Cited by 119Alzheimer's disease research and treatmentsNeuroinflammation and Neurodegeneration MechanismsNeurological Disease Mechanisms and Treatments

The DOI matches its Crossref record; 43 of the 43 references it cites were found in a registry or an index.

Neuroinflammation‐induced acceleration of amyloid deposition in the APPV717F transgenic mouse

Qiao, Xiaoxi, Cummins, David J., Paul, Steven M.·2001·European Journal of Neuroscience

DOI 10.1046/j.0953-816x.2001.01666.x

Open this paper in CoChat — free account

Abstract

It has been postulated that neuroinflammation plays a critical role in the pathogenesis of Alzheimer's disease (AD). To directly test whether an inflammatory stimulus can accelerate amyloid deposition in vivo, we chronically administered the bacterial endotoxin, lipopolysaccharide (LPS), intracerebroventricularly (i.c.v.) to 2‐month‐old APP V717F+/+ transgenic (TG) mice, which overexpress a mutant human amyloid precursor protein (APP 717V‐F) with or without apolipoprotein E (apoE) for 2 weeks. Two weeks following central LPS administration a striking global reactive astrocytosis with increased GFAP immunoreactivity was found throughout the brains of all LPS‐treated wild‐type and transgenic mice including the contralateral brain hemisphere. Localized microglial activation was also evident from lectin immunostaining adjacent to the cannula track of LPS‐treated mice. Quantification of thioflavine‐S‐positive Aβ deposits revealed a marked acceleration of amyloid deposition in LPS‐treated APP V717F+/+–apoE+/+ mice compared to nontreated or vehicle‐treated APP V717F+/+–apoE+/+ mice (P = 0.005). By contrast, no amyloid deposits were detected by thioflavine‐S staining in LPS or vehicle‐treated apoE‐deficient APP V717F TG mice. Our data suggest that neuroinflammation can accelerate amyloid deposition in the APP V717F+/+ mouse model of AD and that this process requires the expression of apoE.

Integrity signals

Registry

Crossref · 10.1046/j.0953-816x.2001.01666.x

Cites

43 of 43 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Claims the paper makes

This paper’s full text isn’t openly available, so its claims and self-check weren’t run. The registry and citation checks still apply.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Gene Dose of Apolipoprotein E Type 4 Allele and the Risk of Alzheimer's Disease in Late Onset Families
Corder, E. H., Saunders, A. M., Strittmatter, W. J., Schmechel, D. E., Gaskell, P. C., Small, G. W., Roses, A. D., Haines, J. L., & Pericak-Vance, M. A. (1993) · Science · doi:10.1126/science.8346443 · Cited by 9,429
Apolipoprotein E: high-avidity binding to beta-amyloid and increased frequency of type 4 allele in late-onset familial Alzheimer disease.
Strittmatter, W. J., Saunders, A. M., Schmechel, D., Pericak-Vance, M., Enghild, J., Salvesen, G. S., & Roses, A. D. (1993) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.90.5.1977 · Cited by 4,268
Correlative Memory Deficits, Aβ Elevation, and Amyloid Plaques in Transgenic Mice
Hsiao, K., Chapman, P., Nilsen, S., Eckman, C., Harigaya, Y., Younkin, S., Yang, F., & Cole, G. (1996) · Science · doi:10.1126/science.274.5284.99 · Cited by 4,210
Apolipoprotein E: Cholesterol Transport Protein with Expanding Role in Cell Biology
Mahley, R. W. (1988) · Science · doi:10.1126/science.3283935 · Cited by 4,028
Alzheimer-type neuropathology in transgenic mice overexpressing V717F β-amyloid precursor protein
Games, D., Adams, D., Alessandrini, R., Barbour, R., Borthelette, P., Blackwell, C., Carr, T., Clemens, J., Donaldson, T., Gillespie, F., et al. (1995) · Nature · doi:10.1038/373523a0 · Cited by 2,516
Bacterial endotoxin: molecular relationships of structure to activity and function
Rietschel, E., Kirikae, T., Schade, F. U., Mamat, U., Schmidt, G., Loppnow, H., Ulmer, A. J., Zähringer, U., Seydel, U., Padova, F. D., et al. (1994) · The FASEB Journal · doi:10.1096/fasebj.8.2.8119492 · Cited by 1,608
Theory and Practice of Histological Techniques
Warren, B. A. (1996) · Pathology · doi:10.1016/s0031-3025(16)35146-7 · Cited by 1,572
Accelerated Amyloid Deposition in the Brains of Transgenic Mice Coexpressing Mutant Presenilin 1 and Amyloid Precursor Proteins
Borchelt, D. R., Ratovitski, T., van Lare, J., Lee, M. K., Gonzales, V., Jenkins, N. A., Copeland, N. G., Price, D. L., & Sisodia, S. S. (1997) · Neuron · doi:10.1016/s0896-6273(00)80974-5 · Cited by 1,023
Apolipoprotein E isoform-dependent amyloid deposition and neuritic degeneration in a mouse model of Alzheimer's disease
Holtzman, D. M., Bales, K. R., Tenkova, T., Fagan, A. M., Parsadanian, M., Sartorius, L. J., Mackey, B., Olney, J., McKeel, D., Wozniak, D., et al. (2000) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.050004797 · Cited by 937
Self-citation
Reactive microglia in patients with senile dementia of the Alzheimer type are positive for the histocompatibility glycoprotein HLA-DR
McGeer, P. L., Itagaki, S., Tago, H., & McGeer, E. G. (1987) · Neuroscience Letters · doi:10.1016/0304-3940(87)90696-3 · Cited by 836

Show all 43 references

Research works printed but not linked: 2

10.1002/1531-8249(200003)47:3<365::AID-ANA13>3.0.CO;2-G · DOI
Qiao X., 1999, Effects of intracerebroventricular administration of lipopolysaccharide on amyloid deposition in the APPV717F transgenic mouse, Soc. Neurosci. Abstr., 25, 1858

Sorted by citations

Innate immune activation in neurodegenerative disease
Heneka, M. T., Kummer, M. P., & Latz, E. (2014) · Nature Reviews Immunology · doi:10.1038/nri3705 · Cited by 1,437
Microglia in Alzheimer's disease
Sarlus, H., & Heneka, M. T. (2017) · Journal of Clinical Investigation · doi:10.1172/jci90606 · Cited by 911
“In contrast, studies of acute (109) and chronic LPS exposure reported accelerated amyloidosis and increased microglial activation that localized to plaques in LPS-treated brains (112, 113).”
Background
Does neuroinflammation fan the flame in neurodegenerative diseases?
Frank-Cannon, T. C., Alto, L. T., McAlpine, F. E., & Tansey, M. G. (2009) · Molecular Neurodegeneration · doi:10.1186/1750-1326-4-47 · Cited by 751
“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].”
The role of microglia in amyloid clearance from the AD brain
Lee, C. Y. D., & Landreth, G. E. (2010) · Journal of Neural Transmission · doi:10.1007/s00702-010-0433-4 · Cited by 701
“On the other hand, chronic administration of LPS by daily infusion of LPS into the lateral ventricles for 2 weeks in APP mice or weekly injection of LPS intraperitoneally in APPSwe mice resulted in enhanced Ab deposition (Qiao et al. 2001; Sheng et al. 2003).”
Background
Interplay between innate immunity and Alzheimer disease: APOE and TREM2 in the spotlight
Shi, Y., & Holtzman, D. M. (2018) · Nature Reviews Immunology · doi:10.1038/s41577-018-0051-1 · Cited by 595
Janus-faced microglia: beneficial and detrimental consequences of microglial phagocytosis
Sierra, A., Abiega, O., Shahraz, A., & Neumann, H. (2013) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2013.00006 · Cited by 574
“In vivo, LPS administered locally either transiently reduced (Herber et al., 2004), or enhanced (Qiao et al., 2001) Aβ load in mouse models of AD.”
Background
The role of interleukin-1 in neuroinflammation and Alzheimer disease: an evolving perspective
Shaftel, S. S., Griffin, W. S. T., & O'Banion, M. K. (2008) · Journal of Neuroinflammation · doi:10.1186/1742-2094-5-7 · Cited by 565
Extensive innate immune gene activation accompanies brain aging, increasing vulnerability to cognitive decline and neurodegeneration: a microarray study
Cribbs, D. H., Berchtold, N. C., Perreau, V., Coleman, P. D., Rogers, J., Tenner, A. J., & Cotman, C. W. (2012) · Journal of Neuroinflammation · doi:10.1186/1742-2094-9-179 · Cited by 499
“Consistent with the idea that activation of the immune system in the brain is harmful, the majority of recent studies in transgenic mouse models of AD support the notion that immune activation can precipitate the onset of AD-like pathology [5-10] (but see [11-13]).”
Background
Microglial Phagocytosis Induced by Fibrillar β-Amyloid and IgGs Are Differentially Regulated by Proinflammatory Cytokines
Koenigsknecht-Talboo, J., & Landreth, G. E. (2005) · The Journal of Neuroscience · doi:10.1523/jneurosci.1808-05.2005 · Cited by 477
“Moreover, LPS treatment has been demonstrated to increase neuroinflammation and accelerate fA deposition in animal models of AD attributable to microglial cytokine production (Qiao et al., 2001).”
Background
The neuroinflammatory hypothesis of delirium
Cerejeira, J., Firmino, H., Vaz‐Serra, A., & Mukaetova‐Ladinska, E. B. (2010) · Acta Neuropathologica · doi:10.1007/s00401-010-0674-1 · Cited by 494
Lipopolysaccharide-induced-neuroinflammation increases intracellular accumulation of amyloid precursor protein and amyloid β peptide in APPswe transgenic mice
Sheng, J. (2003) · Neurobiology of Disease · doi:10.1016/s0969-9961(03)00069-x · Cited by 388
TLR4 Cross-Talk With NLRP3 Inflammasome and Complement Signaling Pathways in Alzheimer's Disease
Yang, J., Wise, L., & Fukuchi, K.-I. (2020) · Frontiers in Immunology · doi:10.3389/fimmu.2020.00724 · Cited by 387
Review: Systemic inflammation andAlzheimer's disease
Holmes, C. (2013) · Neuropathology and Applied Neurobiology · doi:10.1111/j.1365-2990.2012.01307.x · Cited by 356
Immunology and immunotherapy of Alzheimer's disease
Weiner, H. L., & Frenkel, D. (2006) · Nature Reviews Immunology · doi:10.1038/nri1843 · Cited by 335
“; indeed, other investigators have reported increased amyloid-β levels in response to LP”
Background
The Impact of Systemic Inflammation on Alzheimer’s Disease Pathology
Xie, J., Van Hoecke, L., & Vandenbroucke, R. E. (2022) · Frontiers in Immunology · doi:10.3389/fimmu.2021.796867 · Cited by 324
“Studies in Tg2576 (43), PDAPP (44), APPSwe (45), APP/PS1 (40, 46) and App (47) mice show an increase in Ab deposition upon LPS-induced systemic inflammation.”
Background
Inhibition of soluble TNF signaling in a mouse model of Alzheimer's disease prevents pre-plaque amyloid-associated neuropathology
McAlpine, F. E., Lee, J., Harms, A. S., Ruhn, K. A., Blurton-Jones, M. M., Hong, J. J., Das, P., Golde, T. E., LaFerla, F. M., Oddo, S., et al. (2009) · Neurobiology of Disease · doi:10.1016/j.nbd.2009.01.006 · Cited by 274
Bone-marrow-derived cells contribute to the recruitment of microglial cells in response to β-amyloid deposition in APP/PS1 double transgenic Alzheimer mice
Malm, T. M., Koistinaho, M., Pärepalo, M., Vatanen, T., Ooka, A., Karlsson, S., & Koistinaho, J. (2005) · Neurobiology of Disease · doi:10.1016/j.nbd.2004.09.009 · Cited by 301
The roles of TNF in brain dysfunction and disease
Clark, I. A., Alleva, L. M., & Vissel, B. (2010) · Pharmacology & Therapeutics · doi:10.1016/j.pharmthera.2010.08.007 · Cited by 239
Intracranially Administered Anti-Αβ Antibodies Reduce β-Amyloid Deposition by Mechanisms Both Independent of and Associated with Microglial Activation
Wilcock, D. M., DiCarlo, G., Henderson, D., Jackson, J., Clarke, K., Ugen, K. E., Gordon, M. N., & Morgan, D. (2003) · The Journal of Neuroscience · doi:10.1523/jneurosci.23-09-03745.2003 · Cited by 232
Neuroprotective and neurotoxic properties of glial cells in the pathogenesis of Alzheimer's disease
Farfara, D., Lifshitz, V., & Frenkel, D. (2008) · Journal of Cellular and Molecular Medicine · doi:10.1111/j.1582-4934.2008.00314.x · Cited by 216
“In these studies, LPS was given intravenously [155], intracerebroventricularly [156] or intraperitoneally [157].”
Method
Tumor necrosis factor-α synthesis inhibitor 3,6′-dithiothalidomide attenuates markers of inflammation, Alzheimer pathology and behavioral deficits in animal models of neuroinflammation and Alzheimer’s disease
Tweedie, D., Ferguson, R. A., Fishman, K., Frankola, K. A., van Praag, H., Holloway, H. W., Luo, W., Li, Y., Caracciolo, L., Russo, I., et al. (2012) · Journal of Neuroinflammation · doi:10.1186/1742-2094-9-106 · Cited by 208
“Its administration into the lateral ventricle of mice has been widely used to model neuroinflammation and induce these ADrelated impairments [32,70-72], which in the present study resulted in the activation of microglia and neuronal degeneration within the DG, accompanied by a learning impairment in the Morris Water M…”
Systemic injection of LPS induces region-specific neuroinflammation and mitochondrial dysfunction in normal mouse brain
Noh, H., Jeon, J., & Seo, H. (2014) · Neurochemistry International · doi:10.1016/j.neuint.2014.02.008 · Cited by 216
Toll-Like Receptor 2 Signaling in Response to Brain Injury: An Innate Bridge to Neuroinflammation
Babcock, A. A., Wirenfeldt, M., Holm, T. H., Nielsen, H. H., Dissing‐Olesen, L., Toft‐Hansen, H., Millward, J. M., Landmann, R. M., Rivest, S., Finsen, B. R., et al. (2006) · Journal of Neuroscience · doi:10.1523/jneurosci.4937-05.2006 · Cited by 188
“, 2005), although contradictory results were obtained in younger mice (Qiao et al., 2001).”
Result
Dynamic Complexity of the Microglial Activation Response in Transgenic Models of Amyloid Deposition: Implications for Alzheimer Therapeutics
Morgan, D., Gordon, M. N., Tan, J., Wilcock, D. M., & Rojiani, A. M. (2005) · Journal of Neuropathology & Experimental Neurology · doi:10.1097/01.jnen.0000178444.33972.e0 · Cited by 176
“Manipulations of Microglial Activation in Transgenic Mice Publication Manipulation Effects DiCarlo et al (32) Herber et al (33) Acute LPS ICI Cleared diffuse Ab, not Congo red, activated microglia Quinn et al (35) Acute LPS IP Cleared Ab; increased IL-1, IL-1ra, RANTES, decreased IL-12 Malm et al (36) Acute LPS ICI Cl…”
Background
3-Hydroxy-3-Methylglutaryl-Coenzyme A Reductase Inhibitors Attenuate β-Amyloid-Induced Microglial Inflammatory Responses
Cordle, A. C., & Landreth, G. E. (2005) · Journal of Neuroscience · doi:10.1523/jneurosci.2544-04.2005 · Cited by 177
The Role of Peroxisome Proliferator-Activated Receptor-γ (PPARγ) in Alzheimer’s Disease
Jiang, Q., Heneka, M. T., & Landreth, G. E. (2008) · CNS Drugs · doi:10.2165/00023210-200822010-00001 · Cited by 176
“[76] reported that lipopolysaccharide accelerated matory cytokines.”
A dual role for apolipoprotein e in neuroinflammation: anti- and pro-inflammatory activity
Guo, L., LaDu, M. J., & Van Eldik, L. J. (2004) · Journal of Molecular Neuroscience · doi:10.1385/jmn:23:3:205 · Cited by 175
“In addition, neuroinflammation was found to accelerate amyloid deposition in APP transgenic mice, a process that required apoE expression (Qiao et al., 2001).”
Background
Role of CD40 ligand in amyloidosis in transgenic Alzheimer's mice
Tan, J., Town, T., Crawford, F., Mori, T., DelleDonne, A., Crescentini, R., Obregon, D., Flavell, R. A., & Mullan, M. J. (2002) · Nature Neuroscience · doi:10.1038/nn968 · Cited by 217
“However, chronic administration of lipopolysaccharide results in a strong increase in Aβ/β-amyloid pathology in Tg APP sw mice, suggesting that chronic microglial activation contributes to Aβ/β-amyloid patholog”
Background
Chronic Inflammation and Amyloidogenesis in Alzheimer's Disease -- Role of Spirochetes1
Miklossy, J. (2008) · Journal of Alzheimer s Disease · doi:10.3233/jad-2008-13404 · Cited by 168
“LPS induced acceleration of amyloid deposition in LPS-treated APPV717F transgenic mice was also reported [80].”
Induction of Toll-Like Receptor 9 Signaling as a Method for Ameliorating Alzheimer's Disease-Related Pathology
Scholtzova, H., Kascsak, R. J., Bates, K. A., Boutajangout, A., Kerr, D. J., Meeker, H. C., Mehta, P. D., Spinner, D. S., & Wisniewski, T. (2009) · The Journal of Neuroscience · doi:10.1523/jneurosci.5715-08.2009 · Cited by 166
“…which large doses of the LPS were administer to mice intraperitoneally, however reported deleterious effects, including the exacerbation of amyloid deposition and cognitive declines and/or increased neuroinflammation and neuronal death (Qiao et al., 2001; Cunningham et al., 2005; Lee et al., 2008).”
Background
Apolipoprotein E4 enhances brain inflammation by modulation of the NF-κB signaling cascade
Ophir, G., Amariglio, N., Jacob‐Hirsch, J., Elkon, R., Rechavi, G., & Michaelson, D. M. (2005) · Neurobiology of Disease · doi:10.1016/j.nbd.2005.05.002 · Cited by 167
Alzheimer's disease β‐secretase BACE1 is not a neuron‐specific enzyme
Roßner, S., Lange‐Dohna, C., Zeitschel, U., & Perez-Polo, J. R. (2004) · Journal of Neurochemistry · doi:10.1111/j.1471-4159.2004.02857.x · Cited by 174
“…a single intrahippocampal lipopolysaccharide (LPS) injection fails to increase the b-amyloid load in APP/presenilin-1 transgenic mice (DiCarlo et al. 2001), but the chronic intracerebroventricular infusion of LPS accelerates b-amyloid deposition in APPV717F transgenic mice (Qiao et al. 2001).”
Background
Clearance of Amyloid-β Peptides By Microglia and Macrophages: the Issue of What, When and Where
Lai, A. Y., & McLaurin, J. (2012) · Future Neurology · doi:10.2217/fnl.12.6 · Cited by 166
Apolipoprotein E and Alzheimer's disease
Troutwine, B., Hamid, L., Lysaker, C. R., Strope, T. A., & Wilkins, H. (2021) · Acta Pharmaceutica Sinica B · doi:10.1016/j.apsb.2021.10.002 · Cited by 179
Astrocytic expression of the Alzheimer's disease β‐secretase (BACE1) is stimulus‐dependent
Hartlage‐Rübsamen, M., Zeitschel, U., Apelt, J., Gärtner, U., Franke, H., Stahl, T., Günther, A., Schliebs, R., Penkowa, M., Bigl, V., et al. (2002) · Glia · doi:10.1002/glia.10178 · Cited by 160
“…with the observation that a single intrahippocampal LPS injection failed to increase -amyloid load in APP/presenilin-1 transgenic mice (DiCarlo et al., 2001), but chronic intracerebroventricular infusion of LPS accelerated -amyloid deposition in APPV717F transgenic mice (Qiao et al., 2001).”
Background
The Important Interface Between Apolipoprotein E and Neuroinflammation in Alzheimer’s Disease
Kloske, C. M., & Wilcock, D. M. (2020) · Frontiers in Immunology · doi:10.3389/fimmu.2020.00754 · Cited by 152
“In one study, APP mice with and without ApoE were chronically administered LPS and it was found that in the presence of ApoE, the mice had increased gliosis and Aβ deposition suggesting a role for ApoE to increase inflammation in AD models (104).”
Background
Intracellular Aβ-oligomers and early inflammation in a model of Alzheimer's disease
Ferretti, M. T., Bruno, M. A., Ducatenzeiler, A., Klein, W. L., & Cuello, A. C. (2011) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2011.01.007 · Cited by 151
Oxidative stress and neuroinflammation in Alzheimer's disease and amyotrophic lateral sclerosis: Common links and potential therapeutic targets
Mhatre, M., Floyd, R. A., & Hensley, K. (2004) · Journal of Alzheimer s Disease · doi:10.3233/jad-2004-6206 · Cited by 148
Time-dependent reduction in Aβ levels after intracranial LPS administration in APP transgenic mice
Herber, D. L., Roth, L. M., Wilson, D. H., Wilson, N., Mason, J. E., Morgan, D., & Gordon, M. N. (2004) · Experimental Neurology · doi:10.1016/j.expneurol.2004.07.007 · Cited by 151
Microglial Activation is Required for Aβ Clearance After Intracranial Injection of Lipopolysaccharide in APP Transgenic Mice
Herber, D. L., Mercer, M., Roth, L. M., Symmonds, K., Maloney, J. L., Wilson, N., Freeman, M. J., Morgan, D., & Gordon, M. N. (2007) · Journal of Neuroimmune Pharmacology · doi:10.1007/s11481-007-9069-z · Cited by 143
“In opposition to our results, administration of LPS has been reported by some investigators to increase APP and Aβ levels in young mice at ages prior to extracellular amyloid deposition (Qiao et al. 2001; Sly et al. 2001; Sheng et al. 2003).”
BackgroundResult
Inflammation occurs early during the Aβ deposition process in TgCRND8 mice
Dudal, S., Krzywkowski, P., Paquette, J., Morissette, C., Lacombe, D., Tremblay, P., & Gervais, F. (2004) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2003.08.008 · Cited by 138
“The inflammatory microenvironment may also provide further driving conditions to favor the formation of densely compacted senile plaques [1,3,45,51].”
Background
Inflammatory changes are tightly associated with neurodegeneration in the brain and spinal cord of the APP/PS1KI mouse model of Alzheimer's disease
Wirths, O., Breyhan, H., Marcello, A., Côtel, M.-C., Brück, W., & Bayer, T. A. (2008) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2008.06.011 · Cited by 140
Inflammasomes as therapeutic targets for A lzheimer's disease
White, C., Lawrence, C. B., Brough, D., & Rivers‐Auty, J. (2016) · Brain Pathology · doi:10.1111/bpa.12478 · Cited by 136
“This is supported by research demonstrating that chronic inflammation induced by head trauma (26, 67), infection (44), obesity (77, 97) or bacterial toxins (121, 126) accelerates amyloid deposition and memory deficits (112) (Figure 1).”
Background
Involvement of inflammation in Alzheimer’s disease pathogenesis and therapeutic potential of anti-inflammatory agents
Shadfar, S., Hwang, C. J., Lim, M., Choi, D., & Hong, J. T. (2015) · Archives of Pharmacal Research · doi:10.1007/s12272-015-0648-x · Cited by 136
“Another study demonstrated detrimental effects of activated microglia in AD (Qiao et al. 2001).”
Background
Microglia in Alzheimer’s disease: A multifaceted relationship
ElAli, A., & Rivest, S. (2016) · Brain, Behavior, and Immunity · doi:10.1016/j.bbi.2015.07.021 · Cited by 134
“For instance, the chronic intracerebroventricular administration of LPS (10 µg/µl in PBS, daily for 2 weeks) significantly accelerated the deposition of cerebral Aβ, concomitantly with a marked microglial cell activation in APP(V717F) mice (Qiao et al., 2001).”
Background
Anti-TLR2 antibody triggers oxidative phosphorylation in microglia and increases phagocytosis of β-amyloid
Rubio‐Araiz, A., Finucane, O. M., Keogh, S., & Lynch, M. A. (2018) · Journal of Neuroinflammation · doi:10.1186/s12974-018-1281-7 · Cited by 117
Osteoarthritis accelerates and exacerbates Alzheimer's disease pathology in mice
Kyrkanides, S., Tallents, R. H., Miller, J. H., Olschowka, M. E., Johnson, R. E., Yang, M., Olschowka, J. A., Brouxhon, S. M., & O’Banion, M. K. (2011) · Journal of Neuroinflammation · doi:10.1186/1742-2094-8-112 · Cited by 116
“In contrast, LPS administration to AD mouse models has given mixed results, with some investigators reporting exacerbation [12-14] and others improvement of pathology due to an inflammationinduced phagocytic activity [15-17].”
Result
A Review of the Brain-Gut-Microbiome Axis and the Potential Role of Microbiota in Alzheimer’s Disease
Sun, M., Ma, K., Wen, J., Wang, G., Zhang, C., Li, Q., Bao, X., & Wang, H. (2020) · Journal of Alzheimer’s Disease · doi:10.3233/jad-190872 · Cited by 113
Apolipoprotein E, Amyloid, and Alzheimer Disease
Bales, K. R. (2002) · Molecular Interventions · doi:10.1124/mi.2.6.363 · Cited by 114
Atorvastatin attenuates the production of IL-1β, IL-6, and TNF-α in the hippocampus of an amyloid β1-42-induced rat model of Alzheimer’s disease
Li, X.-H., Li, X.-H., Zhang, Y.-Y., Wang, M., & Wang, D. (2013) · Clinical Interventions in Aging · doi:10.2147/cia.s40405 · Cited by 108
Deletion of CD14 Attenuates Alzheimer's Disease Pathology by Influencing the Brain's Inflammatory Milieu
Reed-Geaghan, E. G., Reed, Q. W., Cramer, P. E., & Landreth, G. E. (2010) · Journal of Neuroscience · doi:10.1523/jneurosci.2637-10.2010 · Cited by 106
“, 2009) or injected into the brain (Qiao et al., 2001), induced intraneuronal A deposition and accelerated/enhanced plaque deposition, supporting the view that chronic microglial activation contributes to disease progression and severity and alters the kinetics of plaque deposition.”
Background
Microglia in Alzheimer's Disease: It's All About Context
Weitz, T. M., & Town, T. (2012) · International Journal of Alzheimer's Disease · doi:10.1155/2012/314185 · Cited by 95
Ibuprofen Suppresses Interleukin-1β Induction of Pro-Amyloidogenic α1-Antichymotrypsin to Ameliorate β-Amyloid (Aβ) Pathology in Alzheimer's Models
Morihara, T., Teter, B., Yang, F., Lim, G. P., Boudinot, S. G., Boudinot, F. D., Frautschy, S. A., & Cole, G. M. (2005) · Neuropsychopharmacology · doi:10.1038/sj.npp.1300668 · Cited by 96
“Chronic proinflammatory LPS injection into APP Tg apoE wild-type mice has been reported to induce extensive GFAP-positive astrocytes and to accelerate amyloidosis, while LPS failed to increase amyloid deposition in APP Tg apoE-knockout mice (Qiao et al, 2001).”
Background
Loss of tau rescues inflammation-mediated neurodegeneration
Maphis, N., Xu, G., Kokiko-Cochran, O. N., Cardona, A. E., Ransohoff, R. M., Lamb, B. T., & Bhaskar, K. (2015) · Frontiers in Neuroscience · doi:10.3389/fnins.2015.00196 · Cited by 91
“…evidence for alterations in inflammatory cells/molecules prior to the development of brain pathologies in several different mouse models of AD (Qiao et al., 2001; Li et al., 2003; Dudal et al., 2004; Kitazawa et al., 2005; Frontiers in Neuroscience | www.frontiersin.org 8 June 2015 | Volume 9…”
Background
Microglial response to LPS increases in wild-type mice during aging but diminishes in an Alzheimer's mouse model: Implication of TLR4 signaling in disease progression
Go, M., Kou, J., Lim, J.-E., Yang, J., & Fukuchi, K.-I. (2016) · Biochemical and Biophysical Research Communications · doi:10.1016/j.bbrc.2016.09.073 · Cited by 89
“Previous studies reported that LPS injection prematurely induced thioflavin-positive Ab deposition [14] or accumulation of intracellular Ab and C-terminal APP fragments [15,16] in AD mouse models.”
Cognitive impairment in PDAPP mice depends on ApoE and ACT-catalyzed amyloid formation
Nilsson, L. N. G., Arendash, G. W., Leighty, R. E., Costa, D. A., Low, M. A., Garcia, M. F., Cracciolo, J. R., Rojiani, A. M., Wu, X., Bales, K. R., et al. (2004) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2003.12.011 · Cited by 88
“Thus, the present findings provide an explanation for the involvement of inflammation and the prophylactic benefit of NSAIDs in AD [2,37,44,53] and point to novel targets for anti-inflammatory therapy.”
BackgroundSelf-citation
Apolipoprotein E: Essential Catalyst of the Alzheimer Amyloid Cascade
Potter, H., & Wısnıewskı, T. (2012) · International Journal of Alzheimer s Disease · doi:10.1155/2012/489428 · Cited by 84
Inflammation and cerebral amyloidosis are disconnected in an animal model of Alzheimer's disease
Quinn, J. (2003) · Journal of Neuroimmunology · doi:10.1016/s0165-5728(03)00037-7 · Cited by 102
“The trend to lower levels of beta amyloid plaque after systemic LPS is counter to the hypothesis that inflammatory events promote Alzheimer’s disease and contrasts with a report that chronic intraventricular LPS promotes beta amyloid pathology (Qiao et al., 2001) in a similar transgenic mouse model of AD.”
Result
Inflammatory Signaling Pathways Regulating ApoE Gene Expression in Macrophages
Gafencu, A. V., Robciuc, M. R., Fuior, E. V., Zannis, V. I., Kardassis, D., & Simionescu, M. (2007) · Journal of Biological Chemistry · doi:10.1074/jbc.m611422200 · Cited by 80
Loss of Interleukin Receptor-Associated Kinase 4 Signaling Suppresses Amyloid Pathology and Alters Microglial Phenotype in a Mouse Model of Alzheimer's Disease
Cameron, B., Tse, W., Lamb, R., Li, X., Lamb, B. T., & Landreth, G. E. (2012) · Journal of Neuroscience · doi:10.1523/jneurosci.1729-12.2012 · Cited by 76
“, 2001); however, sustained TLR4 activation resulted in increased amyloid deposition (Qiao et al., 2001; Sheng et al., 2003).”
Background
Lipolysaccharide-Induced Neuroinflammation Is Associated with Alzheimer-Like Amyloidogenic Axonal Pathology and Dendritic Degeneration in Rats
Deng, X., Li, M., Ai, W., He, L., Lu, D., Patrylo, P. R., Cai, H., Luo, X., Li, Z., & Yan, X. (2014) · Advances in Alzheimer s Disease · doi:10.4236/aad.2014.32009 · Cited by 73
“In transgenic models of AD, LPS administration is shown to increase APP and Aβ immunoreactivity in neuronal somata [65], elevate γ-secretase activity [66] and accelerate plaque deposition [67].”
Background
Neuroinflammation in Alzheimer’s disease: Pleiotropic roles for cytokines and neuronal pentraxins
Swanson, A., Wolf, T., Sitzmann, A., & Willette, A. A. (2018) · Behavioural Brain Research · doi:10.1016/j.bbr.2018.02.015 · Cited by 72
Accelerated accumulation of N‐ and C‐terminal βAPP fragments and delayed recovery of microtubule‐associated protein 1B expression following stroke in aged rats
Badan, I., Dinca, I., Buchhold, B., Suofu, Y., Walker, L. C., Gratz, M., Platt, D., Kessler, C., & Popa‐Wagner, A. (2004) · European Journal of Neuroscience · doi:10.1111/j.0953-816x.2004.03323.x · Cited by 70
Caffeic acid phenethyl ester (CAPE) prevents inflammatory stress in organotypic hippocampal slice cultures
Montpied, P., de Bock, F., Rondouin, G., Niel, G., Briant, L., Courseau, A.-S., Lerner‐Natoli, M., & Bockaert, J. (2003) · Molecular Brain Research · doi:10.1016/s0169-328x(03)00178-5 · Cited by 68
The amyloid hypothesis: let sleeping dogmas lie?
Bishop, G. M., & Robinson, S. R. (2002) · Neurobiology of Aging · doi:10.1016/s0197-4580(02)00050-7 · Cited by 67
“[28] Qiao X, Cummins DJ, Paul SM.”
Background
Protective properties of lysozyme on β-amyloid pathology: implications for Alzheimer disease
Helmfors, L., Boman, A., Civitelli, L., Nath, S., Sandin, L., Janefjord, C., McCann, H., Zetterberg, H., Blennow, K., Halliday, G. M., et al. (2015) · Neurobiology of Disease · doi:10.1016/j.nbd.2015.08.024 · Cited by 62
“Several reports from transgenic mice studies indicated that immune activation might prime the brain for Alzheimer disease pathology, such as Aβ plaques and tau aggregation (Qiao et al., 2001; Sheng et al., 2003; Kitazawa et al., 2005 ).”
Sustained Trem2 stabilization accelerates microglia heterogeneity and Aβ pathology in a mouse model of Alzheimer’s disease
Dhandapani, R., Neri, M., Bernhard, M., Brzak, I., Schweizer, T., Rudin, S., Joller, S., Berth, R., Kernen, J., Neuhaus, A., et al. (2022) · Cell Reports · doi:10.1016/j.celrep.2022.110883 · Cited by 60
Review: Experimental manipulations of microglia in mouse models of Alzheimer's pathology: activation reduces amyloid but hastens tau pathology
Lee, D. C., Rizer, J., Hunt, J. B., Selenica, M. ‐. B., Gordon, M. N., & Morgan, D. (2013) · Neuropathology and Applied Neurobiology · doi:10.1111/nan.12002 · Cited by 57
Perispinal etanercept for neuroinflammatory disorders
Tobinick, E. L. (2008) · Drug Discovery Today · doi:10.1016/j.drudis.2008.10.005 · Cited by 56
Enduring Changes in Neuronal Function upon Systemic Inflammation Are NLRP3 Inflammasome Dependent
Beyer, M. M. S., Lonnemann, N., Remus, A., Latz, E., Heneka, M. T., & Korte, M. (2020) · The Journal of Neuroscience · doi:10.1523/jneurosci.0200-20.2020 · Cited by 55
RETRACTED: Multiple inflammatory pathways are involved in the development and progression of cognitive deficits in APPswe/PS1dE9 mice
Zhang, W., Bai, M., Ye, X., Hao, J., Zhang, Z., Su, C., Lei, G., Miao, J., & Li, Z. (2012) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2011.12.023 · Cited by 53
“, 2008), but their enefit for clearing A is thought to be much limited, ecause mounting evidence indicates that activated glial ells as well as their released proinflammatory mediators ay exacerbate AD-associated pathology (Kitazawa et al., 005; Qiao et al., 2001; Sheng et al., 2003).”
Background
Retracted
Photobiomodulation using a low-level light-emitting diode improves cognitive dysfunction in the 5XFAD mouse model of Alzheimer’s disease
Cho, G. M., Lee, S., Park, J. H., Kim, M. J., Park, K.-J., Choi, B. T., Shin, Y., Kim, N. G., & Shin, H. K. (2018) · The Journals of Gerontology Series A · doi:10.1093/gerona/gly240 · Cited by 53
Microglial TLR4/NLRP3 Inflammasome Signaling in Alzheimer’s Disease
Li, Y., Chen, X., Zhou, M., Feng, S., Peng, X., & Wang, Y. (2023) · Journal of Alzheimer s Disease · doi:10.3233/jad-230273 · Cited by 58
Melatonin attenuated mediators of neuroinflammation and alpha-7 nicotinic acetylcholine receptor mRNA expression in lipopolysaccharide (LPS) stimulated rat astrocytoma cells, C6
Niranjan, R., Nath, C., & Shukla, R. (2012) · Free Radical Research · doi:10.3109/10715762.2012.697626 · Cited by 46
“A transgenic model of AD further emphasized that LPS increases the amyloid beta protein deposition [25].”
Background
The value and limitations of transgenic mouse models used in drug discovery for Alzheimer's disease: an update
Bales, K. R. (2012) · Expert Opinion on Drug Discovery · doi:10.1517/17460441.2012.666234 · Cited by 46
“However, microglia may also produce detrimental pro-inflammatory cytokines that impede efficient Ab clearance, promote tau phosphorylation, neuronal injury and cognitive impairment [94-96].”
Background
Infectivity of amyloid diseases
Sigurdsson, E. M., Wisniewski, T., & Frangione, B. (2002) · Trends in Molecular Medicine · doi:10.1016/s1471-4914(02)02403-6 · Cited by 43
Early intervention attenuates synaptic plasticity impairment and neuroinflammation in 5xFAD mice
Li, K., Wang, X., Jiang, Y., Zhang, X., Liu, Z., Yin, T., & Yang, Z. R. (2021) · Journal of Psychiatric Research · doi:10.1016/j.jpsychires.2021.02.007 · Cited by 45
Neuronal ApoE4 in Alzheimer’s disease and potential therapeutic targets
Zhang, L., Xia, Y., & Gui, Y. (2023) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2023.1199434 · Cited by 41
“Microglia that knock down TLR2 and TLR4 also show a reduced inflammatory response to Aβ (Bales et al., 2000; Qiao et al., 2001).”
Background
Modeling Alzheimer’s Disease in Mouse without Mutant Protein Overexpression: Cooperative and Independent Effects of Aβ and Tau
Guo, Q., Li, H., Cole, A. L., Hur, J., Li, Y., & Zheng, H. (2013) · PLoS ONE · doi:10.1371/journal.pone.0080706 · Cited by 41
“For example, it is well-accepted that neuroinflammation plays an important role in human AD pathogenesis for both Aβ pathology and tau hyperphosphorylation [27-31], which is also supported by mouse model studies that artificially induce brain inflammation [32-34].”
Background
Compound of icariin, astragalus, and puerarin mitigates iron overload in the cerebral cortex of Alzheimer's disease mice
Chai, X.-Q., Zhang, Y., & Kong, W.-N. (2018) · Neural Regeneration Research · doi:10.4103/1673-5374.230302 · Cited by 35
“Moreover, released inflammatory cytokines can disrupt the blood-brain barrier (Blasko et al., 2001; Qiao et al., 2001; Sastre et al., 2003), increasing vascular permeability, and allowing iron to enter and accumulate in the brain .”
Background
Microglia and Cholesterol Handling: Implications for Alzheimer’s Disease
Herrera, O. M. M., & Zivkovic, A. M. (2022) · Biomedicines · doi:10.3390/biomedicines10123105 · Cited by 38
“In murine models chronic LPS activation leads to increased Aβ deposition [96,97].”
Background
Challenges and Future Perspectives in Modeling Neurodegenerative Diseases Using Organ‐on‐a‐Chip Technology
Pramotton, F. M., Spitz, S., & Kamm, R. D. (2024) · Advanced Science · doi:10.1002/advs.202403892 · Cited by 33
The Interplay of Inflammation and Gut-Microbiota Dysbiosis in Alzheimer’s Disease: Mechanisms and Therapeutic Potential
Samat, H. N. A., Razali, N. N., Mahadzir, H., Muhammad, T. S. T., Ling, K., Mansor, N. I., & Abidin, S. Z. (2025) · International Journal of Molecular Sciences · doi:10.3390/ijms26188905 · Cited by 34
What Can Rodent Models Tell Us About Cognitive Decline in Alzheimer's Disease?
Davis, S., & Laroche, S. (2003) · Molecular Neurobiology · doi:10.1385/mn:27:3:249 · Cited by 32
Post-symptomatic NLRP3 inhibition rescues cognitive impairment and mitigates amyloid and tau driven neurodegeneration
Auger, A., Faidi, R., Rickman, A. D., Peña-Martinez, C., Fajfer, A., Carling, J., Hilyard, A., Ali, M., Ono, R., Cleveland, C., et al. (2025) · npj Dementia · doi:10.1038/s44400-025-00011-5 · Cited by 31
Environmental Experience Modulates Ischemia-Induced Amyloidogenesis and Enhances Functional Recovery
Briones, T. L., Rogozinska, M., & Woods, J. (2009) · Journal of Neurotrauma · doi:10.1089/neu.2008.0707 · Cited by 24
“It is believed that the generation of CT-b APP is a pathological event because these fragments can promote synaptic degeneration and neuronal death (Qiao et al., 2001) by increasing the production of A b (Kim et al., 1998).”
Retracted
Organophosphates Induced Alzheimer's Disease: An Epigenetic Aspect
Yadav, S. S., Singh, M. K., & Yadav, R. S. (2016) · Journal of Clinical Epigenetics · Cited by 21
New players in old amyloid precursor protein‐processing pathways
Roßner, S. (2004) · International Journal of Developmental Neuroscience · doi:10.1016/j.ijdevneu.2004.07.004 · Cited by 20
Systemic LPS-induced Aβ-solubilization and clearance in AβPP-transgenic mice is diminished by heparanase overexpression
Jendresen, C., Digre, A., Cui, H., Zhang, X., Vlodavsky, I., Li, J.-P., & Nilsson, L. N. G. (2019) · Scientific Reports · doi:10.1038/s41598-019-40999-4 · Cited by 19
Low levels of amyloid-beta and its transporters in neonatal rats with and without hydrocephalus
Deren, K. E., Forsyth, J., Abdullah, O., Hsu, E. W., Klinge, P. M., Silverberg, G. D., Johanson, C. E., & McAllister, J. P. (2009) · Cerebrospinal Fluid Research · doi:10.1186/1743-8454-6-4 · Cited by 19
“[25], Funato et al[21] and Sasaki et al[53] state that there is a possibility that astrocytes engulf Aβ diffused plaques and attempt to degrade them in lysosomes in the aged brain.”
Background
Is there a molecular logic that sustains neuronal functional integrity and survival? Lipid signaling is necessary for neuroprotective neuronal transcriptional programs
Bazan, N. G. (2014) · Molecular Neurobiology · doi:10.1007/s12035-014-8897-0 · Cited by 15
“Also, the onset of AD is accelerated by neuroinflammation [17, 18] and is enhanced by systemic immune/ inflammatory dysfunctions [19] that trigger early events resembling AD pathology [13, 14].”
Background
Potential Roles of Myeloid Differentiation Factor 2 on Neuroinflammation and Its Possible Interventions
Oo, T. T., Pratchayasakul, W., Chattipakorn, N., & Chattipakorn, S. C. (2020) · Molecular Neurobiology · doi:10.1007/s12035-020-02066-2 · Cited by 15
Apolipoprotein ε in Brain and Retinal Neurodegenerative Diseases
Abyadeh, M., Gupta, V., Paulo, J. A., Sheriff, S., Shadfar, S., Fitzhenry, M. J., Amirkhani, A., Gupta, V. B., Salekdeh, G. H., Haynes, P. A., et al. (2023) · Aging and Disease · doi:10.14336/ad.2023.0312-1 · Cited by 15
Transfer of three transcription factors via a lentiviral vector ameliorates spatial learning and memory impairment in a mouse model of Alzheimer's disease
Chen, P., Yan, Q., Wang, S., Wang, C., & Zhao, P. (2016) · Gene · doi:10.1016/j.gene.2016.04.032 · Cited by 14
Expression of antimicrobial host defence peptides in the central nervous system during health and disease
Smith, K. J., & Findlay, E. G. (2022) · Discovery Immunology · doi:10.1093/discim/kyac003 · Cited by 16
“They reference a study [158] showing intracerebroventricular injection of LPS promoted A β deposition in transgenic mice that overexpress mutated human APP, and suggest this provides evidence that A β can bind pathogens [157].”
Background
Multitarget Effects of Coconut Oil (Virgin Type) on Aβ-Induced Alzheimer’s Disease Animal Model
Mirzaei, F., Khazaei, M., Komaki‬, A., Amiri, I., & Jalili, C. (2019) · Archives of Neuroscience · doi:10.5812/ans.85715 · Cited by 12
Discovery of a New Class of Synthetic Protein Kinase Inhibitors that Suppress Selective Aspects of Glial Activation and Protect Against β-Amyloid Induced Injury: A Foundation for Future Medicinal Chemistry Efforts Focused on Targeting Alzheimer's Disease Progression
Watterson, D. M., Velentza, A. V., Zasadzki, M., Craft, J. M., Haiech, J., & Eldik, L. J. V. (2003) · Journal of Molecular Neuroscience · doi:10.1385/jmn:20:3:411 · Cited by 12
“For example, various models of chronic neuroinflammation result in accelerated amyloid deposition, selective neuronal injury of degeneration, and behavioral abnormalities (see, e.g., Qiao et al., 2001; Hauss-Wegrzyniak and Wenk, 2002; Hauss-Wegrzyniak et al., 2002; Popovich et al., 2002).”
Background
From the Bush to the Brain: Preclinical Stages of Ethnobotanical Anti-Inflammatory and Neuroprotective Drug Discovery—An Australian Example
Kumar, P., Mathew, S., Gamage, R. V., Bodkin, F., Doyle, K., Rosetti, I., Wagnon, I. M., Zhou, X., Raju, R., Gyengési, E., et al. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms241311086 · Cited by 12
Recruiting the innate immune system with GM-CSF to fight viral diseases, including West Nile Virus encephalitis and COVID-19
Potter, H., Boyd, T. D., Clarke, P., Pelak, V. S., & Tyler, K. L. (2020) · F1000Research · doi:10.12688/f1000research.23729.1 · Cited by 11
Lipopolysaccharide stimulates the secretion of the amyloid precursor protein via a protein kinase C-mediated pathway
Small, C. I., Lyles, G. A., & Breen, K. C. (2005) · Neurobiology of Disease · doi:10.1016/j.nbd.2005.01.013 · Cited by 10

Authors: Qiao, X., Cummins, D. J., & Paul, S. M.
Affiliations: Louisiana State University (US)
Eli Lilly (United States) (US)
Corresponding author: Paul, Steven M.
ORCID: Qiao, Xiaoxi
Paul, Steven M.
Venue: European Journal of Neuroscience
Publisher: Wiley
Published: 2001-08
Volume: 14
Issue: 3
Pages: 474-482
ISSN: 0953-816X (ISSN-L)
1460-9568
DOI: 10.1046/j.0953-816x.2001.01666.x
OpenAlex: W2048400917
Cited by: 119
References: 43
Citations by year: 2026: 2 · 2025: 3 · 2024: 3 · 2023: 5 · 2022: 5 · 2021: 3 · 2020: 7 · 2019: 3 · 2018: 5 · 2017: 1 · 2016: 4 · 2015: 4 · 2014: 5 · 2013: 3 · 2012: 11
FWCI: 4.32
Type: journal article
Language: en
Open access: closed
Licence: onlinelibrary.wiley.com/termsAndConditions#vor (vor, 141 d)
Locations: European Journal of Neuroscience (publishedVersion)
PubMed (publishedVersion)
Topics: Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
Keywords: neuroinflammation, amyloid deposition, Alzheimer's disease, lipopolysaccharide, reactive astrogliosis, microglial activation, apolipoprotein E, amyloid precursor protein, intracerebroventricular administration
MeSH terms: Amyloid, Animals, Apolipoproteins E, Encephalitis, Fluorescent Dyes, Immunohistochemistry, Injections, Intraventricular, Lipopolysaccharides, Male, Mice, Transgenic, Neuroglia, RNA, Messenger, Thiazoles, Amyloid beta-Protein Precursor, Mice, Benzothiazoles

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review

Neuroinflammation‐induced acceleration of amyloid deposition in the APPV717F transgenic mouse

Abstract

Overview

Integrity signals

Verification

Claims the paper makes

Claims other papers make about this one

Citations

Cites

Cited by

Related

Metadata

Record

About these checks