The DOI matches its Crossref record; 107 of the 108 references it cites were found in a registry or an index.
Significance of NF-κB as a pivotal therapeutic target in the neurodegenerative pathologies of Alzheimer’s disease and multiple sclerosis
Open accessAbstract
INTRODUCTION: Advances in molecular pathogenesis suggest that the chronic inflammation is a shared mechanism in the initiation and progression of multiple neurodegenerative diseases with diverse clinical manifestations such as Alzheimer's disease (AD) and Multiple sclerosis (MS). Restricted cell renewal and regenerative capacity make the neural tissues extremely vulnerable to the uncontrolled inflammatory process leading to irreversible tissue damage. AREAS COVERED: A predominant consequence of increased inflammatory signaling is the upregulation of the transcription factor, NF-κB with subsequent neuroprotective or deleterious effects depending on the strength of the signal and the type of NF-κB dimers activated. We discuss the interplay between neuroinflammation and neurodegeneration keeping in focus NF-κB signaling as the point of convergence of multiple pathways associated with the development of the neurodegenerative pathologies, AD and MS. EXPERT OPINION: Considerable interest exists in developing efficient NF-κB inhibitors for neurodegenerative diseases. The review includes an overview of natural compounds and rationally designed agents that inhibit NF-κB and mediate neuroprotection in AD and MS. The key chemical moieties of the natural and the synthetic compounds provide efficient leads for the development of effective small molecule inhibitors that selectively target NF-κB activation; this would result in the desired benefit to risk therapeutic effects.
Overview
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
Cites
Statistics
Verification
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?
In the citing paper
“Neuroinflammation is one of the major factors of AD and other disorders related to cholinergic transmission. It can be attenuated by reducing the expression of NF-κB-p65 via NLRP3 pathways.”
From Acetylcholinesterase Inhibitory Potential of Various Sesquiterpene Analogues for Alzheimer’s Disease Therapy (2021) · cites this paper as [142]
In the citing paper
“Thus targeting the transcription factor (NF-κβp65) could be the novel approach for the treatment of AD.”
From Acetylcholinesterase Inhibitory Potential of Various Sesquiterpene Analogues for Alzheimer’s Disease Therapy (2021) · cites this paper as [142]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
1 retracted
Wang, P., Su, C., Li, R., Wang, H., Ren, Y., Sun, H., Yang, J., Sun, J., Shi, J., Tian, J., et al. (2014) · Journal of Neuroscience Research · doi:10.1002/jnr.23322 · Cited by 65
RetractedMechanisms underlying inflammation in neurodegeneration
Glass, C. K., Saijo, K., Winner, B., Marchetto, M. C., & Gage, F. H. (2010) · Cell · doi:10.1016/j.cell.2010.02.016 · Cited by 3,580
Yang, F., Lim, G. P., Begum, A. N., Ubeda, O. J., Simmons, M. R., Ambegaokar, S. S., Chen, P. P., Kayed, R., Glabe, C. G., Frautschy, S. A., et al. (2005) · Journal of Biological Chemistry · doi:10.1074/jbc.m404751200 · Cited by 2,336
MAP Kinases in the Immune Response
Dong, C., Davis, R. J., & Flavell, R. A. (2002) · Annual Review of Immunology · doi:10.1146/annurev.immunol.20.091301.131133 · Cited by 1,684
Kauppinen, A., Suuronen, T., Ojala, J. O., Kaarniranta, K., & Salminen, A. (2013) · Cellular Signalling · doi:10.1016/j.cellsig.2013.06.007 · Cited by 1,016
Why neurodegenerative diseases are progressive: uncontrolled inflammation drives disease progression
Gao, H., & Hong, J. (2008) · Trends in Immunology · doi:10.1016/j.it.2008.05.002 · Cited by 852
Inhibiting NF-κB activation by small molecules as a therapeutic strategy
Gupta, S. C., Sundaram, C., Reuter, S., & Aggarwal, B. B. (2010) · Biochimica et Biophysica Acta (BBA) - Gene Regulatory Mechanisms · doi:10.1016/j.bbagrm.2010.05.004 · Cited by 762
SIRT1 Protects against Microglia-dependent Amyloid-β Toxicity through Inhibiting NF-κB Signaling
Chen, J., Zhou, Y., Mueller-Steiner, S., Chen, L.-F., Kwon, H., Yi, S., Mucke, L., & Gan, L. (2005) · Journal of Biological Chemistry · doi:10.1074/jbc.m509329200 · Cited by 740
Glucocorticoids increase amyloid-β and tau pathology in a mouse model of alzheimer’s disease
Green, K. N., Billings, L. M., Roozendaal, B., McGaugh, J. L., & LaFerla, F. M. (2006) · The Journal of Neuroscience · doi:10.1523/jneurosci.2797-06.2006 · Cited by 623
Kaltschmidt, B., Uherek, M., Volk, B., Baeuerle, P. A., & Kaltschmidt, C. (1997) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.94.6.2642 · Cited by 619
Cited by
Sorted by citations
Mechanisms of NF-κB p65 and strategies for therapeutic manipulation
Giridharan, S., & Srinivasan, M. (2018) · Journal of Inflammation Research · doi:10.2147/jir.s140188 · Cited by 686
microRNA dysregulation in neurodegenerative diseases: A systematic review
Juźwik, C. A., S. Drake, S., Zhang, Y., Paradis-Isler, N., Sylvester, A., Amar-Zifkin, A., Douglas, C., Morquette, B., Moore, C. S., & Fournier, A. E. (2019) · Progress in Neurobiology · doi:10.1016/j.pneurobio.2019.101664 · Cited by 426
The Pivotal Role of NF-kB in the Pathogenesis and Therapeutics of Alzheimer’s Disease
Sun, E., Motolani, A., Campos, L., & Lu, T. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms23168972 · Cited by 381
Targeting Transcription Factors for Cancer Treatment
Lambert, M., Jambon, S., Depauw, S., & David‐Cordonnier, M. (2018) · Molecules · doi:10.3390/molecules23061479 · Cited by 359
Nanotechnology-based drug delivery systems for the treatment of Alzheimer’s disease
Fonseca‐Santos, B., Chorilli, M., & Gremião, M. P. D. (2015) · International Journal of Nanomedicine · doi:10.2147/ijn.s87148 · Cited by 320
Metadata
- Authors
- Srinivasan, M., & Lahiri, D. K.
- Affiliations
- Indiana University (US)
- Indiana University School of Medicine (US)
- Venue
- Expert Opinion on Therapeutic Targets
- Publisher
- Informa UK Limited
- Published
- 2015-02-04
- Volume
- 19
- Issue
- 4
- Pages
- 471-487
- ISSN
- 1472-8222 (ISSN-L)
- 1744-7631
- PMC
- PMC5873291
- OpenAlex
- W1973257468
- Cited by
- 164
- References
- 108
- Citations by year
- 2026: 10 · 2025: 12 · 2024: 11 · 2023: 13 · 2022: 16 · 2021: 21 · 2020: 19 · 2019: 16 · 2018: 19 · 2017: 10 · 2016: 10 · 2015: 6
- FWCI
- 4.96
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Expert Opinion on Therapeutic Targets (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- IUScholarWorks (Indiana University) (submittedVersion)
- Purdue University Indianapolis (Indiana University) (submittedVersion)
- Author eBooks
- Funders
- National Institutes of Health (5r21ag042804-02)
- National Institute on Aging (R21-AG042804, 5R21AG042804, 1R21AG047)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Keywords
- NF-κB signaling, Alzheimer's disease, multiple sclerosis, neuroinflammation, neurodegeneration, NF-κB inhibitors, neuroprotection, natural compounds, small molecule inhibitors, chronic inflammation
- MeSH terms
- Alzheimer Disease, Animals, Humans, Multiple Sclerosis, Drug Design, Signal Transduction, Up-Regulation, NF-kappa B, Neuroprotective Agents
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
