From Inflammaging to Dementia: Cellular and Molecular Drivers of Cognitive Decline
A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Neuroscience".
Deadline for manuscript submissions: 31 August 2026 | Viewed by 181
Special Issue Editors
2. Neuroscience Institute, University of Tennessee Health Science Center, Memphis, TN, USA
3. Department of Anatomy & Neurobiology, College of Medicine, University of Tennessee Health Science Center, Memphis, TN 38163, USA
Interests: cognitive decline; neuroinflammation; Alzheimer's disease; neurodegeneration; neuroprotection
2. Center for Muscle, Metabolism and Neuropathology, Division of Regenerative and Rehabilitation Sciences and Department of Physical Therapy, College of Health Professions, University of Tennessee Health Science Center, Memphis, TN 38163, USA
3. Neuroscience Institute, University of Tennessee Health Science Center, Memphis, TN 38163, USA
Interests: Alzheimer’s disease; Parkinson’s disease; stroke; DNA damage; neuroinflammation; oxidative stress and antioxidants; regulation of motor function; gut microbiota in neurological diseases; long noncoding RNAs and CNS in regulation of muscle weakness
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Special Issue Information
Dear Colleagues,
Background
Although aging is the dominant risk factor for cognitive decline, dementia, and neurodegenerative diseases, chronological aging alone is insufficient to explain the inter-individual variability in cognitive trajectories observed among older individuals. While some maintain cognitive integrity into late life, others develop progressive impairment that culminates in dementia, indicating that age-associated biological processes shape the susceptibility to cognitive dysfunction. A growing body of evidence implicates neuroinflammation as a central mechanism linking aging, vulnerability to neurodegeneration, and cognitive dysfunction, operating across neurons, glia, vascular cells, and peripheral immune systems.
Inflammaging, characterized by chronic, low-grade activation of inflammatory pathways that accompanies aging, acts as a critical upstream driver of sustained neuroinflammatory states in the aging brain. This process reshapes neuro-immune communication at both the cellular and molecular levels, influencing synaptic function, neuronal resilience, and cerebrovascular integrity. Elucidating these mechanisms is essential for identifying the early drivers of cognitive decline and translating biological insight into effective therapeutic strategies. Addressing these questions requires integrative approaches that span molecular pathways, neural circuits, and brain-wide systems with direct relevance to disease prediction, prevention, and intervention. The scope of this Special Issue includes normal aging, prodromal cognitive impairment, dementia, and neurodegenerative diseases, while emphasizing cell-type specificity, temporal dynamics, and translational relevance.
Aims of This Special Issue
This Special Issue aims to advance our understanding of the role of neuroinflammation in age-related cognitive decline and dementia. Our aims are as follows:
- To define the mechanistic pathways through which aging affects neuro-immune signaling.
- To explore the causal and compensatory roles of neuroinflammation in cognitive decline.
- To integrate the cellular-, circuit-, and systems-level contributions of neuroinflammation to age-related cognitive decline and dementia.
- To describe the emerging tools and therapeutic strategies that target neuro-immune systems.
Prof. Dr. Michael P. McDonald
Dr. Mohammad Moshahid Khan
Guest Editors
Manuscript Submission Information
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Keywords
- neuroimmune crosstalk
- brain-immune signaling
- neuroinflammation
- microglial activation
- astrocytic reactivity
- complement-mediated synaptic loss
- cytokine modulation of synaptic plasticity
- inflammasome signaling
- blood–brain barrier dysfunction
- neurovascular inflammation
- immune-cell trafficking
- synaptic dysfunction
- biomarkers
- DNA damage and repair
- interferons responses
- immune-targeted therapeutics
- cognitive decline
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