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Review
. 2024 Aug 28;148(1):31.
doi: 10.1007/s00401-024-02790-2.

Inflammatory aspects of Alzheimer's disease

Affiliations
Review

Inflammatory aspects of Alzheimer's disease

Pablo Botella Lucena et al. Acta Neuropathol. .

Abstract

Alzheimer´s disease (AD) stands out as the most common chronic neurodegenerative disorder. AD is characterized by progressive cognitive decline and memory loss, with neurodegeneration as its primary pathological feature. The role of neuroinflammation in the disease course has become a focus of intense research. While microglia, the brain's resident macrophages, have been pivotal to study central immune inflammation, recent evidence underscores the contributions of other cellular entities to the neuroinflammatory process. In this article, we review the inflammatory role of microglia and astrocytes, focusing on their interactions with AD's core pathologies, amyloid beta deposition, and tau tangle formation. Additionally, we also discuss how different modes of regulated cell death in AD may impact the chronic neuroinflammatory environment. This review aims to highlight the evolving landscape of neuroinflammatory research in AD and underscores the importance of considering multiple cellular contributors when developing new therapeutic strategies.

Keywords: Activation; Alzheimer’s disease; Cytokine; Immune mediator; Innate immunity; Neurodegeneration; Neuroinflammation.

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References

    1. Abdul HM, Sama MA, Furman JL, Mathis DM, Beckett TL, Weidner AM et al (2009) Cognitive decline in Alzheimer’s disease is associated with selective changes in calcineurin/NFAT signaling. J Neurosci Off J Soc Neurosci 29:12957–12969. https://doi.org/10.1523/JNEUROSCI.1064-09.2009 - DOI
    1. Acosta C, Anderson HD, Anderson CM (2017) Astrocyte dysfunction in Alzheimer disease. J Neurosci Res 95:2430–2447. https://doi.org/10.1002/jnr.24075 - DOI - PubMed
    1. Acosta JC, Banito A, Wuestefeld T, Georgilis A, Janich P, Morton JP et al (2013) A complex secretory program orchestrated by the inflammasome controls paracrine senescence. Nat Cell Biol 15:978–990. https://doi.org/10.1038/ncb2784 - DOI - PubMed - PMC
    1. Alonso AC, Grundke-Iqbal I, Iqbal K (1996) Alzheimer’s disease hyperphosphorylated tau sequesters normal tau into tangles of filaments and disassembles microtubules. Nat Med 2:783–787. https://doi.org/10.1038/nm0796-783 - DOI - PubMed
    1. Alzheimer A (1907) Uber eine eigenartige Erkrankung der Hirnrinde. Zentralbl Nervenh Psych 18:177–179

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