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| 9762518 | amyloid | amyloid | 2.3 | Accumulations of amyloid and extracellular tangles apparently act as irritants causing the activation | Junguk Hur |  |
| 9762518 | amyloid | amyloid | 2.3 | chromogranin A ( Taupenot et al . 1996 and _amp_#x3b2 -amyloid protein ( Klegeris et al . 1994 as well as | Junguk Hur | |
| 9762518 | amyloid | amyloid | 2.3 | activators of complement have for example been found in AD amyloid deposits | Junguk Hur | |
| 9762518 | amyloid | amyloid | 2.3 | The most prominent is _amp_#x3b2 -amyloid protein | Junguk Hur | |
| 9762518 | amyloid | amyloid | 2.3 | Others are amyloid P C-reactive protein and the Hageman factor ( McGeer and | Junguk Hur | |
| 9762518 | amyloid | amyloid | 2.3 | Subsequent immunohistochemical and other studies have revealed that the amyloid deposits in AD are also associated with many other extracellular | Junguk Hur | |
| 9769023 | amyloid | amyloid | 1.0 | Accumulations of amyloid extracellular tangles or Lewy bodies apparently act as irritants causing | Junguk Hur | |
| 9850924 | amyloid | amyloid | 1.0 | Accumulations of amyloid and extracellular tangles apparently act as irritants causing the activation | Junguk Hur | |
| 10417811 | amyloid | amyloid | 1.3 | amyotrophic lateral sclerosis and (5) 5 transgenic mice overexpressing mutant amyloid precursor protein which exhibits age-related amyloid deposition characteristic of Alzheimer's | Junguk Hur | |
| 10417811 | amyloid | amyloid | 1.3 | transgenic mice overexpressing mutant amyloid precursor protein which exhibits age-related amyloid deposition characteristic of Alzheimer's disease | Junguk Hur | |
| 10525172 | amyloid | amyloid | 1.0 | generated by microglial cells activated by pro-inflammatory cytokines or _amp_#x3b2 -amyloid peptide (_amp_#x3b2;-A) _amp_#x3b2 -A and by neurons in three different | Junguk Hur | |
| 10525172 | amyloid | amyloid | 1.0 | cytokines IL-1 IL-6 and TNF_amp_#x3b1 as well as by _amp_#x3b2 -amyloid peptide (_amp_#x3b2;-A) _amp_#x3b2 -A 82 90 the first 42 amino | Junguk Hur | |
| 10525172 | amyloid | amyloid | 1.0 | _amp_#x3b2 -A 82 90 the first 42 amino acids of amyloid precursor protein (APP) APP ( Fig 6 | Junguk Hur | |
| 10525172 | APP | APP | 0.3 | the first 42 amino acids of amyloid precursor protein (APP) APP ( Fig 6 | | |
| 10525172 | amyloid | amyloid | 1.0 | and thus peroxynitrite the soluble _amp_#x3b2 -A monomer a diffuse amyloid deposit and mature filamentous amyloid plaques | Junguk Hur | |
| 10525172 | amyloid | amyloid | 1.0 | _amp_#x3b2 -A monomer a diffuse amyloid deposit and mature filamentous amyloid plaques | Junguk Hur | |
| 10525172 | amyloid | amyloid | 1.0 | a pathway for peroxynitrite formation may be postulated in cerebral amyloid angiopathy which is frequently associated with AD 84 93 | Junguk Hur | |
| 11173059 | amyloid | amyloid | 17.4 | the formation of Lewy bodies and its aggregation in insoluble amyloid fibrils seems to precede the accumulation of ubiquitin and neurofilaments | Junguk Hur | |
| 11173059 | amyloid | amyloid | 17.4 | plaques are spherical multicellular lesions containing extracellular deposits of _amp_#x3b2 -amyloid protein which is mostly in a fibrillar form ( Selkoe | Junguk Hur | |
| 11173059 | amyloid | amyloid | 17.4 | Role of the _amp_#x3b2 -amyloid protein | Junguk Hur | |
| 11173059 | amyloid | amyloid | 17.4 | It is a widely accepted concept that deposition of _amp_#x3b2 -amyloid protein is the key event in the pathogenesis of Alzheimer | Junguk Hur | |
| 11173059 | amyloid | amyloid | 17.4 | Alzheimer disease _amp_#x3b2 -Amyloid protein derives from a precursor named amyloid precursor protein which in neurons consists of 695-amino acid residues | Junguk Hur | |
| 11173059 | amyloid | amyloid | 17.4 | The amyloid precursor protein is a transmembrane molecule with a long extracellular | Junguk Hur | |
| 11173059 | amyloid | amyloid | 17.4 | Under physiological conditions a small amount of amyloid precursor protein undergoes secretory cleavage of a long extracellular portion | Junguk Hur | |
| 11173059 | amyloid | amyloid | 17.4 | In Alzheimer disease the processing of amyloid precursor protein is significantly altered | Junguk Hur | |
| 11173059 | amyloid | amyloid | 17.4 | Increased amounts of amyloid precursor protein are cleaved by another endoprotease named _amp_#x3b2 -secretase | Junguk Hur | |
| 11173059 | amyloid | amyloid | 17.4 | the putative intramembranous portion leads to the generation of _amp_#x3b2 -amyloid protein molecules of 40 or 42 amino acid residues _amp_#x3b2 | Junguk Hur | |
| 11173059 | amyloid | amyloid | 17.4 | of disease and are accounted for by mutations of the amyloid precursor protein presenilin-1 (PS-1), PS-1 or presenilin-2 gene (PS-2) PS-2 | Junguk Hur | |
| 11173059 | amyloid | amyloid | 17.4 | The gene of amyloid precursor protein maps on chromosome 21q21.2 and at least 7 | Junguk Hur | |
| 11173059 | amyloid | amyloid | 17.4 | _amp_#x3b3 -secretase cleavage sites altering the normal proteolysis of the amyloid precursor protein | Junguk Hur | |
| 11173059 | amyloid | amyloid | 17.4 | they may act as or cooperate with _amp_#x3b3 -secretase in amyloid precursor protein processing ( Selkoe 1999 | Junguk Hur | |
| 11173059 | amyloid | amyloid | 17.4 | a wide consensus on the hypothesis that missense mutations of amyloid precursor protein PS-1 and PS-2 genes may share a common | Junguk Hur | |
| 11173059 | amyloid | amyloid | 17.4 | common pathogenetic mechanism finally leading to the accumulation of _amp_#x3b2 -amyloid protein as a byproduct of abnormal amyloid precursor protein metabolism | Junguk Hur | |
| 11173059 | amyloid | amyloid | 17.4 | accumulation of _amp_#x3b2 -amyloid protein as a byproduct of abnormal amyloid precursor protein metabolism ( Selkoe 1999 | Junguk Hur | |
| 11173059 | amyloid | amyloid | 17.4 | Experimental data for transgenic mice which overexpress mutant human amyloid precursor protein and develop Alzheimer-like pathology demonstrated that immunization with | Junguk Hur | |
| 11173059 | amyloid | amyloid | 17.4 | protein and develop Alzheimer-like pathology demonstrated that immunization with _amp_#x3b2 -amyloid protein may prevent neuritic plaque formation and that peripheral administration | Junguk Hur | |
| 11173059 | amyloid | amyloid | 17.4 | prevent neuritic plaque formation and that peripheral administration of anti-_amp_#x3b2 -amyloid protein antibodies reduces neuritic plaque burden ( Schenk and Bard | Junguk Hur | |
| 11173059 | amyloid | amyloid | 17.4 | humans are currently underway and if safe immunization with _amp_#x3b2 -amyloid protein may become the first-line treatment for asymptomatic subjects with | Junguk Hur | |
| 11173059 | amyloid | amyloid | 17.4 | treatment for patients with Alzheimer disease carrying mutations of the amyloid precursor protein PS1 or PS2 gene | Junguk Hur | |
| 11173059 | amyloid | amyloid | 17.4 | 4 may be due to its higher affinity for _amp_#x3b2 -amyloid protein compared to other alleles and to its propensity to | Junguk Hur | |
| 11173059 | amyloid | amyloid | 17.4 | to enhance the aggregation or reduce the clearance of _amp_#x3b2 -amyloid protein ( Selkoe 1999 | Junguk Hur | |
| 11173059 | amyloid | amyloid | 17.4 | of them code for proteins which may participate in _amp_#x3b2 -amyloid protein processing or aggregation in neuritic plaques -1-Antichymotrypsin is a | Junguk Hur | |
| 11173059 | amyloid | amyloid | 17.4 | a protease inhibitor and an acute-phase protein also found in amyloid deposits in Alzheimer disease brains ( Abraham et al. 1988 | Junguk Hur | |
| 11173059 | amyloid | amyloid | 17.4 | ( Licastro et al. 2000a and contribute to enhance _amp_#x3b2 -amyloid protein aggregation ( Ma et al. 1994 or hamper its | Junguk Hur | |
| 11173059 | amyloid | amyloid | 17.4 | -2-Macroglobulin another proteinase inhibitor is detected in amyloid plaques and interacts with the lipoprotein receptor related protein (LRP), | Junguk Hur | |
| 11173059 | amyloid | amyloid | 17.4 | LRP as do a number of other ligands including _amp_#x3b2 -amyloid protein amyloid precursor protein ApoE and cholesterol ( Rosenberg 2000 | Junguk Hur | |
| 11173059 | amyloid | amyloid | 17.4 | do a number of other ligands including _amp_#x3b2 -amyloid protein amyloid precursor protein ApoE and cholesterol ( Rosenberg 2000 -2-Macroglobulin also | Junguk Hur | |
| 11173059 | amyloid | amyloid | 17.4 | and cholesterol ( Rosenberg 2000 -2-Macroglobulin also binds to _amp_#x3b2 -amyloid protein and such complexes may be cleared through binding to | Junguk Hur | |
| 11173059 | amyloid | amyloid | 17.4 | may be cleared through binding to LRP or deposition in amyloid plaques | Junguk Hur | |
| 11173059 | amyloid | amyloid | 17.4 | may reflect a genetically-determined defective removal of -2-macroglobulin/_amp_#x3b2;-amyloid -2-macroglobulin _amp_#x3b2 -amyloid protein complexes | Junguk Hur | |
| 11173059 | amyloid | amyloid | 17.4 | believed to contribute to the clearance of ApoE/_amp_#x3b2;-amyloid ApoE _amp_#x3b2 -amyloid protein and -2-macroglobulin/_amp_#x3b2;-amyloid -2-macroglobulin _amp_#x3b2 -amyloid protein complexes ( Hyman | Junguk Hur | |
| 11173059 | amyloid | amyloid | 17.4 | of ApoE/_amp_#x3b2;-amyloid ApoE _amp_#x3b2 -amyloid protein and -2-macroglobulin/_amp_#x3b2;-amyloid -2-macroglobulin _amp_#x3b2 -amyloid protein complexes ( Hyman et al. 2000 | Junguk Hur | |
| 11173059 | amyloid | amyloid | 17.4 | by lovastatin and methyl-_amp_#x3b2 -cyclodextrine inhibits the production of _amp_#x3b2 -amyloid protein by cultured hippocampal neurons ( Simons et al. 1998 | Junguk Hur | |
| 11173059 | amyloid | amyloid | 17.4 | a neutralizing anti-NGF recombinant antibody developed an Alzheimer-like pathology including amyloid plaques and neurofibrillary tangles ( Capsoni et al. 2000 | Junguk Hur | |
| 11173059 | amyloid | amyloid | 17.4 | 1999 and insulin-like growth factor-1 shows protective effects against _amp_#x3b2 -amyloid protein neurotoxicity ( Dore et al. 1999 | Junguk Hur | |
| 11173059 | amyloid | amyloid | 17.4 | 1 exhibits opposing activities because it protects neurons against _amp_#x3b2 -amyloid protein toxicity ( Prehn et al. 1996 but enhances _amp_#x3b2 | Junguk Hur | |
| 11173059 | amyloid | amyloid | 17.4 | protein toxicity ( Prehn et al. 1996 but enhances _amp_#x3b2 -amyloid protein deposition in amyloid precursor protein transgenic mice ( Wyss-Coray | Junguk Hur | |
| 11173059 | amyloid | amyloid | 17.4 | et al. 1996 but enhances _amp_#x3b2 -amyloid protein deposition in amyloid precursor protein transgenic mice ( Wyss-Coray et al. 1997 | Junguk Hur | |
| 11173059 | amyloid | amyloid | 17.4 | in vitro ( Mattson et al. 1997 and reduces _amp_#x3b2 -amyloid protein production ( Xu et al. 1998 | Junguk Hur | |
| 11173059 | amyloid | amyloid | 17.4 | formation of Alzheimer disease plaques by upregulating the secretion of amyloid precursor protein ( Rogers et al. 1999 | Junguk Hur | |
| 11173059 | amyloid | amyloid | 17.4 | Therefore a self-amplifying circuit may occur between _amp_#x3b2 -amyloid protein and cytokines ultimately fostering the sustained formation of plaques | Junguk Hur | |
| 11173059 | amyloid | amyloid | 17.4 | obscure but several data suggest that chronic deposition of _amp_#x3b2 -amyloid protein may be crucial _amp_#x3b2 -Amyloid protein up-regulates pro-apoptotic molecules | Junguk Hur | |
| 11173059 | amyloid | amyloid | 17.4 | In turn caspases may support _amp_#x3b2 -amyloid protein synthesis by altering the normal proteolytic pathway of amyloid | Junguk Hur | |
| 11173059 | amyloid | amyloid | 17.4 | -amyloid protein synthesis by altering the normal proteolytic pathway of amyloid precursor protein ( Wellington and Hayden 2000 contributing to the | Junguk Hur | |
| 11173059 | amyloid | amyloid | 17.4 | to the accumulation and ultimately to the aggregation of _amp_#x3b2 -amyloid protein into fibrils | Junguk Hur | |
| 11173059 | amyloid | amyloid | 17.4 | In addition mutated PS-1 may promote apoptosis independently of _amp_#x3b2 -amyloid protein intervention by down-regulating neuronal survival factors ( Weihl et | Junguk Hur | |
| 14739060 | amyloid | amyloid | 1.0 | forms missense mutation have been identified for gene encoding _amp_#x3b2 -amyloid precursor protein as well as presenilin 1 (PSEN1) PSEN1 and | Junguk Hur | |
| 14739060 | amyloid | amyloid | 1.0 | for the former accumulation of several aggregated proteins (_amp_#x3b2;-amyloid, _amp_#x3b2 -amyloid especially its toxic form A_amp_#x3b2 42 APOE 43 hyperphosphorylated tau | Junguk Hur | |
| 14739060 | amyloid | amyloid | 1.0 | 2 with an inflammatory reaction around the deposit of _amp_#x3b2 -amyloid for the latter 38 | Junguk Hur | |
| 15210305 | amyloid | amyloid | 1.6 | of AD pathology possibly established and maintained by a significant amyloid beta deposition | Junguk Hur | |
| 15210305 | amyloid | amyloid | 1.6 | The amyloid precursor protein/presenilin-1 protein presenilin-1 (APP+PS1) APP PS1 transgenic mouse is | Junguk Hur | |
| 15210305 | APP | APP | 0.6 | The amyloid precursor protein/presenilin-1 protein presenilin-1 (APP+PS1) APP PS1 transgenic mouse is a model for amyloid deposition and | | |
| 15210305 | amyloid | amyloid | 1.6 | presenilin-1 (APP+PS1) APP PS1 transgenic mouse is a model for amyloid deposition and as in AD the mice develop memory deficits | Junguk Hur | |
| 15210305 | amyloid | amyloid | 1.6 | and as in AD the mice develop memory deficits and amyloid deposits accumulate | Junguk Hur | |
| 15210305 | amyloid | amyloid | 1.6 | lipopolysaccharide and IFN-gamma as well as prion protein (PrP) PrP amyloid 5 | Junguk Hur | |
| 15453089 | amyloid | amyloid | 1.0 | The characteristic neuropathological signs of the disease are amyloid deposition of the proteinase-resistant prion protein (PrP PrP res or | Junguk Hur | |
| 15453089 | amyloid | amyloid | 1.0 | in the elderly characterized by senile plaques neurofibrillary tangles and amyloid angiopathy | Junguk Hur | |
| 15453089 | amyloid | amyloid | 1.0 | neurons expressing COX-2 negatively correlated with the Braak score for amyloid deposits although a moderate albeit non-significant COX-2 increase was found | Junguk Hur | |
| 15453089 | amyloid | amyloid | 1.0 | be mainly expressed by microglial cells found in association with amyloid deposits regardless their ramified or activated morphology ( 71 | Junguk Hur | |
| 15571972 | amyloid | amyloid | 1.0 | work suggesting that tetracyclines can inhibit the formation of _amp_#x3b2 -amyloid aggregates and are able to disassemble preformed fibrils ( Forloni | Junguk Hur | |
| 15681814 | ABETA | Abeta | 1.0 | factor p53 is activated by the Alzheimer's disease toxic peptide Abeta as well as by excess glutamate and hypoxia to trigger | | |
| 16120782 | amyloid | amyloid | 1.3 | various mechanisms (Landreth Landreth and Heneka 2001 gamma agonists reduce amyloid beta peptide and cytokine mediated neuroinflammation and neurotoxicity in vitro | Junguk Hur | |
| 16445350 | amyloid | amyloid | 1.0 | discusses differences in critical pathways of immune/inflammation immune inflammation and amyloid formation between Parkinson's disease and amyotrophic lateral sclerosis as well | Junguk Hur | |
| 16624536 | amyloid | amyloid | 1.0 | Protection against _amp_#x3b2 -amyloid and glutamate excitotoxicity has been achieved through control of microglial | Junguk Hur | |
| 16647138 | amyloid | amyloid | 1.5 | It possesses protective effects against the neurotoxicity of _amp_#x3b2 -amyloid protein a protein probably causative in the generation of Alzheimer's | Junguk Hur | |
| 16647138 | amyloid | amyloid | 1.5 | The accumulation and aggregation of _amp_#x3b2 -amyloid peptide is believed to be an important event in the | Junguk Hur | |
| 16647138 | amyloid | amyloid | 1.5 | by which COX-1 and COX-2 promote amyloidogenic accumulation of _amp_#x3b2 -amyloid peptide is not fully understood | Junguk Hur | |
| 16647138 | amyloid | amyloid | 1.5 | COX-1 and COX-2 potentiate _amp_#x3b2 -amyloid peptide generation through mechanisms that involve _amp_#x3b3 -secretase activity ( | Junguk Hur | |
| 16647138 | amyloid | amyloid | 1.5 | synthesis and _amp_#x3b3 -secretase activity may not only modulate _amp_#x3b2 -amyloid peptide deposition but also induce neuroinflammation in AD brain ( | Junguk Hur | |
| 16753239 | amyloid | amyloid | 1.0 | (2000) 2000 demonstrated that conditioned media from _amp_#x3b2 -amyloid treated primary mouse microglia was toxic to mouse cortical neurons | Junguk Hur | |
| 16753239 | amyloid | amyloid | 1.0 | However troglitazone treatment of microglia suppressed _amp_#x3b2 -amyloid mediated neuron cell death | Junguk Hur | |
| 16753239 | amyloid | amyloid | 1.0 | PPAR-_amp_#x3b3 agonists including TZDs 15d-PGJ 2 and NSAIDS blocked _amp_#x3b2 -amyloid induction of neurotoxic molecules by monocytes | Junguk Hur | |
| 16753239 | amyloid | amyloid | 1.0 | 6 months beginning at an age of 10 months when amyloid plaques first develop exhibited decreased glial activation amyloid deposition and | Junguk Hur | |
| 16753239 | amyloid | amyloid | 1.0 | months when amyloid plaques first develop exhibited decreased glial activation amyloid deposition and dystrophic neuritis relative to untreated animals | Junguk Hur | |
| 16753239 | APP | APP | 0.3 | In addition these studies demonstrated that ibuprofen altered APP processing resulting in decreased production of A_amp_#x3b2 42 in vitro | | |
| 16766086 | amyloid | amyloid | 1.0 | demonstrated in studies of hippocampal neurons challenged with neurotoxic beta amyloid (A_amp_#x3b2;) A_amp_#x3b2 peptides ( Inestrosa et al. 2005 | Junguk Hur | |
| 16766086 | APP | APP | 0.3 | 1997 treated 1-year-old Tg2576 mice bearing a mutant form of APP (KM670/671NL) KM670 671NL for 4 months with oral pioglitazone or | | |
| 16766086 | APP | hAPP | 0.3 | Mice overexpressing the hAPP V717I mutation were treated for 7 days with a higher | | |
| 16766086 | APP | APP | 0.3 | ability of inflammatory cyokines to stimulate the expression of the APP processing enzyme BACE1 ( Sastre et al. 2003 | | |
| 16766086 | APP | APP | 0.3 | reported that PPAR_amp_#x3b3 activation can lead to suppression of cellular APP levels through the stimulation of the ubiquitination and subsequent degradation | | |
| 16766086 | APP | APP | 0.3 | through the stimulation of the ubiquitination and subsequent degradation of APP ( d_amp_#x2019 Abramo et al. 2005 | | |
| 16766086 | APP | APP | 0.3 | reduced A_amp_#x3b2 peptide levels and plaque burden observed in pioglitazone-treated APP overexpressing transgenic mice | | |
| 16781706 | amyloid | amyloid | 1.0 | al. 2003 and cannabinoid CB 2 receptor activation blocks _amp_#x3b2 -amyloid induced microglial activation ( Ramirez et al. 2005 | Junguk Hur | |
| 16781706 | amyloid | amyloid | 1.0 | Cannabinoid CB 2 receptor activation blocks _amp_#x3b2 -amyloid induced microglial activation ( Ramirez et al. 2005 | Junguk Hur | |
| 16983747 | amyloid | amyloid | 1.0 | inflammation genetic mutations inappropriate protein aggregates (e.g., e.g. Lewy bodies amyloid plaques and biochemical defects leading to apoptosis such as oxidative | Junguk Hur | |
| 17191135 | amyloid | amyloid | 1.3 | as a novel nutritional approach to reduce oxidative damage and amyloid pathology in AD | Junguk Hur | |
| 17191135 | amyloid | amyloid | 1.3 | It is characterized pathologically by deposition of amyloid B-peptide (AB) AB in senile (neuritic) neuritic plaques and the | Junguk Hur | |
| 17191135 | amyloid | amyloid | 1.3 | intracellular immunoreactive deposits as well as the formation of intracellular amyloid 89 | Junguk Hur | |
| 17191135 | amyloid | amyloid | 1.3 | received considerable attention as it has been demonstrated that the amyloid precursor protein (APP) APP decreases HO activity thus reducing the | Junguk Hur | |
| 17191135 | APP | APP | 0.3 | it has been demonstrated that the amyloid precursor protein (APP) APP decreases HO activity thus reducing the intracellular levels of bilirubin | | |
| 17191135 | amyloid | amyloid | 1.3 | s quality control system becomes overwhelmed conformational changes occur to amyloid polypeptide intermediates generating stable oligomers with an anti-parallel crossed B-pleated | Junguk Hur | |
| 17191135 | amyloid | amyloid | 1.3 | Although it is clear why mutant proteins form amyloid it is harder to rationalize why a wild-type protein adopts | Junguk Hur | |
| 17191135 | amyloid | amyloid | 1.3 | discrepancy suggests that another event likely triggers misfolding in sporadic amyloid disease | Junguk Hur | |
| 17306794 | APP | APP | 0.6 | SOD1-G93A and the Alzheimer's disease double transgenic mouse model APP/PS1 APP PS1 | | |
| 17306794 | amyloid | amyloid | 1.3 | Transgenic mice expressing the human amyloid precursor protein (APP) APP with the Swedish mutation (K670M/N671L) K670M | Junguk Hur | |
| 17306794 | APP | APP | 0.6 | Transgenic mice expressing the human amyloid precursor protein (APP) APP with the Swedish mutation (K670M/N671L) K670M N671L and the human | | |
| 17306794 | APP | APP | 0.6 | mice were crossed to generate mice carrying both transgenes (APP/PS1) APP PS1 | | |
| 17306794 | amyloid | amyloid | 1.3 | The presence of amyloid plaques in APP/PS1 APP PS1 transgenic mice and AD tissues | Junguk Hur | |
| 17306794 | APP | APP | 0.6 | The presence of amyloid plaques in APP/PS1 APP PS1 transgenic mice and AD tissues was confirmed using thioflavine | | |
| 17306794 | APP | APP | 0.6 | APP/PS1 APP PS1 and human AD tissue | | |
| 17306794 | APP | APP | 0.6 | At the age of 9_amp_#xa0 months mice overexpressing both mutant APP and mutant presenilin 1 (APP/PS1) APP PS1 showed numerous thioflavine | | |
| 17306794 | APP | APP | 0.6 | mice overexpressing both mutant APP and mutant presenilin 1 (APP/PS1) APP PS1 showed numerous thioflavine S-positive plaques in the cerebral cortex | | |
| 17306794 | APP | APP | 0.6 | In coincidence with the brain of APP/PS1 APP PS1 mice thioflavine S(+) S plaques were surrounded by CATX-loaded | | |
| 17306794 | APP | APP | 0.6 | mouse and (v) v associated with plaques in the APP/PS1 APP PS1 transgenic mouse and human AD cerebral cortex | | |
| 17306794 | APP | APP | 0.6 | transgenic mouse model SOD1-G93A and around senile plaques of APP/PS1 APP PS1 transgenics and AD patients | | |
| 17306794 | APP | APP | 0.6 | Fig 8._amp_#xa0 CATX expression in APP/PS1 APP PS1 bigenic mice and Alzheimer patients | | |
| 17306794 | APP | APP | 0.6 | (A_amp_#x2013;D) A_amp_#x2013 D APP/PS1 APP PS1 bigenic animals | | |
| 17306794 | amyloid | amyloid | 1.3 | A A_amp_#x2032 Thioflavine and CATX staining of an amyloid plaque in the cerebral cortex of a 9-month-old APP/PS1 APP | Junguk Hur | |
| 17306794 | APP | APP | 0.6 | amyloid plaque in the cerebral cortex of a 9-month-old APP/PS1 APP PS1 bigenic animal | | |
| 17350694 | amyloid | amyloid | 1.0 | discovery of MHC class II antigens in the microglia surrounding amyloid plaques and dystrophic neuritis several inflammatory processes have been described | Junguk Hur | |
| 17569578 | amyloid | amyloid | 1.0 | in response to neurodegeneration and to extracellular deposition of _amp_#x3b2 -amyloid peptides | Junguk Hur | |
| 17569578 | APP | APP | 0.3 | been investigated in animal models of AD that overexpress human APP | | |
| 17569578 | amyloid | amyloid | 1.0 | The finding that PPAR_amp_#x3b3 agonists elicited a reduction in amyloid pathology in animal models of the disease may be the | Junguk Hur | |
| 17569578 | APP | APP | 0.3 | Similarly Heneka et al found that oral pioglitazone treatment of APP transgenic mice reduced BACE1 transcription and expression | | |
| 17569578 | APP | APP | 0.3 | of independent studies found that PPAR_amp_#x3b3 activation regulated both cellular APP levels and A_amp_#x3b2 production by stimulating the ubiquitin-mediated degradation of | | |
| 17569578 | APP | APP | 0.3 | levels and A_amp_#x3b2 production by stimulating the ubiquitin-mediated degradation of APP 45 | | |
| 17569578 | amyloid | amyloid | 1.0 | IDE acts to proteolytically degrade amyloid peptides and has been genetically linked to AD 139 | Junguk Hur | |
| 17574754 | amyloid | amyloid | 1.0 | In addition in a model of amyloid deposition the EP2 receptor similarly promotes an increase in neuronal | Junguk Hur | |
| 17574754 | amyloid | amyloid | 1.0 | receptor signaling in the LPS 17 19 and 20 and amyloid models 13 lends support to this hypothesis | Junguk Hur | |
| 17597167 | amyloid | amyloid | 1.0 | of IL-1 signalling in the brain on the production of amyloid precursor protein (APP) APP was suggested by the finding that | Junguk Hur | |
| 17597167 | APP | APP | 0.3 | the brain on the production of amyloid precursor protein (APP) APP was suggested by the finding that the heterozygotic but not | | |
| 17597167 | APP | APP | 0.3 | the heterozygotic but not homozygotic mice had decreased levels of APP in the cerebellum 12 | | |
| 17597167 | APP | APP | 0.3 | the reciprocal interactions between cytokines IL-1 and IL-6 and APP/_amp_#x3b2;-amyloid APP _amp_#x3b2 -amyloid (A_amp_#x3b2;) A_amp_#x3b2 peptide | | |
| 17597167 | amyloid | amyloid | 1.0 | interactions between cytokines IL-1 and IL-6 and APP/_amp_#x3b2;-amyloid APP _amp_#x3b2 -amyloid (A_amp_#x3b2;) A_amp_#x3b2 peptide | Junguk Hur | |
| 17597167 | APP | APP | 0.3 | Thus the cytokines stimulate synthesis release and metabolism of APP 28 and 29 while the cleavage product A_amp_#x3b2 peptide induces | | |
| 17597167 | amyloid | amyloid | 1.0 | early expression of IL-6 mRNA prior to the appearance of amyloid plaques in mice with overexpression of human APP with the | Junguk Hur | |
| 17597167 | APP | APP | 0.3 | appearance of amyloid plaques in mice with overexpression of human APP with the so called Swedish mutation 31 and gliosis in | | |
| 17901552 | amyloid | amyloid | 1.0 | activity with nonsteroidal anti-inflammatory drugs (NSAIDs) NSAIDs reduces inflammation and amyloid accumulation in murine transgenic models of Familial Alzheimer's disease and | Junguk Hur | |
| 17997855 | amyloid | amyloid | 1.0 | Co-stimulation of microglia with host-derived compounds (_amp_#x003b2;-amyloid, _amp_#x003b2 -amyloid fibronectin advanced glycation end products and bacterial products can lead | Junguk Hur | |
| 17997855 | amyloid | amyloid | 1.0 | Endogenous compounds deposited in the extracellular space (e.g., e.g. _amp_#x003b2 -amyloid 17 entering the brain through the leaky blood-brain barrier (e.g., | Junguk Hur | |
| 18040778 | amyloid | amyloid | 1.0 | or endogenous proteins that have taken on pathological properties e.g. amyloid B peptide (AB) AB in AD and A-synuclein in PD | Junguk Hur | |
| 18464925 | amyloid | amyloid | 1.0 | ibuprofen reduced the neurotoxicity of microglial cells exposed to _amp_#x003b2 -amyloid fibrils 80 | Junguk Hur | |
| 18464925 | amyloid | amyloid | 1.0 | 2216 in an AD animal model the reduction of cerebral amyloid load accompanied by a sustained microglial activation 82 | Junguk Hur | |
| 18464925 | amyloid | amyloid | 1.0 | the ability of PPAR-_amp_#x003b3 agonists to reduced inflammation and the amyloid burden by various mechanisms have found some validation in a | Junguk Hur | |
| 10417811 | amyloid-beta protein | amyloid beta protein | 1.0 | amyloid beta protein precursor|isoenzymes|nerve tissue proteins|superoxide dismutase|phospholipases a|phospholipases a2| | | |
| 17306794 | amyloid-beta protein | amyloid beta protein | 1.0 | amyloid beta protein precursor|nerve tissue proteins|presenilin 1|sod1 g93a protein|superoxide dismutase|cathepsins| | | |