Cited by 85Neuroinflammation and Neurodegeneration MechanismsAlzheimer's disease research and treatmentsDementia and Cognitive Impairment Research

The Potential Role of Cytokines and Growth Factors in the Pathogenesis of Alzheimer’s Disease

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Ogunmokun, Gilbert, Dewanjee, Saikat, Chakraborty, Pratik, Valupadas, Chandrasekhar, Chaudhary, Anupama, Kolli, Viswakalyan, Anand, Uttpal, Vallamkondu, Jayalakshmi +6 more·2021·Cells

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Abstract

Alzheimer’s disease (AD) is one of the most prominent neurodegenerative diseases, which impairs cognitive function in afflicted individuals. AD results in gradual decay of neuronal function as a consequence of diverse degenerating events. Several neuroimmune players (such as cytokines and growth factors that are key players in maintaining CNS homeostasis) turn aberrant during crosstalk between the innate and adaptive immunities. This aberrance underlies neuroinflammation and drives neuronal cells toward apoptotic decline. Neuroinflammation involves microglial activation and has been shown to exacerbate AD. This review attempted to elucidate the role of cytokines, growth factors, and associated mechanisms implicated in the course of AD, especially with neuroinflammation. We also evaluated the propensities and specific mechanism(s) of cytokines and growth factors impacting neuron upon apoptotic decline and further shed light on the availability and accessibility of cytokines across the blood-brain barrier and choroid plexus in AD pathophysiology. The pathogenic and the protective roles of macrophage migration and inhibitory factors, neurotrophic factors, hematopoietic-related growth factors, TAU phosphorylation, advanced glycation end products, complement system, and glial cells in AD and neuropsychiatric pathology were also discussed. Taken together, the emerging roles of these factors in AD pathology emphasize the importance of building novel strategies for an effective therapeutic/neuropsychiatric management of AD in clinics.

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  • Numerous cytokines and chemokines have been shown to contribute to the pathogenesis of neurodegenerative diseases.

    “Numerous cytokines and chemokines have been shown to contribute to the pathogenesis of neurodegenerative diseases as summarized by the recent reviews.9,253,412”

    From Role of neuroinflammation in neurodegeneration development (2023) · cites this paper as [412]

    The Introduction says cytokines and chemokines play key roles in neurodegeneration in Alzheimer’s disease, and Section 4 describes how they contribute to its inflammatory cycle and plaque formation. The review supports the claim for Alzheimer’s disease and AD-like conditions, but does not establish it across neurodegenerative diseases generally. (LLM, conf=0.82)

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Authors
Ogunmokun, G., Dewanjee, S., Chakraborty, P., Valupadas, C., Chaudhary, A., Kolli, V., Anand, U., Vallamkondu, J., Goel, P., Paluru, H. P. R., Gill, K. D., Reddy, P. H., De Feo, V., & Kandimalla, R.
Affiliations
  • The University of Texas Health Science Center at Houston (US)
  • Jadavpur University (IN)
  • Kakatiya Medical College (IN)
  • Orinin-BioSystems, LE-52, Lotus Road 4, CHD City, Karnal 132001, India
  • GITAM University (IN)
  • Ben-Gurion University of the Negev (IL)
  • National Institute of Technology Warangal (IN)
  • Maharishi Markandeshwar University, Mullana (IN)
  • Sri Krishnadevaraya University (IN)
  • Post Graduate Institute of Medical Education and Research (IN)
  • Texas Tech University (US)
  • Department of Pharmacy, University of Salerno, 84084 Fisciano, Italy
Corresponding author
Kandimalla, Ramesh
Venue
Cells
Publisher
MDPI AG
Published
2021-10-18
Volume
10
Issue
10
Pages
2790
ISSN
2073-4409 (ISSN-L)
OpenAlex
W3205901847
Cited by
85
References
22
Citations by year
2026: 10 · 2025: 24 · 2024: 18 · 2023: 20 · 2022: 12 · 2021: 1
FWCI
1.52
Type
journal article
Language
en
Open access
Locations
  • Cells (publishedVersion, cc-by)
  • Preprints.org (acceptedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
  • Jadavpur University
  • Department of Biotechnology, Ministry of Science and Technology, India (BT/RLF/Re-entry/22/2016, 102/IFD/SAN/1117/2018-19)
  • Council of Scientific and Industrial Research, India (02(0275)/16/EMR-II)
Topics
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
Keywords
Alzheimer's disease, cytokines, growth factors, neuroinflammation, microglial activation, neuronal apoptosis, blood-brain barrier, choroid plexus, macrophage migration, neurotrophic factors, hematopoietic growth factors, tau phosphorylation, advanced glycation end products, complement system, glial cells, neuropsychiatric symptoms
MeSH terms
Alzheimer Disease, Humans, Inflammation, Models, Biological, Cytokines, Chemokines, Intercellular Signaling Peptides and Proteins

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 ›

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