Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2025 Mar 28:9:25424823241306772.
doi: 10.1177/25424823241306772. eCollection 2025 Jan-Dec.

Cerebrospinal fluid cytokine levels affect electroencephalographic activity in Alzheimer's disease

Matilde Bruno  1 , Chiara Giuseppina Bonomi  1 , Alessandro Castelli  2 , Francesca Izzi  2 , Fabio Placidi  2 , Silvia Falletti  1 , Nicola Biagio Mercuri  3 , Caterina Motta  1 , Alessandro Martorana  1
Affiliations

Cerebrospinal fluid cytokine levels affect electroencephalographic activity in Alzheimer's disease

Matilde Bruno et al. J Alzheimers Dis Rep. .

Abstract

To investigate the role of neuroinflammation as mediator of amyloid-β-induced cortical activity changes in Alzheimer's disease (AD), we examined the relationship between cerebrospinal fluid (CSF) inflammatory cytokines (IL-1β, IL-2, IL-4, IL-6, IL-7, IL-8, IL-10, IL-12, IL-13, IL-17, TNF-α, IFN-γ, GM-CSF, G-CSF, MIP-1α, MCP-1) and electroencephalographic (EEG) abnormalities in a cohort of biologically defined AD patients (n = 55, M:F = 19:36, median age 73, Mini-Mental State Examination ≥ 22). We retrieved a positive association between IL-4 CSF levels and EEG background activity frequency; IL-7, IL-8, and IL-12 CSF levels were positively associated with the presence of interictal epileptiform discharges. Neuroinflammation accompanying AD pathology may enhance the amyloid's epileptogenic potential while also counteracting neurodegenerative damage.

Keywords: Alzheimer's disease; EEG; cytokines; epileptiform activity; neuroinflammation.

PubMed Disclaimer

Conflict of interest statement

The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

References

    1. Kashyap G, Bapat D, Das D, et al. Synapse loss and progress of Alzheimer’s disease -A network model. Sci Rep 2019; 9: 6555. - PMC - PubMed
    1. Li S, Hong S, Shepardson NE, et al. Soluble oligomers of amyloid β protein facilitate hippocampal long-term depression by disrupting neuronal glutamate uptake. Neuron 2009; 62: 788–801. - PMC - PubMed
    1. Palop JJ, Mucke L. Network abnormalities and interneuron dysfunction in Alzheimer disease. Nat Rev Neurosci 2016; 17: 777–792. - PMC - PubMed
    1. Kazim SF, Seo JH, Bianchi R, et al. Neuronal network excitability in Alzheimer’s disease: the puzzle of similar versus divergent roles of amyloid β and tau. eNeuro 2021; 8: ENEURO.0418-20.2020. - PMC - PubMed
    1. Hiragi T, Ikegaya Y, Koyama R. Microglia after seizures and in epilepsy. Cells 2018; 7: 26. - PMC - PubMed

LinkOut - more resources