The neuroimmune-axis and ageing in Parkinson’s Disease
- Submission status
- Open
- Submission deadline
This Collection supports and amplifies research related to SDG 3.
Age is the greatest risk factor for Parkinson’s Disease (PD), yet the contribution of the aging immune system has arguably been underappreciated and understudied to date. Preclinical research has increasingly highlighted the neuroimmune axis as a critical mediator in the ageing-related vulnerability to PD. Ageing promotes a pro-inflammatory environment in the brain, characterized by microglial priming, increased cytokine release, and impaired resolution of inflammation, all of which exacerbate α-synuclein pathology and dopaminergic neuron loss in animal models. Moreover, peripheral immune changes such as increased monocyte infiltration and altered T cell responses further amplify neurodegeneration in the aged brain. These insights support the neuroimmune axis as both a contributor to and a potential therapeutic target for PD in the context of ageing.
This Collection will showcase research that brings additional knowledge to our current understanding of the age-related changes to the neuroimmune axis in the context of PD and how this knowledge may be leveraged for potential therapeutics. We particularly welcome submissions on topics such as:
- Mechanisms underlying age-dependent microglial reactivity and its role in α-synuclein aggregation.
- Mechanisms regulating peripheral immune cell trafficking into the aged brain during early PD pathology.
- The impact of age-related changes in adaptive immunity (e.g., T cell senescence) on neurodegeneration.
- Interactions between systemic inflammation, metabolic ageing, and central immune responses in PD.
- The development and use of peripheral immune signatures as biomarkers to monitor immune aging and disease risk.
- Inflammaging and how this may relate to disease progression and/or severity in PD.
- Sex and immune aging differences in PD and healthy aging.
- Imaging neuroinflammation and age-related changes in neuroinflammation in humans.
Editors
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Muthuraman Muthuraman, PhD
Institute of Computer Science, Augsburg, Germany Universitätsklinikum Würzburg Department of Neurology, Germany
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Rebecca Wallings, DPhil
Stark Neurosciences Research Institute, Department of Neurology, Indiana University, United States
The Collection will publish original research Articles, Reviews, Perspectives and Comments (full details on content types can be found here). Papers will be published in npj Parkinson's Disease as soon as they are accepted and then collected together and promoted on the Collection homepage. All Guest Edited Collections are associated with a call for papers and are managed by one or more of our Editorial Board Members and the journal's Editors.
This Collection welcomes submissions from all authors – and not by invitation only – on the condition that the manuscripts fall within the scope of the Collection and of npj Parkinson's Disease more generally. See our editorial process page for more details.
All submissions are subject to the same peer review process and editorial standards as regular npj Parkinson's Disease articles, including the journal’s policy on competing interests. The Guest Editors have no competing interests with the submissions, which they handle through the peer-review process. The peer review of any submissions for which the Guest Editors have competing interests is handled by another Editorial Board Member who has no competing interests. See our Collections guidelines for more details.
This Collection is not supported by sponsorship.
