Neuroinflammatory mechanisms play an important role in the progression, or lack thereof, of various aging-associated dementias. Although an active area of research, the complexity of the mechanisms involved leave much work to be done. The current collection of articles explores several specific anti-inflammatory modulators, with mixed results in various models of disease associated with neuroinflammatory damage. Chesworth et al. describe the anti-inflammatory effects of the plant flavonoid Apigenin in a mouse model of chronic neuroinflammation driven by overexpression of astrocyte IL-6. While the compound worked to normalize several markers of microglial inflammation, there was no functional rescue of impaired spatial memory (Chesworth et al.). Similarly, a study by Zajac et al. examined the effect of long-term supplementation of short-chain fatty acids on microbiome and amyloid beta-associated neuropathology in the APPswe/PS1dE9 mouse model of Alzheimer's disease (AD). While they found significant alterations in microbiome, these changes were by themselves insufficient to alter neuropathological or behavioral endpoints. In contrast, treatment with Glatiramer (an FDA-approved treatment for multiple sclerosis) was able to rescue both neuroinflammatory markers as well as behavioral deficits in the combined tau and amyloid 3xTg model of AD (Dionisio-Santos et al.). Taken together, these studies indicate that while systemic administration of anti-inflammatory compounds have the potential to reduce pathology and functional deficits, the details are vital: broadly anti-inflammatory treatments are unlikely to provide much benefit unless they are targeted to key pathologies based on the disease in question. Two reviews aim to synthesize and address some of this nuance: one by Rickenbach and Gericke that describes the role of the adaptive immune response in brain aging, and another by Garland et al. that focuses on the crosstalk between astrocytes and microglia. While the appropriate targeting of neuroinflammatory mechanisms remains a promising strategy in mitigating cognitive decline in the context of aging-associated diseases such as AD, the ongoing challenge remains to better define the “appropriate” targets for each stage and disease.
Publisher's note
All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher.
Statements
Author contributions
DB wrote the editorial. MG, EW, and CS reviewed and approved it. All authors contributed to the article and approved the submitted version.
Conflict of interest
The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
Summary
Keywords
neuroinflammation, aging, dementia, Alzheimer's disease, immune system
Citation
Braun DJ, Weekman EM, Gordon MN and Späni CB (2022) Editorial: Modulation of neuroimmune systems to preserve brain function in aging and dementia. Front. Neurosci. 16:995409. doi: 10.3389/fnins.2022.995409
Received
15 July 2022
Accepted
22 July 2022
Published
03 August 2022
Volume
16 - 2022
Edited and reviewed by
Fabricio Ferreira de Oliveira, Elysian Clinic, Brazil
Updates
Copyright
© 2022 Braun, Weekman, Gordon and Späni.
This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
*Correspondence: David J. Braun david.braun1@uky.edu
This article was submitted to Neurodegeneration, a section of the journal Frontiers in Neuroscience
Disclaimer
All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.