The Effects of Music on Inflammation: A Bibliometric Study from 1989 to 2024

 

 I bet your incompetent? doctor never created a music protocol for your stroke recovery and this will do nothing to change that mind! How long before s/he is fired for incompetence?

music (94 posts back to March 2011)

music therapy (85 posts back to October 2014)

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singing (12 posts to July 2013)

• music playing (2 posts to April 2023)

The Effects of Music on Inflammation: A Bibliometric Study from 1989 to 2024

Authors Saleh AY ORCID logo, Yogi Saputra DA, Valentina R, Susanto TD

Received 4 November 2025

Accepted for publication 4 August 2026

Published 21 August 2026 Volume 2026:19 562618

DOI https://doi.org/10.2147/JIR.S562618

Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 2

Editor who approved publication: Professor Ning Quan

Abstract: 

This bibliometric study maps the scientific landscape of research on music and inflammation from 1989 to 2024. Using Scopus data analyzed through Biblioshiny and VOSviewer, we examined publication trends, influential authors, thematic evolution, and co‑occurrence patterns of inflammation‑related biomarkers. The expanded search strategy incorporated biological mediators such as cytokines, IL‑6, TNF‑α, CRP, and cortisol to ensure comprehensive coverage of mechanistic literature. Results show a shift from early musculoskeletal‑focused studies to recent clinical applications of music in systemic inflammatory conditions. Co‑occurrence analysis highlights cortisol and stress‑related pathways as dominant research themes, while detailed music‑type reporting remains limited. This study identifies key research gaps and proposes standardized frameworks for future biomarker‑based investigations of music interventions.

Study offers insight into how long-term inflammation may contribute to cognitive decline

Is your competent? doctor testing for this AND HAS EXACT PROTOCOLS TO STOP THE INFLAMMATION? NO? So, escaping responsibility and just blaming the stroke for your cognitive decline! I'd suggest screaming and talking to the president to get this person fired! 

 Study offers insight into how long-term inflammation may contribute to cognitive decline

The King's College London study, published in Nature Communications, offers insight into how long-term inflammation may contribute to cognitive decline in disorders such as Alzheimer's disease, aging, depression, and the lingering neurological effects of viral infections.

The scientists discovered that adding a molecule, that is involved in the inflammatory response, to stem cells from the hippocampus prevents the development of new neurons. The formation of new neurons in this region, known as hippocampal neurogenesis, is essential for learning, memory and mood regulation. It is one of the few parts of the human brain where new neurons are made in adults. Altered adult hippocampal neurogenesis is associated with aging, neurodegeneration, and mood disorders such as depression.

The study focused on cytokines, which are chemical signals that are released by the body in response to a threat, such as a viral infection. Cytokines ultimately act as triggers for the rest of the immune response, which helps the body fight the infection. High cytokine levels are also a hallmark of chronic inflammation.

Viral infection has previously been linked to changes in the ability to create new neurons in part of the hippocampus. However, how exactly infection and inflammatory cytokines affect creation of new neurons was previously unknown.

When researchers added one particular cytokine, called TNF‑α, to human hippocampal stem cells, it prevented them from developing into neurons. Instead, they switched into an "immune alert" state, releasing signals that can attract key immune cells, known as T cells, that drive inflammation, while simultaneously reducing the production of new nerve cells.

First author Dr Tinne A. D. Nissen, who completed the research as part of her PhD at King's College London, said: "What surprised us most was that the stem cells were not simply impaired by inflammation, they actively adopted behaviors that could potentially sustain immune responses in the brain."

Our findings reveal a new link between chronic inflammation and the brain's reduced ability to generate new neurons.

Inflammatory signals can effectively redirect hippocampal stem cells away from their normal role of producing neurons and toward supporting immune activity instead."

Professor Sandrine Thuret, co-corresponding author, Professor of Neuroscience, King's College London

The researchers also identified an unexpected signalling pathway behind this effect involving type I interferons, molecules typically associated with the body's antiviral defense. By blocking interferon signalling with an existing therapeutic antibody, some of the effects of inflammation were reversed – by restoring production of new neurons and preventing the attraction of T cells involved in the immune response.

Co-corresponding author Professor Linda S. Klavinskis, Professor of Viral Immunology, King's College London, added: "Our work uncovers a new mechanism that may help explain why ongoing inflammation is so damaging to brain health. Importantly, it also points to possible treatments to protect or restore the brain's regenerative capacity."

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This research was a collaboration between the Department of Infectious Diseases at the Faculty of Life Sciences & Medicine and the Department of Basic and Clinical Neuroscience at the Institute of Psychiatry, Psychology & Neuroscience, King's College London.

This research was funded by the Wellcome Trust as part of the "Neuro-Immune Interactions in Health & Disease Wellcome Trust PhD Programme, the Medical Research Council UK, a Medical Research Council Discovery Award, a PhD Studentship awarded by the Medical Research Council UK, The Galen and Hilary Weston Foundation, the National Institute for Health Research (NIHR) Biomedical Research Centre based at Guy's and St Thomas' NHS Foundation Trust and King's College London.

Source:

King's College London

Journal reference:

Nissen, T. A. D., et al. (2026) TNF-α induces type I IFN signalling to suppress neurogenesis and recruit T cells. Nature Communications. DOI: 10.1038/s41467-026-74104-x. https://www.nature.com/articles/s41467-026-74104-x

Molecular 'switch' reverses chronic inflammation and aging

I would much rather use this route to reduce the risk of stroke and heart attacks since inflammation is the reason cholesterol is grabbed out of the bloodstream and packed into plaque. Now if we can get our doctors and stroke hospitals to ensure further research is done to create an intervention for this. But since your hospital has never ensured earlier research is done, this will not be completed either. Oh well, we'll just have to wait until stroke survivors are in charge.

Molecular 'switch' reverses chronic inflammation and aging

ScienceDaily | February 07, 2020

Chronic inflammation, which results when old age, stress or environmental toxins keep the body's immune system in overdrive, can contribute to a variety of devastating diseases, from Alzheimer and Parkinson to diabetes and cancer.
Now, scientists at the University of California, Berkeley, have identified a molecular "switch" that controls the immune machinery responsible for chronic inflammation in the body. The finding, which appears online Feb. 6 in the journal Cell Metabolism, could lead to new ways to halt or even reverse many of these age-related conditions.
"My lab is very interested in understanding the reversibility of aging," said senior author Danica Chen, associate professor of metabolic biology, nutritional sciences and toxicology at UC Berkeley. "In the past, we showed that aged stem cells can be rejuvenated. Now, we are asking: to what extent can aging be reversed? And we are doing that by looking at physiological conditions, like inflammation and insulin resistance, that have been associated with aging-related degeneration and diseases."
In the study, Chen and her team show that a bulky collection of immune proteins called the NLRP3 inflammasome—responsible for sensing potential threats to the body and launching an inflammation response—can be essentially switched off by removing a small bit of molecular matter in a process called deacetylation.
Overactivation of the NLRP3 inflammasome has been linked to a variety of chronic conditions, including multiple sclerosis, cancer, diabetes and dementia. Chen's results suggest that drugs targeted toward deacetylating, or switching off, this NLRP3 inflammasome might help prevent or treat these conditions and possibly age-related degeneration in general.

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"This acetylation can serve as a switch," Chen said. "So, when it is acetylated, this inflammasome is on. When it is deacetylated, the inflammasome is off."
By studying mice and immune cells called macrophages, the team found that a protein called SIRT2 is responsible for deacetylating the NLRP3 inflammasome. Mice that were bred with a genetic mutation that prevented them from producing SIRT2 showed more signs of inflammation at the ripe old age of two than their normal counterparts. These mice also exhibited higher insulin resistance, a condition associated with type 2 diabetes and metabolic syndrome.
The team also studied older mice whose immune systems had been destroyed with radiation and then reconstituted with blood stem cells that produced either the deacetylated or the acetylated version of the NLRP3 inflammasome. Those who were given the deacetylated, or "off," version of the inflammasome had improved insulin resistance after six weeks, indicating that switching off this immune machinery might actually reverse the course of metabolic disease.
"I think this finding has very important implications in treating major human chronic diseases," Chen said. "It's also a timely question to ask, because in the past year, many promising Alzheimer's disease trials ended in failure. One possible explanation is that treatment starts too late, and it has gone to the point of no return. So, I think it's more urgent than ever to understand the reversibility of aging-related conditions and use that knowledge to aid a drug development for aging-related diseases."