CoChat
Sign Up
Cited by 587Neuroinflammation and Neurodegeneration MechanismsAlzheimer's disease research and treatmentsNeurological Disease Mechanisms and Treatments

The DOI matches its Crossref record; 233 of the 234 references it cites were found in a registry or an index.

Microglia, neuroinflammation, and beta-amyloid protein in Alzheimer’s disease

Cai, Zhiyou, Hussain, M. Delwar, Yan, Liang-Jun·2014·International Journal of Neuroscience
DOI 10.3109/00207454.2013.833510
Open this paper in CoChat — free account

Abstract

Compelling evidence from basic molecular biology has demonstrated the dual roles of microglia in the pathogenesis of Alzheimer's disease (AD). On one hand, microglia are involved in AD pathogenesis by releasing inflammatory mediators such as inflammatory cytokines, complement components, chemokines, and free radicals that are all known to contribute to beta-amyloid (Aβ) production and accumulation. On the other hand, microglia are also known to play a beneficial role in generating anti-Aβ antibodies and stimulating clearance of amyloid plaques. Aβ itself, an inducer of microglia activation and neuroinflammation, has been considered as an underlying and unifying factor in the development of AD. A vicious cycle of inflammation has been formed between Aβ accumulation, activated microglia, and microglial inflammatory mediators, which enhance Aβ deposition and neuroinflammation. Thus, inhibiting the vicious cycle seems to be a promising treatment to restrain further development of AD. With increasing research efforts on microglia in AD, intervention of microglia activation and neuroinflammation in AD may provide a potential target for AD therapy in spite of the provisional failure of nonsteroidal antiinflammatory drugs in clinical trials.

Overview

Integrity signals

Registry

Crossref · 10.3109/00207454.2013.833510

Cites

233 of 233 references verified0 citation errors · 0 not checkable

Statistics

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

Verification

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?

Citations

Cites

Show all 234 references

Research works printed but not linked: 24

  1. Dubinina EE, 2007, Adv Gerontol, 20, 109
  2. Weitz TM, 2012, Int J Alzheimer's Dis, 2012, 314185
  3. Imamoto K, 1981, Prog Clin Biol Res, 59, 125
  4. Wierzba-Bobrowicz T, 2002, Folia Neuropathol, 40, 125
  5. Krause DL, 2010, Int J Alzheimer's Dis, 2010, doi: 10.4061/20 · DOI
  6. Sochocka M, 2013, CNS Neurol Disord Drug Targets
  7. Lampron A, 2013, J Comp Neurol
  8. McLarnon JG, 2012, Am J Neurodegener Dis, 1, 199
  9. Thanopoulou K, 2010, Proc Natl Acad Sci USA, 107, 20816, 10.1073/pnas.1005888107 · DOI · Paper page
  10. Pflanzner T, 2010, Neurobiol Aging, 32, 2323
  11. Lee KW, 2009, J Neurochem, 108, 165
  12. 10.1002/glia.10108 · DOI
  13. Eckman EA, 2005, Biochem Soc Trans, 33, 1101, 10.1042/BST0331101 · DOI
  14. 10.1111/j.14714159.2010.06899.x · DOI
  15. Zou K, 2008, Rev Neurosci, 19, 203
  16. 10.1523/JNEUROSCI.0616-08.2008 · DOI · Paper page
  17. Chiarini A, 2006, Ital J Anat Embryol, 111, 221
  18. Samuelsson M, 2005, Int J Mol Med, 16, 449
  19. Yan SD, 1998, Restor Neurol Neurosci, 12, 167
  20. Gan L, 2004, J Biol Chem, 279, 5565, 10.1074/jbc.M306183200 · DOI
  21. Lee HS, 2007, Pharmazie, 62, 937
  22. Wilkinson K, 2012, Int J Alzheimer's Dis, 2012, 489456
  23. Nakamura K, 2006, J Neurosci Res, 84, 874, 10.1002/jnr.20992 · DOI
  24. Christie RH, 1996, Am J Pathol, 148, 399

Cited by

Sorted by citations

See all 587

Related

Metadata

Authors
Cai, Z., Hussain, M. D., & Yan, L.-J.
Affiliations
  • Anhui Medical University (CN)
  • Texas A&M Health Science Center (US)
  • University of North Texas Health Science Center (US)
Corresponding author
Cai, Zhiyou
ORCID
Venue
International Journal of Neuroscience
Publisher
Informa UK Limited
Published
2013-09-12
Volume
124
Issue
5
Pages
307-321
ISSN
  • 0020-7454 (ISSN-L)
  • 1543-5245
DOI
10.3109/00207454.2013.833510
OpenAlex
W2096407545
Cited by
583
References
234
Citations by year
2026: 17 · 2025: 45 · 2024: 72 · 2023: 86 · 2022: 67 · 2021: 82 · 2020: 72 · 2019: 54 · 2018: 45 · 2017: 13 · 2016: 14 · 2015: 12 · 2014: 3 · 2013: 1
FWCI
0.97
Type
journal article
Language
en
Open access
closed
Locations
  • International Journal of Neuroscience (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
microglia, neuroinflammation, amyloid-beta, Alzheimer's disease, microglial activation, inflammatory cytokines, complement system, chemokines, free radicals, amyloid plaque clearance, anti-amyloid antibodies, anti-inflammatory therapy
MeSH terms
Alzheimer Disease, Humans, Inflammation, Amyloid beta-Peptides, Microglia

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