The DOI matches its Crossref record; 61 of the 61 references it cites were found in a registry or an index.
Recent advances in molecular pathways and therapeutic implications targeting neuroinflammation for Alzheimer’s disease
Open accessAbstract
Alzheimer's disease (AD) is a major contributor of dementia leading to the degeneration of neurons in the brain with major symptoms like loss of memory and learning. Many evidences suggest the involvement of neuroinflammation in the pathology of AD. Cytokines including TNF-α and IL-6 are also found increasing the BACE1 activity and expression of NFκB resulting in generation of Aβ in AD brain. Following the interaction of Aβ with microglia and astrocytes, other inflammatory molecules also get translocated to the site of inflammation by chemotaxis and exaggerate neuroinflammation. Various pathways like NFκB, p38 MAPK, Akt/mTOR, caspase, nitric oxide and COX trigger microglia to release inflammatory cytokines. PPARγ agonists like pioglitazone increases the phagocytosis of Aβ and reduces inflammatory cytokine IL-1β. Celecoxib and roficoxib like selective COX-2 inhibitors also ameliorate neuroinflammation. Non-selective COX inhibitor indomethacin is also potent inhibitor of inflammatory mediators released from microglia. Mitophagy process is considered quite helpful in reducing inflammation due to microglia as it promotes the phagocytosis of over activated microglial cells and other inflammatory cells. Mitophagy induction is also beneficial in the removal of damaged mitochondria and reduction of infiltration of inflammatory molecules at the site of accumulation of the damaged mitochondria. Targeting these pathways and eventually ameliorating the activation of microglia can mitigate neuroinflammation and come out as a better therapeutic option for the treatment of Alzheimer's disease.
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?
The source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Several pathological factors in AD, such as Aβ, pro-inflammatory cytokines, and oxidative stress, activate microglia and initiate downstream signaling pathways such as MAPK, NF-κB, and PI3K/Akt.”
From Recent advances in Alzheimer's disease: Mechanisms, clinical trials and new drug development strategies. (2024) · cites this paper as [240]
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“The activation of these pathways further promotes the activation of microglia and the production of inflammatory mediators, exacerbating neurotoxicity.238–240”
From Recent advances in Alzheimer's disease: Mechanisms, clinical trials and new drug development strategies. (2024) · cites this paper as [240]
The cited source says what the claim attributes to it.
In the citing paper
“A significant trigger for astrocyte reactivity is neuroinflammation, involving pro-inflammatory molecules like cytokines and chemokines (11–14).”
From Varicose projection astrocytes: Conserved reactive cells in brain pathology (2026) · cites this paper as [12]
In the citing paper
“A growing amount of evidence has revealed that a sustained inflammatory state in the brain is a major contributor in the AD pathogenesis (Dhapola et al., 2021).”
From Exploring the Therapeutic Potential of Phytochemicals in Alzheimer’s Disease: Focus on Polyphenols and Monoterpenes (2022) · cites this paper as Dhapola et al., 2021
In the citing paper
“Neuroinflammation has been identified as a key contributor to the pathobiology of AD [2–4]”
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, H.-Y., Lee, K.-C., Pei, Z., Khan, A., Bakshi, K. P., & Burns, L. H. (2017) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2017.03.016 · Cited by 48
Retracted2019 Alzheimer’s disease facts and figures.
Alzheimer's Association (2019) · Alzheimer's & Dementia · doi:10.1016/j.jalz.2019.01.010 · Cited by 2,461 · cited 1×
“Gradually the person becomes bedridden and ultimately leads to death of the Alzheimer’s Association (2019).”
BackgroundNeuroinflammation in Alzheimer's disease: current evidence and future directions
Calsolaro, V., & Edison, P. (2016) · Alzheimer's & Dementia · doi:10.1016/j.jalz.2016.02.010 · Cited by 1,726
Vascular dysfunction—The disregarded partner of Alzheimer's disease
Sweeney, M. D., Montagne, A., Sagare, A. P., Nation, D. A., Schneider, L. S., Chui, H. C., Harrington, M. G., Pa, J., Law, M., Wang, D. J. J., et al. (2019) · Alzheimer's & Dementia · doi:10.1016/j.jalz.2018.07.222 · Cited by 711
Alzheimer's disease drug development pipeline: 2018
Cummings, J., Lee, G., Ritter, A., & Zhong, K. (2018) · Alzheimer's & Dementia: Translational Research & Clinical Interventions · doi:10.1016/j.trci.2018.03.009 · Cited by 697
Neuroinflammation pathways: a general review
Shabab, T., Khanabdali, R., Moghadamtousi, S. Z., Kadir, H. A., & Mohan, G. (2016) · International Journal of Neuroscience · doi:10.1080/00207454.2016.1212854 · Cited by 657
The Alzheimer’s Disease Clinical Spectrum
Atri, A. (2019) · Medical Clinics of North America · doi:10.1016/j.mcna.2018.10.009 · Cited by 623
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
Microglia, neuroinflammation, and beta-amyloid protein in Alzheimer’s disease
Cai, Z., Hussain, M. D., & Yan, L.-J. (2014) · International Journal of Neuroscience · doi:10.3109/00207454.2013.833510 · Cited by 583
Aging and Alzheimer's disease pathology
Sengoku, R. (2019) · Neuropathology · doi:10.1111/neup.12626 · Cited by 316
Cited by
Sorted by citations
Zhang, J., Zhang, Y., Wang, J., Xia, Y., Zhang, J., & Chen, L. (2024) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-024-01911-3 · Cited by 1,138
Inflammatory Processes in Alzheimer’s Disease—Pathomechanism, Diagnosis and Treatment: A Review
Twarowski, B., & Herbet, M. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms24076518 · Cited by 489
Skrzypczak-Wiercioch, A., & Sałat, K. (2022) · Molecules · doi:10.3390/molecules27175481 · Cited by 406
Apoptosis in Alzheimer’s disease: Insight into the signaling pathways and therapeutic avenues
Kumari, S., Dhapola, R., & Reddy, D. H. (2023) · Apoptosis · doi:10.1007/s10495-023-01848-y · Cited by 324
Self-citationGut liver brain axis in diseases: the implications for therapeutic interventions
Yan, M., Man, S., Sun, B., Ma, L., Guo, L., Huang, L., & Gao, W. (2023) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-023-01673-4 · Cited by 314
Metadata
- Authors
- Dhapola, R., Hota, S. S., Sarma, P., Bhattacharyya, A., Medhi, B., & Reddy, D. H.
- Affiliations
- Central University of Punjab (IN)
- Post Graduate Institute of Medical Education and Research (IN)
- Government Medical College and Hospital (IN)
- Venue
- Inflammopharmacology
- Published
- 2021-11-23
- Volume
- 29
- Issue
- 6
- Pages
- 1669-1681
- ISSN
- 0925-4692 (ISSN-L)
- 1568-5608
- PMC
- PMC8608577
- OpenAlex
- W3215739089
- Cited by
- 383
- References
- 61
- Citations by year
- 2026: 72 · 2025: 116 · 2024: 111 · 2023: 55 · 2022: 27
- FWCI
- 5.64
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Inflammopharmacology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
- Keywords
- Alzheimer's disease, neuroinflammation, microglia, amyloid-beta, NF-κB, TNF-α, interleukin-6, p38 MAPK, caspases, nitric oxide, COX-2 inhibitors, PPARγ agonists, pioglitazone, celecoxib, rofecoxib, indomethacin, mitophagy, astrocytes
- MeSH terms
- Neuroinflammatory Diseases, Alzheimer Disease, Animals, Humans, Inflammation, Mitochondria, Cytokines, Inflammation Mediators, Molecular Targeted Therapy, Mitophagy
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
