Cited by 143Alzheimer's disease research and treatmentsNeuroinflammation and Neurodegeneration MechanismsMedicinal Plants and Neuroprotection

Neuroinflammation and Alzheimer's disease: critical roles for cytokine/Aβ-induced glial activation, NF-κB, and apolipoprotein E

Bales, K·2000·Neurobiology of Aging

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Crossref · 10.1016/s0197-4580(00)00143-3

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2 of 2 references verified0 citation errors · 0 not checkable

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  • Glial activation and subsequent apoE induction appear to be mediated, at least in part, by the nuclear factor-κb (NF-κb) transcription factor.

    “Glial activation and subsequent apoE induction appear to be mediated, at least in part, by the nuclear factor-κb (NF-κb) transcription factor (Bales et al., 2000).”

    From The role of apolipoprotein E in Alzheimer's disease (2009) · cites this paper as Bales et al., 2000

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Authors
Bales, K.
Affiliations
Eli Lilly (United States) (US)
Corresponding author
Bales, K
Venue
Neurobiology of Aging
Publisher
Elsevier BV
Published
2000-06
Volume
21
Issue
3
Pages
427-432
ISSN
0197-4580 (ISSN-L)
OpenAlex
W1999584554
Cited by
143
References
2
Citations by year
2026: 3 · 2025: 4 · 2023: 3 · 2022: 9 · 2021: 6 · 2020: 6 · 2019: 2 · 2018: 2 · 2017: 5 · 2016: 7 · 2015: 7 · 2014: 10 · 2013: 7 · 2012: 8
FWCI
2.94
Type
journal article
Language
en
Open access
closed
Locations
  • Neurobiology of Aging (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Health Sciences › Medicine › Complementary and alternative medicine › Medicinal Plants and Neuroprotection
Keywords
Alzheimer's disease, neuroinflammation, amyloid-beta, phytochemicals, acetylcholinesterase inhibition, beta-secretase, caspase-3, oxidative stress, Nrf2/HO-1 pathway, NF-κB signaling, glial activation, cognitive impairment, memory impairment, neuroprotection, apoptosis
MeSH terms
Alzheimer Disease, Animals, Apolipoproteins E, Humans, Inflammation, Macrophage Activation, Mice, Transgenic, Neuroglia, Cytokines, Amyloid beta-Peptides, NF-kappa B, Mice

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