Cited by 501Alzheimer's disease research and treatmentsNeuroinflammation and Neurodegeneration MechanismsDementia and Cognitive Impairment Research

The DOI matches its Crossref record; 54 of the 54 references it cites were found in a registry or an index.

Intrathecal inflammation precedes development of Alzheimer's disease

Open access

Tarkowski, E·2003·Journal of Neurology, Neurosurgery & Psychiatry

DOI 10.1136/jnnp.74.9.1200PMC PMC1738668

Open this paper in CoChat — free account Open PDF

Abstract

OBJECTIVES: To analyse the cerebrospinal fluid (CSF) values of the proinflammatory cytokines, interleukin 1beta (IL1beta), tumour necrosis factor alpha (TNFalpha), GM-CSF, of the anti-inflammatory cytokine TGFbeta, of tau protein, a marker for neurodegeneration, and of beta amyloid (Abeta), a protein involved in the formation of senile plaques, in prospectively followed up patients with mild cognitive impairment (MCI). METHODS: Analyses of CSF levels of TNFalpha, IL1beta, GM-CSF, TGFbeta, betaa, and tau protein were performed using ELISA in 56 patients with MCI who were followed up prospectively and in 25 age matched, healthy controls. RESULTS: Patients with MCI displayed significantly higher levels of TNFalpha and tau protein and significantly lower levels of TGFbeta and Abeta compared with the healthy controls. After nine months of follow up, 25 patients still displayed MCI while the remaining 31 patients had progressed to Alzheimer's disease (AD). Only MCI patients who progressed to AD at follow up, showed significantly higher CSF levels of TNFalpha than controls. In addition, reduced CSF-Abeta42 levels were only found in MCI patients that progressed to AD, further supporting the notion that disturbed metabolism of Abeta is an early finding in AD. CONCLUSIONS: These results demonstrate increased production of the proinflammatory cytokine, TNFalpha and decreased production of the anti-inflammatory cytokine TGFbeta in patients with MCI at risk to develop AD, suggesting a propensity towards inflammation in this patient group and indicating that CNS inflammation is a early hallmark in the pathogenesis of AD.

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

Integrity signals

Registry

Crossref · 10.1136/jnnp.74.9.1200

Cites

54 of 54 references verified0 citation errors · 0 not checkable

Statistics

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

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?

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Diagnostic and Statistical Manual of Mental Disorders
Williams, J. B. W., & First, M. B. (2013) · Oxford University Press eBooks · doi:10.1093/acrefore/9780199975839.013.104 · Cited by 109,845
“Mini-mental state”
Folstein, M. F., Folstein, S. E., & McHugh, P. R. (1975) · Journal of Psychiatric Research · doi:10.1016/0022-3956(75)90026-6 · Cited by 88,282
Clinical diagnosis of Alzheimer's disease: Report of the NINCDS‐ADRDA Work Group* under the auspices of Department of Health and Human Services Task Force on Alzheimer's Disease
McKhann, G., Drachman, D., Folstein, M., Katzman, R., Price, D., & Stadlan, E. M. (1984) · Neurology · doi:10.1212/wnl.34.7.939 · Cited by 27,915
[Japanese version of the Neuropsychiatric Inventory--a scoring system for neuropsychiatric disturbance in dementia patients].
Hirono, N., Mori, E., Ikejiri, Y., Imamura, T., Shimomura, T., Hashimoto, M., Yamashita, H., & Ikeda, M. (1997) · PubMed · Cited by 21,012
Special Care Units and Traditional Care in Dementia: Relationship with Behavior, Cognition, Functional Status and Quality of Life - A Review
Kok, J. S., Berg, I. J., & Scherder, E. J. A. (2013) · Dementia and Geriatric Cognitive Disorders Extra · doi:10.1159/000353441 · Cited by 20,589
Older Adults' Reasons for Using Technology while Aging in Place
Peek, S. T. M., Luijkx, K. G., Rijnaard, M. D., Nieboer, M. E., van der Voort, C. S., Aarts, S., van Hoof, J., Vrijhoef, H. J., & Wouters, E. (2015) · Gerontology · doi:10.1159/000430949 · Cited by 19,852
Sensitivity and False Alarm Rate of a Fall Sensor in Long-Term Fall Detection in the Elderly
Kangas, M., Korpelainen, R., Vikman, I., Nyberg, L., & Jämsä, T. J. (2014) · Gerontology · doi:10.1159/000362720 · Cited by 19,007
Clinical diagnosis of Alzheimer's disease: Report of the NINCDS—ADRDA Work Group under the auspices of Department of Health and Human Services Task Force on Alzheimer's Disease
McKhann, G., Drachman, D., Folstein, M., Katzman, R., Price, D. L., & Stadlan, E. (2011) · Neurology · doi:10.1212/01.wnl.0000400650.92875.cf · Cited by 9,882
Glutamate neurotoxicity and diseases of the nervous system
Choi, D. W. (1988) · Neuron · doi:10.1016/0896-6273(88)90162-6 · Cited by 8,188
Inflammation and Alzheimer’s disease
Akiyama, H. (2000) · Neurobiology of Aging · doi:10.1016/s0197-4580(00)00124-x · Cited by 4,514

Show all 53 references

Research works printed but not linked: 5

Banati RB, Beyreuter K. Alzheimer's disease. In: Kettenman H, Ransom BR, eds. Neuroglia. New York: Oxford University Press, 1995:1027-43.
Tarkowski E, Wallin A, Blennow K, et al. Local production of TNF-α, a potent neuroprotective agent, in Alzheimer disease and vascular dementia. J Clin Immunol 1999;19:223-30.
Tarkowski E, Wallin A, Regland B, et al. Local and systemic cytokine release in patients with Alzheimer disease and vascular dementia. Acta Neurol Scan 2001;103:166-74.
Wallin A, Blennow K, Scheltens PH. Research criteria for clinical diagnosis of "pure" Alzheimer's disease. Drugs of Today 1994;30:265-73.
Holmin S, Mathiesen T. Intracerebral administration of interleukin-1-beta induces neuronal DNA-fragmentation, encephalitis and vasogenic edema. J Neurosurgery 2000;92:108-20.

Sorted by citations

Neuroinflammation in Alzheimer's disease
Heneka, M. T., Carson, M. J., Khoury, J. E., Landreth, G. E., Brosseron, F., Feinstein, D. L., Jacobs, A. H., Wyss-Coray, T., Vitorica, J., Ransohoff, R. M., et al. (2015) · The Lancet Neurology · doi:10.1016/s1474-4422(15)70016-5 · Cited by 6,226
“Some studies highlight elevated CSF cytokines as risk factors for MCI to AD conversion or as correlates of the speed of cognitive decline and disease progression 76,189 .”
Neuroinflammation in neurodegenerative disorders: the roles of microglia and astrocytes
Kwon, H. S., & Koh, S.-H. (2020) · Translational Neurodegeneration · doi:10.1186/s40035-020-00221-2 · Cited by 2,595
Immune attack: the role of inflammation in Alzheimer disease
Heppner, F. L., Ransohoff, R. M., & Becher, B. (2015) · Nature Reviews Neuroscience · doi:10.1038/nrn3880 · Cited by 2,134
Necroptosis and RIPK1-mediated neuroinflammation in CNS diseases
Yuan, J., Amin, P., & Ofengeim, D. (2019) · Nature Reviews Neuroscience · doi:10.1038/s41583-018-0093-1 · Cited by 967
Classification and prediction of clinical Alzheimer's diagnosis based on plasma signaling proteins
Ray, S., Britschgi, M., Herbert, C., Takeda-Uchimura, Y., Boxer, A., Blennow, K., Friedman, L. F., Galasko, D. R., Jutel, M., Karydas, A., et al. (2007) · Nature Medicine · doi:10.1038/nm1653 · Cited by 1,048
Mediterranean Diet and Mild Cognitive Impairment
Scarmeas, N., Stern, Y., Mayeux, R., Manly, J. J., Schupf, N., & Luchsinger, J. A. (2009) · Archives of Neurology · doi:10.1001/archneurol.2008.536 · Cited by 757
Activation of microglia and astrocytes: a roadway to neuroinflammation and Alzheimer’s disease
Kaur, D., Sharma, V., & Deshmukh, R. R. (2019) · Inflammopharmacology · doi:10.1007/s10787-019-00580-x · Cited by 503
Body Fluid Cytokine Levels in Mild Cognitive Impairment and Alzheimer’s Disease: a Comparative Overview
Brosseron, F., Krauthausen, M., Kummer, M., & Heneka, M. T. (2014) · Molecular Neurobiology · doi:10.1007/s12035-014-8657-1 · Cited by 447
“or serum, whereas one study reports downregulation in CSF [3, 19, 32, 51, 52, 63].”
Background
Tumor Necrosis Factor Receptor 1 Is a Negative Regulator of Progenitor Proliferation in Adult Hippocampal Neurogenesis
Iosif, R. E., Ekdahl, C. T., Ahlenius, H., Pronk, C. J., Bonde, S., Kokaia, Z., Jacobsen, S. E. W., & Lindvall, O. (2006) · Journal of Neuroscience · doi:10.1523/jneurosci.2723-06.2006 · Cited by 462
“TNF- is a key player in many pathological processes and is increased in the CSF of patients, e.g., with mild cognitive impairment (Tarkowski et al., 2003b), Alzheimer’s disease and vascular dementia (Tarkowski et al., 2003a), and stroke (Sairanen et al., 2001; Zaremba and Losy, 2001).”
Background
Therapeutic strategies for Alzheimer's disease in clinical trials
Godyń, J., Jończyk, J., Panek, D., & Malawska, B. (2015) · Pharmacological Reports · doi:10.1016/j.pharep.2015.07.006 · Cited by 462
“Abbreviations: ACh, acetylcholine; AD, Alzheimer’s disease; ADAM, disintegrin and metalloproteinase domain; ADAS-cog, Alzheimer’s Disease Assessment Scale-cognitive; ADCS ADL23, Alzheimer’s Disease Cooperative Study – Activities of Daily Living Scale; ADCS-CGIC, Alzheimer’s Disease Cooperative Study – Clinical Global…”
BackgroundInfluential
Role of lutein and zeaxanthin in visual and cognitive function throughout the lifespan
Johnson, E. J. (2014) · Nutrition Reviews · doi:10.1111/nure.12133 · Cited by 444
Glial contributions to neurodegeneration in tauopathies
Leyns, C. E. G., & Holtzman, D. M. (2017) · Molecular Neurodegeneration · doi:10.1186/s13024-017-0192-x · Cited by 409
“TNF-α levels were also found to be elevated in the CSF of AD patients and correlate with disease progression [145, 146].”
Background
Particulate Matter in Polluted Air May Increase Biomarkers of Inflammation in Mouse Brain
Campbell, A., Oldham, M. J., Becaria, A., Bondy, S. C., Meacher, D. M., Sioutas, C., Misra, C., Méndez, L. B., & Kleinman, M. T. (2004) · NeuroToxicology · doi:10.1016/j.neuro.2004.08.003 · Cited by 422
“Furthermore, levels of TNF-a in the cerebrospinal fluid of patients with ‘mild cognitive impairment’, who after nine months progressed to AD, are significantly higher than those of controls (Tarkowski et al., 2003).”
Background
Deletion of tumor necrosis factor death receptor inhibits amyloid β generation and prevents learning and memory deficits in Alzheimer's mice
He, P., Zhong, Z., Lindholm, K., Berning, L., Lee, W., Lemere, C., Staufenbiel, M., Li, R., & Shen, Y. (2007) · The Journal of Cell Biology · doi:10.1083/jcb.200705042 · Cited by 390
Microglia Responses to Pro-inflammatory Stimuli (LPS, IFNγ+TNFα) and Reprogramming by Resolving Cytokines (IL-4, IL-10)
Lively, S. S., & Schlichter, L. C. (2018) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2018.00215 · Cited by 411
“(2) Both cytokines are elevated within the CNS in numerous pathologies and damage models, including stroke, trauma, spinal cord injury, perforant-path axotomy, and in multiple sclerosis (MS) and other neurodegenerative disorders (Benveniste and Benos, 1995; Elliott, 2001; Li et al., 2001; Tarkowski et al., 2003; Yamam…”
Background
RIPK1 mediates a disease-associated microglial response in Alzheimer’s disease
Ofengeim, D., Mazzitelli, S., Ito, Y., DeWitt, J. P., Mifflin, L., Zou, C., Das, S., Adiconis, X., Chen, H., Zhu, H., et al. (2017) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1714175114 · Cited by 395
“In addition, increased levels of TNFα are found in the cerebral spinal fluid (CSF) of patients with mild cognitive impairment (MCI) at risk to develop AD, suggesting that CNS inflammation is an early event during the pathogenesis of AD (8).”
Background
RAGE‐dependent signaling in microglia contributes to neuroinflammation, Aβ accumulation, and impaired learning/memory in a mouse model of Alzheimer's disease
Fang, F., Lue, L.-F., Yan, S., Xu, H., Luddy, J. S., Chen, D., Walker, D. G., Stern, D. M., Yan, S., Schmidt, A. M., et al. (2010) · The FASEB Journal · doi:10.1096/fj.09-139634 · Cited by 335
Intrathecal Chemokine Synthesis in Mild Cognitive Impairment and Alzheimer Disease
Galimberti, D., Schoonenboom, N., Scheltens, P., Fenoglio, C., Bouwman, F., Venturelli, E., Guidi, I., Blankenstein, M. A., Bresolin, N., & Scarpini, E. (2006) · Archives of Neurology · doi:10.1001/archneur.63.4.538 · Cited by 289
“Evaluationofchemokinelevels,combinedwithotherknown CSF markers, including amyloid (1-42), tau, and phosphotau levels(34,35) aswell asotherpossibleneuropsychologicalandneuroimagingtools,(36,37) maybeusefulasearlymarkers in MCI to predict conversion to AD.”
Background
Lipoic acid as a novel treatment for Alzheimer's disease and related dementias
Holmquist, L., Stuchbury, G., Berbaum, K., Muscat, S., Young, S. A., Häger, K., Engel, J., & Münch, G. W. (2006) · Pharmacology & Therapeutics · doi:10.1016/j.pharmthera.2006.07.001 · Cited by 286
Serum TNF-alpha levels are increased and correlate negatively with free IGF-I in Alzheimer disease
Álvarez, A., Cacabelos, R., Sanpedro, C., García-Fantini, M., & Aleixandre, M. (2006) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2006.02.012 · Cited by 278
MicroRNAs: Roles in Regulating Neuroinflammation
Gaudet, A. D., Fonken, L. K., Watkins, L. R., Nelson, R. J., & Popovich, P. G. (2018) · The Neuroscientist · doi:10.1177/1073858417721150 · Cited by 236
TNF-alpha modulation for treatment of Alzheimer's disease: a 6-month pilot study.
Tobinick, E. L., Gross, H., Weinberger, A., & Cohen, H. (2006) · PubMed · Cited by 271
A transdisciplinary perspective of chronic stress in relation to psychopathology throughout life span development
Juster, R.-P., Bizik, G., Picard, M., Arsenault-Lapierre, G., Sindi, S., Trepanier, L., Marin, M.-F., Wan, N., Sekerovic, Z., Lord, C., et al. (2011) · Development and Psychopathology · doi:10.1017/s0954579411000289 · Cited by 268
Relationship between Serum and Brain Carotenoids, α -Tocopherol, and Retinol Concentrations and Cognitive Performance in the Oldest Old from the Georgia Centenarian Study
Johnson, E. J., Vishwanathan, R., Johnson, M. A., Hausman, D. B., Davey, A., Scott, T. M., Green, R. C., Miller, L. S., Gearing, M., Woodard, J. L., et al. (2013) · Journal of Aging Research · doi:10.1155/2013/951786 · Cited by 268
Innate Immune Cell Death in Neuroinflammation and Alzheimer’s Disease
Rajesh, Y., & Kanneganti, T. (2022) · Cells · doi:10.3390/cells11121885 · Cited by 269
TLR4 (toll-like receptor 4) activation suppresses autophagy through inhibition of FOXO3 and impairs phagocytic capacity of microglia
Lee, J.-W., Nam, H., Kim, L. E., Jeon, Y., Min, H., Ha, S., Lee, Y., Kim, S.-Y., Lee, S. J., Kim, E.-K., et al. (2019) · Autophagy · doi:10.1080/15548627.2018.1556946 · Cited by 260
Aging‐dependent changes of microglial cells and their relevance for neurodegenerative disorders
Von Bernhardi, R., Tichauer, J. E., & Eugenín, J. (2010) · Journal of Neurochemistry · doi:10.1111/j.1471-4159.2009.06537.x · Cited by 258
“Over-expression of IL-1b, among other cytokines, and probably glial cell activation and changes on gliotransmission contribute to the impairment of cognitive abilities (Holmes et al. 2003; Tarkowski et al. 2003).”
Background
Rapid cognitive improvement in Alzheimer's disease following perispinal etanercept administration
Tobinick, E. L., & Gross, H. (2008) · Journal of Neuroinflammation · doi:10.1186/1742-2094-5-2 · Cited by 250
“These experimental findings, together with the rapid effects of perispinal etanercept shown here, converge to suggest that synaptic dysregulation produced by excess TNF-alpha [5,7-10,12,14,16,18,23] contributes to cognitive and behavioral dysfunction in Alzheimer's disease.”
Influential
PKC signaling deficits: a mechanistic hypothesis for the origins of Alzheimer's disease
Alkon, D. L., Sun, M., & Nelson, T. J. (2007) · Trends in Pharmacological Sciences · doi:10.1016/j.tips.2006.12.002 · Cited by 244
Tau in neurodegenerative disease
Gao, Y.-L., Wang, N., Sun, F.-R., Cao, X.-P., Zhang, W., & Yu, J.-T. (2018) · Annals of Translational Medicine · doi:10.21037/atm.2018.04.23 · Cited by 222
“As known to all, inflammation significantly contributes to AD pathogenesis and also plays an important role in other tauopathies (121,122).”
Background
TNF-mediated neuroinflammation is linked to neuronal necroptosis in Alzheimer's disease hippocampus
Jayaraman, A., Htike, T. T., James, R., Picón, C., & Reynolds, R. (2021) · Acta Neuropathologica Communications · doi:10.1186/s40478-021-01264-w · Cited by 244
The Role of Microglia and the Nlrp3 Inflammasome in Alzheimer's Disease
Hanslik, K. L., & Ulland, T. K. (2020) · Frontiers in Neurology · doi:10.3389/fneur.2020.570711 · Cited by 236
“, microglia, contribute to AD, and precedes Aβ plaque deposition and AD onset (4, 5).”
Background
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
Lipopolysaccharide-induced microglial activation induces learning and memory deficits without neuronal cell deathin rats
Tanaka, S., Ide, M., Shibutani, T., Ohtaki, H., Numazawa, S., Shioda, S., & Yoshida, T. (2006) · Journal of Neuroscience Research · doi:10.1002/jnr.20752 · Cited by 224
“It has been reported that TNF-a (Tarkowski et al., 2003) and IL-1b (McGeer and McGeer, 1998; Remarque et al., 2001) are elevated in the brains of Alzheimer’s disease patients.”
Background
Biomarkers of Oxidative Damage and Inflammation in Alzheimer's Disease
Galasko, D. R., & Montine, T. J. (2010) · Biomarkers in Medicine · doi:10.2217/bmm.09.89 · Cited by 231
Anti-TNF-α reduces amyloid plaques and tau phosphorylation and induces CD11c-positive dendritic-like cell in the APP/PS1 transgenic mouse brains
Shi, J.-Q., Shen, W., Chen, J., Wang, B.-R., Zhong, L.-L., Zhu, Y.-W., Zhu, H.-Q., Zhang, Q.-Q., Zhang, Y.-D., & Xu, J. (2011) · Brain Research · doi:10.1016/j.brainres.2010.10.053 · Cited by 219
“Many studies have demonstrated the relationship between excess TNF-α in the brain and the pathological features of AD (Tarkowski et al., 1999; Perry et al., 2001; Tarkowski et al., 2003).”
Background
Serum MCP-1 levels are increased in mild cognitive impairment and mild Alzheimer’s disease
Galimberti, D., Fenoglio, C., Lovati, C., Venturelli, E., Guidi, I., Corrà, B., Scalabrini, D., Clerici, F., Mariani, C., Bresolin, N., et al. (2006) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2005.10.007 · Cited by 209
Levels of β-Secretase (BACE1) in Cerebrospinal Fluid as a Predictor of Risk in Mild Cognitive Impairment
Zhong, Z., Ewers, M., Teipel, S., Bürger, K., Wallin, A., Blennow, K., He, P., McAllister, C., Hampel, H., & Shen, Y. (2007) · Archives of General Psychiatry · doi:10.1001/archpsyc.64.6.718 · Cited by 206
A possible role for lutein and zeaxanthin in cognitive function in the elderly
Johnson, E. J. (2012) · American Journal of Clinical Nutrition · doi:10.3945/ajcn.112.034611 · Cited by 207
“600 (NS) [4] 0.”
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
“Studies in subjects with mild cognitive impairment (MCI) that progress to develop AD suggest that increased CSF TNF-α levels are an early event, and their rise correlates with disease progression [44].”
Background
Comparative proteomics of cerebrospinal fluid in neuropathologically-confirmed Alzheimer's disease and non-demented elderly subjects
Castaño, E. M., Roher, A. E., Esh, C. L., Kokjohn, T. A., & Beach, T. G. (2006) · Neurological Research · doi:10.1179/016164106x98035 · Cited by 201
Treatment for Rheumatoid Arthritis and Risk of Alzheimer’s Disease: A Nested Case-Control Analysis
Chou, R. C., Kane, M., Ghimire, S., Gautam, S., & Gui, J. (2016) · CNS Drugs · doi:10.1007/s40263-016-0374-z · Cited by 194
Tumor necrosis factor α Inhibition for Alzheimer’s Disease
Chang, R., Yee, K.-L., & Sumbria, R. K. (2017) · Journal of Central Nervous System Disease · doi:10.1177/1179573517709278 · Cited by 195
Reactive astrocytes in Alzheimer’s disease: A double-edged sword
Chun, H., & Lee, C. J. (2018) · Neuroscience Research · doi:10.1016/j.neures.2017.11.012 · Cited by 176
Targeting neuroinflammation in Alzheimer’s disease: from mechanisms to clinical applications
Si, Z.-Z., Zou, C.-J., Mei, X., Mei, X., Luo, H., Shen, Y., Hu, J., Li, X.-X., Wu, L., & Liu, Y. (2022) · Neural Regeneration Research · doi:10.4103/1673-5374.353484 · Cited by 199
“Interestingly, higher CSF TNF-α levels have been found in individuals with AD, while individuals with mild cognitive impairment and high levels of TNF-α in the CSF are more likely to develop AD (Tarkowski et al., 2003).”
Background
Poly(ADP-Ribose) Polymerase-1 Promotes Microglial Activation, Proliferation, and Matrix Metalloproteinase-9-Mediated Neuron Death
Kauppinen, T. M., & Swanson, R. A. (2005) · The Journal of Immunology · doi:10.4049/jimmunol.174.4.2288 · Cited by 181
Differences of peripheral inflammatory markers between mild cognitive impairment and Alzheimer's disease
Bermejo, P., Martín-Aragón, S., Benedí, J., Susín, C., Felici, E., Gil, P., Ribera, J. M., & Villar, Á. M. (2008) · Immunology Letters · doi:10.1016/j.imlet.2008.02.002 · Cited by 178
Altered plasma cytokine levels in Alzheimer's disease: Correlation with the disease progression
Motta, M., Imbesi, R., Rosa, M. D., Stivala, F., & Malaguarnera, L. (2007) · Immunology Letters · doi:10.1016/j.imlet.2007.09.002 · Cited by 176
“[5] Tarkowski E, Andreasen N, Tarkowski A, Blennow K.”
BackgroundResult
NETosis in Alzheimer’s Disease
Pietronigro, E. C., Bianca, V. D., Zenaro, E., & Constantin, G. (2017) · Frontiers in Immunology · doi:10.3389/fimmu.2017.00211 · Cited by 179
“Higher levels of IL-1β and TNFα are found in the brain and cerebrospinal fluid (CSF) of AD patients, suggesting these molecules may contribute to neutrophil activation and NET formation in AD (114, 115).”
Background
The GABAergic system as a therapeutic target for Alzheimer's disease
Guzmán, B. C., Vinnakota, C., Govindpani, K., Waldvogel, H. J., Faull, R. L. M., & Kwakowsky, A. (2018) · Journal of Neurochemistry · doi:10.1111/jnc.14345 · Cited by 172
Do CSF total tau, phosphorylated tau, and β-amyloid 42 help to predict progression of mild cognitive impairment to Alzheimer's disease? A systematic review and meta-analysis of the literature
Diniz, B. S., Pinto, J. A., & Forlenza, O. V. (2008) · The World Journal of Biological Psychiatry · doi:10.1080/15622970701535502 · Cited by 173
Inflammation, Neurodegenerative Diseases, and Environmental Exposures
Campbell, A. (2004) · Annals of the New York Academy of Sciences · doi:10.1196/annals.1332.008 · Cited by 166
Clinical aspects of inflammation in Alzheimer's disease
Rosenberg, P. B. (2005) · International Review of Psychiatry · doi:10.1080/02646830500382037 · Cited by 158
“…of apoptosis Rosler et al. (2001) 27 AD Not matched IL-6 highest in non-AD dementias 24 non-AD dementia 70 neurological controls 49 healthy controls Tarkowski et al. (2003) 56 MCI Not matched TNF- and TGF- increased in MCI and AD compared to controls 25 controls MCI¼ cog deficits without…”
Background
Alzheimer’s Disease Pathogenesis: Role of Autophagy and Mitophagy Focusing in Microglia
Eshraghi, M., Adlimoghaddam, A., Mahmoodzadeh, A., Sharifzad, F., Yasavoli-Sharahi, H., Lorzadeh, S., Albensi, B. C., & Ghavami, S. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms22073330 · Cited by 158
“It has been shown that activation of microglia precedes Aβ and tau pathologies within the brain of AD patients and animal models [193,194].”
Background
Tumor Necrosis Factor (TNF) blocking agents are associated with lower risk for Alzheimer’s disease in patients with rheumatoid arthritis and psoriasis
Zhou, M., Xu, R., Kaelber, D. C., & Gurney, M. E. (2020) · PLOS ONE · doi:10.1371/journal.pone.0229819 · Cited by 157
“In the brain, elevation of TNF in cerebrospinal fluid collected from subjects with mild cognitive impairment is associated with progression to AD at 6 months follow up [6].”
Background
Increased production of inflammatory cytokines in mild cognitive impairment
Magaki, S., Mueller, C., DICKSON, C., & Kirsch, W. M. (2006) · Experimental Gerontology · doi:10.1016/j.exger.2006.09.015 · Cited by 157
“This is in agreement with findings that intrathecal inflammation is seen before the development of AD (Tarkowski et al., 2003).”
BackgroundResultInfluential
TNF-α-dependent neuronal necroptosis regulated in Alzheimer's disease by coordination of RIPK1-p62 complex with autophagic UVRAG
Xu, C., Wu, J. S., Wu, Y., Ren, Z., Yao, Y., Chen, G., Fang, E. F., Noh, J. H., Liu, Y., Wei, L., et al. (2021) · Theranostics · doi:10.7150/thno.62376 · Cited by 151
“But the question has then been raised, how is neuronal necroptosis in AD initiated? Given the accumulated evidence of elevated TNF-α in the CSF and brains of AD patients [20, 49], we hypothesized that upregulated TNF-α in AD brain might lead to the activation of neuronal necroptosis.”
Background
Imbalance of Circulating Th17 and Regulatory T Cells in Alzheimer’s Disease: A Case Control Study
Oberstein, T. J., Taha, L., Spitzer, P., Hellstern, J., i, M. H., Kornhuber, J., & Maler, J. M. (2018) · Frontiers in Immunology · doi:10.3389/fimmu.2018.01213 · Cited by 153
“Interestingly, low levels of TGF-β were associated with a faster progression from MCI to AD dementia, as it was observed for high levels of total Tau and pTau181 (35, 36, 59).”
Background
Biomarkers as Predictors for Conversion from Mild Cognitive Impairment to Alzheimer-Type Dementia: Implications for Trial Design
van Rossum, I. A., Vos, S. J. B., Handels, R. L. H., & Visser, P. J. (2010) · Journal of Alzheimer s Disease · doi:10.3233/jad-2010-091606 · Cited by 148
“tia compared to healthy controls, but not compared to subjects with stable MCI [25].”
MethodResultInfluential
Alzheimer's disease: Effects of β-amyloid on mitochondria
Tillement, L., Lecanu, L., & Papadopoulos, V. (2010) · Mitochondrion · doi:10.1016/j.mito.2010.08.009 · Cited by 148
“Both activated microglia and T lymphocytes can be a source of cytokine production such as interleukins (IL), and tumor necrosis factor (TNF) (Tarkowski et al., 2003).”
Background
Systemic TNF-α produces acute cognitive dysfunction and exaggerated sickness behavior when superimposed upon progressive neurodegeneration
Hennessy, E., Gormley, S., López-Rodríguez, A. B., Murray, C., Murray, C., & Cunningham, C. M. (2016) · Brain Behavior and Immunity · doi:10.1016/j.bbi.2016.09.011 · Cited by 147
“Elevated baseline TNF-a has also been associated with lower hippocampal volume (Sudheimer et al., 2014) and with greater likelihood of mild cognitive impairment (MCI) patient conversion to AD (Tarkowski et al., 2003) suggesting increased systemic TNF-amay have roles in hippocampal neurodegeneration.”
BackgroundInfluential
Decreased Levels of Circulating Adiponectin in Mild Cognitive Impairment and Alzheimer’s Disease
Teixeira, A. L., Diniz, B. S., Campos, A. C., de Miranda, A. S., Rocha, N. P., Talib, L. L., Gattaz, W. F., & Forlenza, O. V. (2012) · NeuroMolecular Medicine · doi:10.1007/s12017-012-8201-2 · Cited by 138
TNF-α-Induced Optic Nerve Degeneration and Nuclear Factor-κB p65
Kitaoka, Y., Kitaoka, Y., Kwong, J. M. K., Ross‐Cisneros, F. N., Wang, J., Tsai, R., Sadun, A. A., & Lam, T. T. (2006) · Investigative Ophthalmology & Visual Science · doi:10.1167/iovs.05-0299 · Cited by 135
Cerebrospinal fluid markers of neuroinflammation in delirium: A role for interleukin-1β in delirium after hip fracture
Cape, E., Hall, R. J., Munster, B. C. V., de Vries, A., Howie, S., Pearson, A., Middleton, S. D., Gillies, F., Armstrong, I. R., White, T. O., et al. (2014) · Journal of Psychosomatic Research · doi:10.1016/j.jpsychores.2014.06.014 · Cited by 130
“Many studies reporting CSF IL-1β levels find them to be close to or below commercially-available assay LoD [30,32,35–37].”
Background
Heat-Shock Proteins in Neuroinflammation
Dukay, B., Csoboz, B., & Tóth, M. E. (2019) · Frontiers in Pharmacology · doi:10.3389/fphar.2019.00920 · Cited by 139
“org fluid of AD patients and was described to be a risk factor in PD (Tarkowski et al., 2003; Lindenau et al., 2017).”
Background
Therapeutic strategies for tau mediated neurodegeneration
Yoshiyama, Y., Lee, V. M. ‐., & Trojanowski, J. Q. (2012) · Journal of Neurology Neurosurgery & Psychiatry · doi:10.1136/jnnp-2012-303144 · Cited by 137
Selective TNF Inhibition for Chronic Stroke and Traumatic Brain Injury
Tobinick, E. L., Kim, N. M., Reyzin, G., Rodriguez-Romanacce, H., & DePuy, V. (2012) · CNS Drugs · doi:10.1007/s40263-012-0013-2 · Cited by 132
“It may well be that the effects of TNF on neuronal function are concentration dependent; low levels of TNF appear necessary for optimal neuronal function, but excess levels may be deleterious [45, 48, 72, 73].”
Aluminum and copper in drinking water enhance inflammatory or oxidative events specifically in the brain
Becaria, A., Lahiri, D. K., Bondy, S. C., Chen, D., Hamadeh, A., Li, H., Taylor, R., & Campbell, A. (2006) · Journal of Neuroimmunology · doi:10.1016/j.jneuroim.2006.03.025 · Cited by 129
“This is illustrated by the finding that significant increase in CSF TNF-a levels precedes development of AD in patients with mild cognitive impairment (Tarkowski et al., 2003).”
Background
Therapeutic Potential of TNF-α Inhibition for Alzheimer’s Disease Prevention
Torres-Acosta, N., O’Keefe, J. H., O’Keefe, E. L., Isaacson, R., & Small, G. W. (2020) · Journal of Alzheimer s Disease · doi:10.3233/jad-200711 · Cited by 129
“This pro-inflammatory cytokine is elevated in the cerebrospinal fluid of AD patients and correlates directly with disease progression [19].”
Background
Differential contribution of microglia and monocytes in neurodegenerative diseases
Baufeld, C., O'Loughlin, E. K., Calcagno, N., Madore, C., & Butovsky, O. (2017) · Journal of Neural Transmission · doi:10.1007/s00702-017-1795-7 · Cited by 128
“…cytokine levels are found in the CSF of individuals with mild cog- nitive impairment—amnestic type (MCI), who have an increased risk to develop AD, suggesting that this neu- roinflammation occurs early in the disease development and might trigger AD (Tarkowski et al. 2003; Brosseron et al. 2014).”
Background
Cerebrospinal Fluid Biomarkers of Neurovascular Dysfunction in Mild Dementia and Alzheimer'S Disease
Sweeney, M. D., Sagare, A. P., & Zlokovic, B. V. (2015) · Journal of Cerebral Blood Flow & Metabolism · doi:10.1038/jcbfm.2015.76 · Cited by 122
Counteracting the effects of TNF receptor‐1 has therapeutic potential in Alzheimer's disease
Steeland, S., Gorlé, N., Vandendriessche, C., Balusu, S., Brkić, M., Cauwenberghe, C. V., Imschoot, G. V., Wonterghem, E. V., Rycke, R. M. D., Kremer, A., et al. (2018) · EMBO Molecular Medicine · doi:10.15252/emmm.201708300 · Cited by 125
“…A b plaques and the elevated TNF levels in the plasma and cerebrospinal fluid (CSF) of AD patients, both of which have been associated with clinical deterioration (Fillit et al , 1991; Dickson, 1997; Paganelli et al , 2002; Tarkowski et al , 2003a,b; Yasutake et al , 2006; Swardfager et al , 2010).”
Increased plasma levels of lipocalin 2 in mild cognitive impairment
Choi, J., Lee, H., & Suk, K. (2011) · Journal of the Neurological Sciences · doi:10.1016/j.jns.2011.03.023 · Cited by 123
“proinflammatory cytokine TNF-α were significantly increased in patients with MCI compared to the controls [51].”
Result
Tumour Necrosis Factor Modulation for Treatment of Alzheimerʼs Disease: Rationale and Current Evidence
Tobinick, E. (2009) · CNS Drugs · doi:10.2165/11310810-000000000-00000 · Cited by 117
The Role of TNF-α in Alzheimer’s Disease: A Narrative Review
Plantone, D., Pardini, M., Righi, D., Manco, C., Colombo, B. M., & Stefano, N. D. (2023) · Cells · doi:10.3390/cells13010054 · Cited by 125
“Interestingly, MCI patients progressing to AD showed elevated CSF TNF α [96].”
Background
Excess cerebral TNF causing glutamate excitotoxicity rationalizes treatment of neurodegenerative diseases and neurogenic pain by anti-TNF agents
Clark, I. A., & Vissel, B. (2016) · Journal of Neuroinflammation · doi:10.1186/s12974-016-0708-2 · Cited by 123
“However, this text takes no account of the presence of excess cerebral TNF production or its influence on extracellular brain glutamate levels in these and similar diseases [34, 51, 93–95].”
Background
Changes in the levels of plasma soluble fractalkine in patients with mild cognitive impairment and Alzheimer's disease
Kim, T., Lim, H. K., Lee, J. Y., Kim, D., Park, S., Lee, C., & Lee, C. (2008) · Neuroscience Letters · doi:10.1016/j.neulet.2008.03.019 · Cited by 117
Blood–Brain Barrier Penetrating Biologic TNF-α Inhibitor for Alzheimer’s Disease
Chang, R., Knox, J., Chang, J. H., Derbedrossian, A., Vasilevko, V., Cribbs, D. H., Boado, R. J., Pardridge, W. M., & Sumbria, R. K. (2017) · Molecular Pharmaceutics · doi:10.1021/acs.molpharmaceut.7b00200 · Cited by 116
Diagnostic function of the neuroinflammatory biomarker YKL-40 in Alzheimer’s disease and other neurodegenerative diseases
Baldacci, F., Lista, S., Cavedo, E., Bonuccelli, U., & Hampel, H. (2017) · Expert Review of Proteomics · doi:10.1080/14789450.2017.1304217 · Cited by 113
“ment system [20], increased release of chemokines and cytokines [13,21,22], caspase activation [13,23], and higher nitric oxides and reactive oxygen species production [24] have all been reported in AD.”
Background
Selective TNF Inhibition for Chronic Stroke and Traumatic Brain Injury: An Observational Study Involving 629 Consecutive Patients Treated with Perispinal Etanercept
Page, S. J. (2013) · CNS Drugs · doi:10.1007/s40263-013-0057-y · Cited by 112
“However, now, more than a decade after the introduction of biologic TNF inhibitors into clinical practice, there is substantial evidence that excess TNF plays a key role in brain dysfunction, and also that physiological levels of TNF are involved in normal brain physiology [14, 15, 25, 26, 29, 31, 32, 35, 37–49].”
Cerebrospinal Fluid Markers of Alzheimer’s Disease Pathology and Microglial Activation are Associated with Altered White Matter Microstructure in Asymptomatic Adults at Risk for Alzheimer’s Disease
Melah, K. E., Lu, S. Y.-F., Hoscheidt, S. M., Alexander, A. L., Adluru, N., Destiche, D. J., Carlsson, C. M., Zetterberg, H., Blennow, K., Okonkwo, O. C., et al. (2016) · Journal of Alzheimer s Disease · doi:10.3233/jad-150897 · Cited by 109
“Several proinflammatory cytokines, chemokines, and complement proteins are elevated in the AD brain and both human and animal studies suggest inflammation may occur early in the AD process [3–7].”
Rapid improvement in verbal fluency and aphasia following perispinal etanercept in Alzheimer's disease
Tobinick, E. L., & Gross, H. (2008) · BMC Neurology · doi:10.1186/1471-2377-8-27 · Cited by 111
“These caveats notwithstanding, the scientific rationale for the further investigation of anti-TNF-alpha treatment of Alzheimer's disease is compelling, with supporting genetic, epidemiologic, clinical, and basic science evidence [1-19,30,50,52].”
Background
TGF-β1 signalling in Alzheimer’s pathology and cytoskeletal reorganization: a specialized Tau perspective
Kapoor, M., & Chinnathambi, S. (2023) · Journal of Neuroinflammation · doi:10.1186/s12974-023-02751-8 · Cited by 114
“TGF-β has been linked to amelioration of such neurotoxicity by reducing glial activation (microglial pro-inflammatory phenotype), decreasing expression of pro-inflammatory cytokines, such as TNF-α, iNOS and IL-1β, increasing expression of trophic factors essential for neuronal survival-like IGF-1, GDNF, and BDNF, and…”
BackgroundInfluential
Serum high sensitivity C-reactive protein and cognitive function in elderly women
Komulainen, P., Lakka, T. A., Kivipelto, M., Hassinen, M., Penttila, I. M., Helkala, E.-L., Gylling, H. K., Nissinen, A. M., & Rauramaa, R. (2007) · Age and Ageing · doi:10.1093/ageing/afm051 · Cited by 115
“Thus, propensity towards inflammation in those patients may indicate that inflammation in central nervous system may be an early hallmark in the pathogenesis of Alzheimer’s disease [30].”
Background
Dietary carotenoids and cognitive function among US adults, NHANES 2011–2014
Christensen, K. L. Y., Gleason, C. E., & Mares, J. A. (2018) · Nutritional Neuroscience · doi:10.1080/1028415x.2018.1533199 · Cited by 109
Meta-analysis of CSF and MRI biomarkers for detecting preclinical Alzheimer's disease
Schmand, B. A., Huizenga, H. M., & van Gool, W. A. (2009) · Psychological Medicine · doi:10.1017/s0033291709991516 · Cited by 109
T Lymphocytes and Inflammatory Mediators in the Interplay between Brain and Blood in Alzheimer’s Disease: Potential Pools of New Biomarkers
Mietelska‐Porowska, A., & Wojda, U. (2017) · Journal of Immunology Research · doi:10.1155/2017/4626540 · Cited by 111
“Similarly, an increased level of TNF-α and a decreased level of TGFβ in the CSF were previously described as markers of the conversion of MCI to AD [105].”
Background
Alzheimer’s Disease: Recent Concepts on the Relation of Mitochondrial Disturbances, Excitotoxicity, Neuroinflammation, and Kynurenines
Zádori, D., Veres, G., Szalárdy, L., Klivènyi, P., & Vécsei, L. (2018) · Journal of Alzheimer s Disease · doi:10.3233/jad-170929 · Cited by 108
“In particular, elevated levels of the proinflammatory cytokine, TNFα, and its soluble receptors, sTNFR1 and sTNFR2, in the CSF of patients with MCI were reported to predict more rapid conversion to AD dementia [183, 184].”
Beta amyloid aggregates induce sensitised TLR4 signalling causing long-term potentiation deficit and rat neuronal cell death
Hughes, C., Choi, M. L., Yi, J.-H., Kim, S.-C., Drews, A., George-Hyslop, P. S., Bryant, C., Gandhi, S., Cho, K., & Klenerman, D. (2020) · Communications Biology · doi:10.1038/s42003-020-0792-9 · Cited by 107
Longitudinal Inflammation, Cognitive Decline, and Alzheimer’s Disease: A Mini-Review
Bettcher, B. M., & Kramer, J. H. (2014) · Clinical Pharmacology & Therapeutics · doi:10.1038/clpt.2014.147 · Cited by 107
Systemic and Acquired Immune Responses in Alzheimer's Disease
Britschgi, M., & Wyss‐Coray, T. (2007) · International review of neurobiology · doi:10.1016/s0074-7742(07)82011-3 · Cited by 107
Levels of CSF prostaglandin E2, cognitive decline, and survival in Alzheimer's disease
Combrinck, M. I. (2005) · Journal of Neurology Neurosurgery & Psychiatry · doi:10.1136/jnnp.2005.063131 · Cited by 105
“15 18–20 A small number of our patients presented with early symptoms and initial learning scores still in the normal range (12–17) before they subsequently progressed to dementia.”
BackgroundResult
Interleukin-18 increases expression of kinases involved in tau phosphorylation in SH-SY5Y neuroblastoma cells
Ojala, J. O., Sutinen, E. M., Salminen, A., & Pirttilä, T. (2008) · Journal of Neuroimmunology · doi:10.1016/j.jneuroim.2008.09.012 · Cited by 102
“Over-expression of inflammatory molecules such as IL-1β has many detrimental effects in the brain, e.g. it contributes to the impairment of cognitive abilities (Holmes et al., 2003; Tarkowski et al., 2003) and to the generation of neuritic plaques (Chang et al., 1999; Lahiri et al., 2003).”
Background
The dual face of microglia (M1/M2) as a potential target in the protective effect of nutraceuticals against neurodegenerative diseases
Darwish, S. F., Elbadry, A. M. M., Elbokhomy, A. S., Salama, G. A., & Salama, R. M. (2023) · Frontiers in Aging · doi:10.3389/fragi.2023.1231706 · Cited by 110
“In the CSF of mild memory impairment patients who developed AD, researchers discovered higher TNF-α (a pro-inflammatory cytokine) and lower TNF-β (antiinflammatory cytokine) levels compared to controls who had not experienced AD (Tarkowski et al., 2003).”
Background
Astrocytes in Alzheimer's Disease: Emerging Roles in Calcium Dysregulation and Synaptic Plasticity
Vincent, A. J., Gasperini, R., Foa, L. C., & Small, D. H. (2010) · Journal of Alzheimer s Disease · doi:10.3233/jad-2010-101089 · Cited by 106
Exercise as a pro-cognitive, pro-neurogenic and anti-inflammatory intervention in transgenic mouse models of Alzheimer’s disease
Ryan, S. M., & Kelly, A. M. (2016) · Ageing Research Reviews · doi:10.1016/j.arr.2016.03.007 · Cited by 106
“, 2006) and have been associated with increasing the risk of conversion from the mild cognitive impairment to dementia phase of AD (Tarkowski et al., 2003).”
Cerebrospinal Fluid and Plasma Levels of Inflammation Differentially Relate to CNS Markers of Alzheimer’s Disease Pathology and Neuronal Damage
Bettcher, B. M., Johnson, S. C., Fitch, R., Casaletto, K. B., Heffernan, K. S., Asthana, S., Zetterberg, H., Blennow, K., Carlsson, C. M., Neuhaus, J. M., et al. (2018) · Journal of Alzheimer s Disease · doi:10.3233/jad-170602 · Cited by 105
YKL-40 as a Potential Biomarker and a Possible Target in Therapeutic Strategies of Alzheimer’s Disease
Muszyński, P., Groblewska, M., Kulczyńska‐Przybik, A., Kułakowska, A., & Mroczko, B. (2017) · Current Neuropharmacology · doi:10.2174/1570159x15666170208124324 · Cited by 104
“The reports suggest the possible role of elevated CSF levels of pro-inflammatory cytokines as risk factors for conversion of MCI to AD or as markers of the disease progression [54, 55].”
Background
It May Take Inflammation, Phosphorylation and Ubiquitination to ‘Tangle’ in Alzheimer’s Disease
Arnaud, L. T., Robakis, N. K. R. K., & Figueiredo‐Pereira, M. E. (2006) · Neurodegenerative Diseases · doi:10.1159/000095638 · Cited by 104
Higher Serum sTNFR1 Level Predicts Conversion from Mild Cognitive Impairment to Alzheimer's Disease
Diniz, B. S., Teixeira, A. L., Ojopi, E. P. B., Talib, L. L., Mendonça, V. A., Gattaz, W. F., & Forlenza, O. V. (2011) · Journal of Alzheimer s Disease · doi:10.3233/jad-2010-100921 · Cited by 99
“α as compared to controls [2].”
Background

Authors: Tarkowski, E.
Affiliations: University of Gothenburg (SE)
Corresponding author: Tarkowski, E
Venue: Journal of Neurology, Neurosurgery & Psychiatry
Publisher: BMJ
Published: 2003-09-01
Volume: 74
Issue: 9
Pages: 1200-1205
ISSN: 0022-3050 (ISSN-L)
DOI: 10.1136/jnnp.74.9.1200
PMC: PMC1738668
OpenAlex: W2071728536
Cited by: 501
References: 53
Citations by year: 2026: 16 · 2025: 17 · 2024: 45 · 2023: 28 · 2022: 43 · 2021: 51 · 2020: 23 · 2019: 30 · 2018: 32 · 2017: 23 · 2016: 18 · 2015: 16 · 2014: 14 · 2013: 13 · 2012: 18
FWCI: 6.52
Type: journal article
Language: en
Open access: bronze
doi.org
Locations: Journal of Neurology Neurosurgery & Psychiatry (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Funders: Rune och Ulla Amlövs Stiftelse för Neurologisk och Reumatologisk Forskning
Hjärt-Lungfonden
Göteborgs Läkaresällskap
Svenska Läkaresällskapet
Stiftelsen Konung Gustaf V:s 80-årsfond
Medical Research Council
Topics: Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
Keywords: Alzheimer's disease, mild cognitive impairment, cerebrospinal fluid biomarkers, intrathecal inflammation, inflammatory cytokines, TNF-α, IL-1β, GM-CSF, TGF-beta, tau protein, amyloid-beta, amyloid metabolism, neuroinflammation, disease progression
MeSH terms: Aged, Aged, 80 and over, Alzheimer Disease, Central Nervous System, Cognition Disorders, Female, Humans, Inflammation, Interleukin-1, Male, Middle Aged, Prospective Studies, Risk Factors, Tumor Necrosis Factor-alpha, Granulocyte-Macrophage Colony-Stimulating Factor, Amyloid beta-Peptides, tau Proteins, Plaque, Amyloid

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

Intrathecal inflammation precedes development of Alzheimer's disease

Abstract

Overview

Integrity signals

Verification

Claims the paper makes

Claims other papers make about this one

Self-check

Citations

Cites

Cited by

Related

Metadata

Record

About these checks