [66,>>67<<]. Aβ vaccinations were also found successful in reducing Aβ levels in two non-human primates, the rhesus monkey [68] and the Caribbean vervet [69]. A clinical trial of Aβ42 vaccinations was undertaken by Elan Pharmaceuticals in AD
n3:mentions
n2:12470794
Subject Item
_:vb6412207
rdf:type
n3:Context
rdf:value
Aβ vaccinations were also found successful in reducing Aβ levels in two non-human primates, the rhesus monkey [>>68<<] and the Caribbean vervet [69].
n3:mentions
n2:15037022
Subject Item
_:vb6412208
rdf:type
n3:Context
rdf:value
Aβ vaccinations were also found successful in reducing Aβ levels in two non-human primates, the rhesus monkey [68] and the Caribbean vervet [>>69<<]. A clinical trial of Aβ42 vaccinations was undertaken by Elan Pharmaceuticals in AD patients, and the immunizations resulted in significant clearance of Aβ and plaque removal in some of the patients [70,71], as well as a slowing of the
n3:mentions
n2:15215183
Subject Item
_:vb6412209
rdf:type
n3:Context
rdf:value
A clinical trial of Aβ42 vaccinations was undertaken by Elan Pharmaceuticals in AD patients, and the immunizations resulted in significant clearance of Aβ and plaque removal in some of the patients [>>70<<,71], as well as a slowing of the cognitive decline in patients who produced antibodies against the peptide [72].
n3:mentions
n2:17086100
Subject Item
_:vb6412210
rdf:type
n3:Context
rdf:value
A clinical trial of Aβ42 vaccinations was undertaken by Elan Pharmaceuticals in AD patients, and the immunizations resulted in significant clearance of Aβ and plaque removal in some of the patients [70,>>71<<], as well as a slowing of the cognitive decline in patients who produced antibodies against the peptide [72].
n3:mentions
n2:12640446
Subject Item
_:vb6412211
rdf:type
n3:Context
rdf:value
in AD patients, and the immunizations resulted in significant clearance of Aβ and plaque removal in some of the patients [70,71], as well as a slowing of the cognitive decline in patients who produced antibodies against the peptide [>>72<<]. Unfortunately, the immunization also resulted in dangerous T-lymphocyte meningoencephalitis in some patients, causing the arrest of these trials [70,73].
n3:mentions
n2:12765607
Subject Item
_:vb6412212
rdf:type
n3:Context
rdf:value
Unfortunately, the immunization also resulted in dangerous T-lymphocyte meningoencephalitis in some patients, causing the arrest of these trials [>>70<<,73]. Passive immunization of PDAPP mice peripherally infused with antibodies that recognize aggregated Aβ in neuritic plaques rapidly increased microglial clustering around plaques detectable by in vivo multi-photon microscopy [74] and
n3:mentions
n2:17086100
Subject Item
_:vb6412213
rdf:type
n3:Context
rdf:value
Unfortunately, the immunization also resulted in dangerous T-lymphocyte meningoencephalitis in some patients, causing the arrest of these trials [70,>>73<<]. Passive immunization of PDAPP mice peripherally infused with antibodies that recognize aggregated Aβ in neuritic plaques rapidly increased microglial clustering around plaques detectable by in vivo multi-photon microscopy [74] and
n3:mentions
n2:12847155
Subject Item
_:vb6412214
rdf:type
n3:Context
rdf:value
Passive immunization of PDAPP mice peripherally infused with antibodies that recognize aggregated Aβ in neuritic plaques rapidly increased microglial clustering around plaques detectable by in vivo multi-photon microscopy [>>74<<] and reduced plaque burden and AD pathology in PDAPP mice [75].
n3:mentions
n2:19109498
Subject Item
_:vb6412215
rdf:type
n3:Context
rdf:value
infused with antibodies that recognize aggregated Aβ in neuritic plaques rapidly increased microglial clustering around plaques detectable by in vivo multi-photon microscopy [74] and reduced plaque burden and AD pathology in PDAPP mice [>>75<<]. Administration of antibodies specifically directed against oligomers of Aβ improved learning and memory in Tg2576 mice [76].
n3:mentions
n2:10932230
Subject Item
_:vb6412216
rdf:type
n3:Context
rdf:value
Administration of antibodies specifically directed against oligomers of Aβ improved learning and memory in Tg2576 mice [>>76<<]. Therefore, passive immunization may be a safer approach in AD patients. In addition, there is strong evidence that using shorter Aβ peptides is safer than using full-length Aβ40 or 42 as the immunogen [77]. In short, Aβ immunotherapy
n3:mentions
n2:16361260
Subject Item
_:vb6412217
rdf:type
n3:Context
rdf:value
In addition, there is strong evidence that using shorter Aβ peptides is safer than using full-length Aβ40 or 42 as the immunogen [>>77<<]. In short, Aβ immunotherapy holds promise but will need to be made safer and more effective in its ability to generate good antibody titers in the elderly [78]. If these novel immunogens can enhance Aβ antibody generation without the
n3:mentions
n2:17908047
Subject Item
_:vb6412218
rdf:type
n3:Context
rdf:value
In short, Aβ immunotherapy holds promise but will need to be made safer and more effective in its ability to generate good antibody titers in the elderly [>>78<<]. If these novel immunogens can enhance Aβ antibody generation without the adverse events seen in the earlier clinical trial, neuroimmune modulation by vaccination may become an effective way to prevent AD.
n3:mentions
n2:19660650
Subject Item
_:vb6412219
rdf:type
n3:Context
rdf:value
body (Lewy bodies) and processes (Lewy neurites) of specific neurons of the brainstem and a classic motor phenotype resulting from substantial loss of dopaminergic neurons from the substantia nigra pars compacta (SNpc) (reviewed in [>>79<<]). A number of studies have confirmed the presence of inflammatory mediators (including TNF, IL-1β, IL-6, and IFNγ) in the cerebrospinal fluid (CSF) of patients with PD as well as in the post-mortem SNpc in PD patient brains [80-84].
n3:mentions
n2:17413315
Subject Item
_:vb6412220
rdf:type
n3:Context
rdf:value
A number of studies have confirmed the presence of inflammatory mediators (including TNF, IL-1β, IL-6, and IFNγ) in the cerebrospinal fluid (CSF) of patients with PD as well as in the post-mortem SNpc in PD patient brains [>>80<<-84]. Significantly elevated levels of TNF mRNA and protein can be detected in the rodent midbrain substantia nigra within hours of in vivo administration of two neurotoxins widely used to model parkinsonism in rodents, 6-hydroxydopamine
n3:mentions
n2:8934562 n2:10212304 n2:9539333 n2:16182554 n2:3399080
Subject Item
_:vb6412221
rdf:type
n3:Context
rdf:value
elevated levels of TNF mRNA and protein can be detected in the rodent midbrain substantia nigra within hours of in vivo administration of two neurotoxins widely used to model parkinsonism in rodents, 6-hydroxydopamine (6-OHDA) [>>8<<] and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) [85-87].
n3:mentions
n2:16823625
Subject Item
_:vb6412222
rdf:type
n3:Context
rdf:value
in the rodent midbrain substantia nigra within hours of in vivo administration of two neurotoxins widely used to model parkinsonism in rodents, 6-hydroxydopamine (6-OHDA) [8] and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) [>>85<<-87]. Consistent with a role of TNF in contributing to dopaminergic neuron death in chronic parkinsonism, plasma TNF levels were shown to remain elevated in MPTP-treated non-human primates one year after administration of the neurotoxin
n3:mentions
n2:12429221 n2:12205053 n2:15140182
Subject Item
_:vb6412223
rdf:type
n3:Context
rdf:value
Consistent with a role of TNF in contributing to dopaminergic neuron death in chronic parkinsonism, plasma TNF levels were shown to remain elevated in MPTP-treated non-human primates one year after administration of the neurotoxin [>>88<<]. In contrast, studies involving mice deficient in TNF or both TNF receptors have yielded conflicting results in that one group reported lack of TNF receptors altered dopamine metabolism and reduced survival of dopaminergic terminals [86]
n3:mentions
n2:16154791
Subject Item
_:vb6412224
rdf:type
n3:Context
rdf:value
In contrast, studies involving mice deficient in TNF or both TNF receptors have yielded conflicting results in that one group reported lack of TNF receptors altered dopamine metabolism and reduced survival of dopaminergic terminals [>>86<<] and other groups reported TNF-deficient mice to have reduced sensitivity to MPTP-induced neurotoxicity [85,87].
n3:mentions
n2:12429221
Subject Item
_:vb6412225
rdf:type
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rdf:value
in that one group reported lack of TNF receptors altered dopamine metabolism and reduced survival of dopaminergic terminals [86] and other groups reported TNF-deficient mice to have reduced sensitivity to MPTP-induced neurotoxicity [>>85<<,87]. Loss of TNF receptors versus TNF ligand during development might alter the behavior of microglia or other immune cell populations and contribute to conflicting outcomes in these studies.
n3:mentions
n2:15140182
Subject Item
_:vb6412226
rdf:type
n3:Context
rdf:value
in that one group reported lack of TNF receptors altered dopamine metabolism and reduced survival of dopaminergic terminals [86] and other groups reported TNF-deficient mice to have reduced sensitivity to MPTP-induced neurotoxicity [85,>>87<<]. Loss of TNF receptors versus TNF ligand during development might alter the behavior of microglia or other immune cell populations and contribute to conflicting outcomes in these studies.
n3:mentions
n2:12205053
Subject Item
_:vb6412227
rdf:type
n3:Context
rdf:value
In the first model chronic low dose lipopolysaccharide (LPS) infusion into SNpc of rats results in delayed, selective and progressive loss of nigral DA neurons [>>89<<]. In the second model exposure of pregnant rats to LPS and thus, in utero exposure of embryos to the endotoxin, caused a loss of DA neurons in postnatal brains [90]. Most importantly, chronic infusion of dominant negative TNF inhibitor
n3:mentions
n2:12068076
Subject Item
_:vb6412228
rdf:type
n3:Context
rdf:value
In the second model exposure of pregnant rats to LPS and thus, in utero exposure of embryos to the endotoxin, caused a loss of DA neurons in postnatal brains [>>90<<]. Most importantly, chronic infusion of dominant negative TNF inhibitor proteins into SNpc of adult rats protected nigral DA neurons from LPS and 6-OHDA induced degeneration [91] as did a single nigral injection of a lentivirus encoding
n3:mentions
n2:11835448
Subject Item
_:vb6412229
rdf:type
n3:Context
rdf:value
Most importantly, chronic infusion of dominant negative TNF inhibitor proteins into SNpc of adult rats protected nigral DA neurons from LPS and 6-OHDA induced degeneration [>>91<<] as did a single nigral injection of a lentivirus encoding DN-TNF in 6-OHDA hemiparkinsonian rats [92].
n3:mentions
n2:16971520
Subject Item
_:vb6412230
rdf:type
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rdf:value
dominant negative TNF inhibitor proteins into SNpc of adult rats protected nigral DA neurons from LPS and 6-OHDA induced degeneration [91] as did a single nigral injection of a lentivirus encoding DN-TNF in 6-OHDA hemiparkinsonian rats [>>92<<]. Given that TNF receptors are expressed in nigrostriatal dopamine neurons [93,94] and these neurons are selectively vulnerable to TNF-induced toxicity [95-99], these early genetic studies and the more recent chronic inflammation models
n3:mentions
n2:18628756
Subject Item
_:vb6412231
rdf:type
n3:Context
rdf:value
Given that TNF receptors are expressed in nigrostriatal dopamine neurons [>>93<<,94] and these neurons are selectively vulnerable to TNF-induced toxicity [95-99], these early genetic studies and the more recent chronic inflammation models of PD strongly implicate TNF and its downstream targets in neurotoxin- and
n3:mentions
n2:8084523
Subject Item
_:vb6412232
rdf:type
n3:Context
rdf:value
Given that TNF receptors are expressed in nigrostriatal dopamine neurons [93,>>94<<] and these neurons are selectively vulnerable to TNF-induced toxicity [95-99], these early genetic studies and the more recent chronic inflammation models of PD strongly implicate TNF and its downstream targets in neurotoxin- and
n3:mentions
n2:8386591
Subject Item
_:vb6412233
rdf:type
n3:Context
rdf:value
Given that TNF receptors are expressed in nigrostriatal dopamine neurons [93,94] and these neurons are selectively vulnerable to TNF-induced toxicity [>>95<<-99], these early genetic studies and the more recent chronic inflammation models of PD strongly implicate TNF and its downstream targets in neurotoxin- and endotoxin-induced loss of nigral DA neurons.
n3:mentions
n2:11358437 n2:9500954 n2:15583962 n2:11850061 n2:9464656
Subject Item
_:vb6412234
rdf:type
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rdf:value
These polymorphisms are over-represented in specific cohorts of individuals affected with PD and may confer increased susceptibility for the disease [>>100<<-104]. However, most of these findings have not been replicated in independent studies and a meta-analysis of multiple association studies is needed to assess the overall genetic effect of cytokine gene polymorphisms on neurodegenerative
n3:mentions
n2:15648059 n2:11585553 n2:11072751 n2:15834859
Subject Item
_:vb6412235
rdf:type
n3:Context
rdf:value
idiopathic PD have markedly elevated microglia activation in the pons, basal ganglia, striatum, and frontal and temporal cortical regions irrespective of the number of years with the disease compared to healthy age-matched controls [>>81<<]. Persistent activation of the abundant number of microglia in the midbrain region are likely the direct result of elevated levels of cytokines acting in an autocrine manner to potentiate inflammatory responses (e.g., auto-amplification
n3:mentions
n2:16182554
Subject Item
_:vb6412236
rdf:type
n3:Context
rdf:value
elevated levels of cytokines acting in an autocrine manner to potentiate inflammatory responses (e.g., auto-amplification of reactive oxygen species, nitric oxide, and superoxide radicals to form highly oxidizing peroxynitrite species)[>>7<<,105-108]. Given that DA neurons in the midbrain have an inherently elevated oxidative intracellular environment as a result of oxidation reactions required for the synthesis of the neurotransmitter dopamine, chronic neuroinflammation is
n3:mentions
n2:15639313
Subject Item
_:vb6412237
rdf:type
n3:Context
rdf:value
levels of cytokines acting in an autocrine manner to potentiate inflammatory responses (e.g., auto-amplification of reactive oxygen species, nitric oxide, and superoxide radicals to form highly oxidizing peroxynitrite species)[7,>>105<<-108]. Given that DA neurons in the midbrain have an inherently elevated oxidative intracellular environment as a result of oxidation reactions required for the synthesis of the neurotransmitter dopamine, chronic neuroinflammation is
n3:mentions
n2:16978723 n2:17180163 n2:16953112 n2:17017556
Subject Item
_:vb6412238
rdf:type
n3:Context
rdf:value
Huntington's disease (HD) is an autosomal dominant neurodegenerative disorder that has been linked to mutations in the huntingtin gene (htt) [>>109<<]. CAG repeat expansions in the htt gene result in an increased number of glutamine residues in the huntingtin protein (polyglutamine expansion).
n3:mentions
n2:8458085
Subject Item
_:vb6412239
rdf:type
n3:Context
rdf:value
The R6/2 mouse model of HD displays increased serum levels of IL-6 and in downstream IL-6 effectors, such as alpha-2-macroglobulin (A2 M) and complement components [>>110<<]. In the CNS, microarray profiling of several brain regions from HD patients and controls revealed increased gliosis and expression of inflammation-related genes, including GFAP and complement proteins. Increases were most pronounced in
n3:mentions
n2:17552550
Subject Item
_:vb6412240
rdf:type
n3:Context
rdf:value
Increases were most pronounced in the caudate putamen where brain pathology is most severe in HD patients [>>111<<]. Increases in labeling of complement proteins in neurons and astrocytes and a 2-5 fold increase in activators and regulators of the classical complement pathway have also been detected in human HD brains by RT-PCR [112]. Lastly, clinical
n3:mentions
n2:16467349
Subject Item
_:vb6412241
rdf:type
n3:Context
rdf:value
Increases in labeling of complement proteins in neurons and astrocytes and a 2-5 fold increase in activators and regulators of the classical complement pathway have also been detected in human HD brains by RT-PCR [>>112<<]. Lastly, clinical plasma samples from HD gene carriers contain increased levels of pro-inflammatory cytokines involved in the innate immune response, such as IL-6 [113].
n3:mentions
n2:10506508
Subject Item
_:vb6412242
rdf:type
n3:Context
rdf:value
Lastly, clinical plasma samples from HD gene carriers contain increased levels of pro-inflammatory cytokines involved in the innate immune response, such as IL-6 [>>113<<].
n3:mentions
n2:18625748
Subject Item
_:vb6412243
rdf:type
n3:Context
rdf:value
innate immune response before the onset of clinical symptoms and investigators have been able to discriminate controls from presymptomatic HD mutation carriers by measuring the levels of 3 cytokines, IL-5, IL-6, and IL-10 in plasma [>>113<<]. In brains of mutant htt carriers, microglia are activated before onset of symptoms and increased microglial activation correlates with an increased chance of developing HD symptoms in 5 years [114].
n3:mentions
n2:18625748
Subject Item
_:vb6412244
rdf:type
n3:Context
rdf:value
In brains of mutant htt carriers, microglia are activated before onset of symptoms and increased microglial activation correlates with an increased chance of developing HD symptoms in 5 years [>>114<<]. Once symptoms have manifested, microglial activation correlates with disease severity [115,116]. In the 3-nitroproprionic acid neurotoxin model of HD in rats, treatment with Celastrol, an anti-inflammatory and antioxidant compound
n3:mentions
n2:17400599
Subject Item
_:vb6412245
rdf:type
n3:Context
rdf:value
Once symptoms have manifested, microglial activation correlates with disease severity [>>115<<,116]. In the 3-nitroproprionic acid neurotoxin model of HD in rats, treatment with Celastrol, an anti-inflammatory and antioxidant compound derived from plants, reduced striatal lesion volume [117], indicating that controlling an
n3:mentions
n2:16769933
Subject Item
_:vb6412246
rdf:type
n3:Context
rdf:value
Once symptoms have manifested, microglial activation correlates with disease severity [115,>>116<<]. In the 3-nitroproprionic acid neurotoxin model of HD in rats, treatment with Celastrol, an anti-inflammatory and antioxidant compound derived from plants, reduced striatal lesion volume [117], indicating that controlling an inflammatory
n3:mentions
n2:11273004
Subject Item
_:vb6412247
rdf:type
n3:Context
rdf:value
In the 3-nitroproprionic acid neurotoxin model of HD in rats, treatment with Celastrol, an anti-inflammatory and antioxidant compound derived from plants, reduced striatal lesion volume [>>117<<], indicating that controlling an inflammatory response could be therapeutically beneficial as HD progresses.
n3:mentions
n2:16092942
Subject Item
_:vb6412248
rdf:type
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rdf:value
However, treatment with acetylsalicylate or rofecoxib, anti-inflammatory drugs commonly used in the clinic, was not neuroprotective in either the R6/2 or N171-82Q transgenic mouse models of HD [>>118<<].
n3:mentions
n2:15474369
Subject Item
_:vb6412249
rdf:type
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rdf:value
Microglia from YAC128 and R6/2 mouse models of HD respond in a similar overactive manner [>>113<<]. Mutant htt is found in glial nuclei where it can act to alter gene expression, probably because of its aberrant interactions with transcription factors that are made possible by glutamine expansion-related conformational changes in the
n3:mentions
n2:18625748
Subject Item
_:vb6412250
rdf:type
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rdf:value
found in glial nuclei where it can act to alter gene expression, probably because of its aberrant interactions with transcription factors that are made possible by glutamine expansion-related conformational changes in the htt protein [>>119<<]. Interestingly, mutant, but not normal htt activates the IKK complex, the major kinase that leads to phosphorylation-induced degradation of IκBs, leading to increased translocation of NF-κB dimers to the nucleus in mouse striatal cells
n3:mentions
n2:12711212
Subject Item
_:vb6412251
rdf:type
n3:Context
rdf:value
Interestingly, mutant, but not normal htt activates the IKK complex, the major kinase that leads to phosphorylation-induced degradation of IκBs, leading to increased translocation of NF-κB dimers to the nucleus in mouse striatal cells [>>120<<]. Since NF-κB can promote expression of IL-6 and other inflammatory cytokines in glia, such an interaction provides a candidate mechanism by which mutant htt could alter the activity of immune cells leading to an abnormally robust
n3:mentions
n2:15371500
Subject Item
_:vb6412252
rdf:type
n3:Context
rdf:value
Areas where degenerating motor neurons are present in both ALS patients and mouse models are marked by the presence of cytokines and immune cells, including T cells, activated microglia, and astrocytes [>>121<<,122]. In addition PET imaging of ALS patients showed an increase in activated microglia in the motor cortex that correlates with upper motor neuron symptoms [123]. In some ALS disease models the presence of immune cells precedes the
n3:mentions
n2:14755726
Subject Item
_:vb6412253
rdf:type
n3:Context
rdf:value
Areas where degenerating motor neurons are present in both ALS patients and mouse models are marked by the presence of cytokines and immune cells, including T cells, activated microglia, and astrocytes [121,>>122<<]. In addition PET imaging of ALS patients showed an increase in activated microglia in the motor cortex that correlates with upper motor neuron symptoms [123]. In some ALS disease models the presence of immune cells precedes the disease
n3:mentions
n2:1347673
Subject Item
_:vb6412254
rdf:type
n3:Context
rdf:value
In addition PET imaging of ALS patients showed an increase in activated microglia in the motor cortex that correlates with upper motor neuron symptoms [>>123<<]. In some ALS disease models the presence of immune cells precedes the disease phenotype [124], and the chemokine MCP-1, a potent chemotactic stimulus for microglia [125] is elevated in the CSF of ALS patients [126], suggesting that
n3:mentions
n2:15056468
Subject Item
_:vb6412255
rdf:type
n3:Context
rdf:value
In some ALS disease models the presence of immune cells precedes the disease phenotype [>>124<<], and the chemokine MCP-1, a potent chemotactic stimulus for microglia [125] is elevated in the CSF of ALS patients [126], suggesting that neuroinflammation could contribute to disease progression.
n3:mentions
n2:16337133
Subject Item
_:vb6412256
rdf:type
n3:Context
rdf:value
In some ALS disease models the presence of immune cells precedes the disease phenotype [124], and the chemokine MCP-1, a potent chemotactic stimulus for microglia [>>125<<] is elevated in the CSF of ALS patients [126], suggesting that neuroinflammation could contribute to disease progression.
n3:mentions
n2:10642753
Subject Item
_:vb6412257
rdf:type
n3:Context
rdf:value
In some ALS disease models the presence of immune cells precedes the disease phenotype [124], and the chemokine MCP-1, a potent chemotactic stimulus for microglia [125] is elevated in the CSF of ALS patients [>>126<<], suggesting that neuroinflammation could contribute to disease progression.
n3:mentions
n2:19236470
Subject Item
_:vb6412258
rdf:type
n3:Context
rdf:value
In addition, the levels of general markers of inflammation in the serum of ALS patients correlate positively with the severity of their disability [>>127<<]. While multiple genetic loci have been identified as causal in familial forms of ALS, 20% of familial cases involve a gain of function mutation in Cu/Zn superoxide dismutase I (SOD1) [128]. In addition to the well-established role of
n3:mentions
n2:18976328
Subject Item
_:vb6412259
rdf:type
n3:Context
rdf:value
While multiple genetic loci have been identified as causal in familial forms of ALS, 20% of familial cases involve a gain of function mutation in Cu/Zn superoxide dismutase I (SOD1) [>>128<<]. In addition to the well-established role of SOD1 as a critical anti-oxidant enzyme, evidence suggests that part of its normal function is to protect against protein aggregation, a phenomenon that is known to hasten neuronal degeneration.
n3:mentions
n2:8446170
Subject Item
_:vb6412260
rdf:type
n3:Context
rdf:value
Nevertheless, several studies have suggested that SOD1 mutations in neurons alone are insufficient to cause ALS and that dysfunction in support glia may contribute to disease development and progression [>>129<<-132]. For example, ablating microglial expression of mutant SOD 1 (mSOD1) or transplanting bone marrow from wild-type mice into mSOD1 transgenic mice increases the life span of mutant mice [133,134], suggesting that SOD1 mutations may
n3:mentions
n2:11331366 n2:14526083 n2:15846792 n2:12077179
Subject Item
_:vb6412261
rdf:type
n3:Context
rdf:value
For example, ablating microglial expression of mutant SOD 1 (mSOD1) or transplanting bone marrow from wild-type mice into mSOD1 transgenic mice increases the life span of mutant mice [>>133<<,134], suggesting that SOD1 mutations may indirectly contribute to neuronal death by affecting glial rather than neuronal function.
n3:mentions
n2:17043238
Subject Item
_:vb6412262
rdf:type
n3:Context
rdf:value
For example, ablating microglial expression of mutant SOD 1 (mSOD1) or transplanting bone marrow from wild-type mice into mSOD1 transgenic mice increases the life span of mutant mice [133,>>134<<], suggesting that SOD1 mutations may indirectly contribute to neuronal death by affecting glial rather than neuronal function.
n3:mentions
n2:16741123
Subject Item
_:vb6412263
rdf:type
n3:Context
rdf:value
Consistent with this idea, mSOD1 mice stimulated with LPS secrete more inflammatory mediators, including TNF [>>135<<], MCP-1, TGF-β[121] and IFN-γ [136], than control mice.
n3:mentions
n2:15378658
Subject Item
_:vb6412264
rdf:type
n3:Context
rdf:value
Consistent with this idea, mSOD1 mice stimulated with LPS secrete more inflammatory mediators, including TNF [135], MCP-1, TGF-β[>>121<<] and IFN-γ [136], than control mice.
n3:mentions
n2:14755726
Subject Item
_:vb6412265
rdf:type
n3:Context
rdf:value
Consistent with this idea, mSOD1 mice stimulated with LPS secrete more inflammatory mediators, including TNF [135], MCP-1, TGF-β[121] and IFN-γ [>>136<<], than control mice.
n3:mentions
n2:15312178
Subject Item
_:vb6412266
rdf:type
n3:Context
rdf:value
Importantly, levels of TNF correlate with severity of motor neuron loss in mouse models of the disease [>>137<<,138] and both TNF receptors are elevated in the serum of ALS patients [139].
n3:mentions
n2:11687290
Subject Item
_:vb6412267
rdf:type
n3:Context
rdf:value
Importantly, levels of TNF correlate with severity of motor neuron loss in mouse models of the disease [137,>>138<<] and both TNF receptors are elevated in the serum of ALS patients [139].
n3:mentions
n2:11796754
Subject Item
_:vb6412268
rdf:type
n3:Context
rdf:value
Importantly, levels of TNF correlate with severity of motor neuron loss in mouse models of the disease [137,138] and both TNF receptors are elevated in the serum of ALS patients [>>139<<].
n3:mentions
n2:10863032
Subject Item
_:vb6412269
rdf:type
n3:Context
rdf:value
In pre-clinical mouse models, certain anti-inflammatory treatments aimed at suppressing microglia activation have been shown to increase the life expectancy of mice expressing human mutant SOD1 by more than 30% [>>140<<]. Anti-inflammatory treatments also prevented neurotoxicity when the CSF of ALS patients was applied to rat spinal cord motor neurons [141].
n3:mentions
n2:15379894
Subject Item
_:vb6412270
rdf:type
n3:Context
rdf:value
Anti-inflammatory treatments also prevented neurotoxicity when the CSF of ALS patients was applied to rat spinal cord motor neurons [>>141<<]. Although a generalized neuroinflammatory response may be driving progressive loss of motor neurons, not all inflammatory mediators have been strongly implicated in ALS. For instance, IL-1β may not be critical to ALS pathogenesis as
n3:mentions
n2:11912107
Subject Item
_:vb6412271
rdf:type
n3:Context
rdf:value
For instance, IL-1β may not be critical to ALS pathogenesis as genetic deletion of IL-1β does not change the lifespan or rate of motor neurodegeneration in mSOD-1 mice [>>142<<].
n3:mentions
n2:11706969
Subject Item
_:vb418708497
rdf:type
n3:RelevantBibliographicResource
n3:RelevantScore
14
n3:hasRelevantPaperId
n2:17180163
Subject Item
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rdf:type
n3:RelevantBibliographicResource
n3:RelevantScore
13
n3:hasRelevantPaperId
n2:20303880
Subject Item
_:vb418708499
rdf:type
n3:RelevantBibliographicResource
n3:RelevantScore
12
n3:hasRelevantPaperId
n2:15831717
Subject Item
_:vb418708500
rdf:type
n3:RelevantBibliographicResource
n3:RelevantScore
11
n3:hasRelevantPaperId
n2:17203472
Subject Item
_:vb418708501
rdf:type
n3:RelevantBibliographicResource
n3:RelevantScore
10
n3:hasRelevantPaperId
n2:10858586
Subject Item
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rdf:type
n3:RelevantBibliographicResource
n3:RelevantScore
10
n3:hasRelevantPaperId
n2:25792098
Subject Item
_:vb418708503
rdf:type
n3:RelevantBibliographicResource
n3:RelevantScore
10
n3:hasRelevantPaperId
n2:12165466
Subject Item
_:vb418708504
rdf:type
n3:RelevantBibliographicResource
n3:RelevantScore
8
n3:hasRelevantPaperId
n2:20234358
Subject Item
_:vb418708505
rdf:type
n3:RelevantBibliographicResource
n3:RelevantScore
8
n3:hasRelevantPaperId
n2:20012068
Subject Item
_:vb418708506
rdf:type
n3:RelevantBibliographicResource
n3:RelevantScore
8
n3:hasRelevantPaperId
n2:16148231
Subject Item
_:vb418708507
rdf:type
n3:RelevantBibliographicResource
n3:RelevantScore
8
n3:hasRelevantPaperId
n2:19913097
Subject Item
_:vb418708508
rdf:type
n3:RelevantBibliographicResource
n3:RelevantScore
7
n3:hasRelevantPaperId
n2:18925972
Subject Item
_:vb418708509
rdf:type
n3:RelevantBibliographicResource
n3:RelevantScore
7
n3:hasRelevantPaperId
n2:19461673
Subject Item
_:vb418708510
rdf:type
n3:RelevantBibliographicResource
n3:RelevantScore
7
n3:hasRelevantPaperId
n2:20644946
Subject Item
_:vb418708511
rdf:type
n3:RelevantBibliographicResource
n3:RelevantScore
7
n3:hasRelevantPaperId
n2:19655259
Subject Item
_:vb418708512
rdf:type
n3:RelevantBibliographicResource
n3:RelevantScore
7
n3:hasRelevantPaperId
n2:17965659
Subject Item
_:vb418708513
rdf:type
n3:RelevantBibliographicResource
n3:RelevantScore
6
n3:hasRelevantPaperId
n2:20887954
Subject Item
_:vb418708514
rdf:type
n3:RelevantBibliographicResource
n3:RelevantScore
6
n3:hasRelevantPaperId
n2:15356140
Subject Item
_:vb418708515
rdf:type
n3:RelevantBibliographicResource
n3:RelevantScore
6
n3:hasRelevantPaperId
n2:18567623
Subject Item
_:vb418708516
rdf:type
n3:RelevantBibliographicResource
n3:RelevantScore
6
n3:hasRelevantPaperId
n2:28099414
Subject Item
_:vb418708517
rdf:type
n3:RelevantBibliographicResource
n3:RelevantScore
6
n3:hasRelevantPaperId
n2:15895084
Subject Item
_:vb418708518
rdf:type
n3:RelevantBibliographicResource
n3:RelevantScore
6
n3:hasRelevantPaperId
n2:8843599
Subject Item
_:vb418708519
rdf:type
n3:RelevantBibliographicResource
n3:RelevantScore
6
n3:hasRelevantPaperId
n2:12379902
Subject Item
_:vb418708520
rdf:type
n3:RelevantBibliographicResource
n3:RelevantScore
6
n3:hasRelevantPaperId
n2:16402109
Subject Item
_:vb418708521
rdf:type
n3:RelevantBibliographicResource
n3:RelevantScore
6
n3:hasRelevantPaperId
n2:15791003
Subject Item
_:vb418708522
rdf:type
n3:RelevantBibliographicResource
n3:RelevantScore
6
n3:hasRelevantPaperId
n2:25991443
Subject Item
_:vb418708523
rdf:type
n3:RelevantBibliographicResource
n3:RelevantScore
6
n3:hasRelevantPaperId
n2:25598354
Subject Item
_:vb418708524
rdf:type
n3:RelevantBibliographicResource
n3:RelevantScore
5
n3:hasRelevantPaperId
n2:12511873
Subject Item
_:vb418708525
rdf:type
n3:RelevantBibliographicResource
n3:RelevantScore
5
n3:hasRelevantPaperId
n2:12824464
Subject Item
_:vb418708526
rdf:type
n3:RelevantBibliographicResource
n3:RelevantScore
5
n3:hasRelevantPaperId
n2:18701698
Subject Item
_:vb418708527
rdf:type
n3:RelevantBibliographicResource
n3:RelevantScore
5
n3:hasRelevantPaperId
n2:19513731
Subject Item
_:vb418708528
rdf:type
n3:RelevantBibliographicResource
n3:RelevantScore
5
n3:hasRelevantPaperId
n2:17720159
Subject Item
_:vb418708529
rdf:type
n3:RelevantBibliographicResource
n3:RelevantScore
5
n3:hasRelevantPaperId
n2:20561356
Subject Item
_:vb418708530
rdf:type
n3:RelevantBibliographicResource
n3:RelevantScore
5
n3:hasRelevantPaperId
n2:22072657
Subject Item
_:vb418708531
rdf:type
n3:RelevantBibliographicResource
n3:RelevantScore
5
n3:hasRelevantPaperId
n2:19302036
Subject Item
_:vb418708532
rdf:type
n3:RelevantBibliographicResource
n3:RelevantScore
5
n3:hasRelevantPaperId
n2:30258234
Subject Item
_:vb418708533
rdf:type
n3:RelevantBibliographicResource
n3:RelevantScore
5
n3:hasRelevantPaperId
n2:22674585
Subject Item
_:vb418708534
rdf:type
n3:RelevantBibliographicResource
n3:RelevantScore
5
n3:hasRelevantPaperId
n2:19269040
Subject Item
_:vb418708535
rdf:type
n3:RelevantBibliographicResource
n3:RelevantScore
5
n3:hasRelevantPaperId
n2:27540165
Subject Item
_:vb418708536
rdf:type
n3:RelevantBibliographicResource
n3:RelevantScore
5
n3:hasRelevantPaperId
n2:19782411
Subject Item
_:vb418708537
rdf:type
n3:RelevantBibliographicResource
n3:RelevantScore
5
n3:hasRelevantPaperId
n2:25800044
Subject Item
_:vb418708538
rdf:type
n3:RelevantBibliographicResource
n3:RelevantScore
5
n3:hasRelevantPaperId
n2:12130773
Subject Item
_:vb418708539
rdf:type
n3:RelevantBibliographicResource
n3:RelevantScore
5
n3:hasRelevantPaperId
n2:23108585
Subject Item
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