Molecular Mechanism and Pathogenesis of Neuroinflammation in Neurological Disorders
A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Neurobiology".
Deadline for manuscript submissions: 25 February 2026
Special Issue Editor
Interests: cerebral amyloid angiopathy; Alzheimer's disease; amyloid-β fibril formation; taxifolin; microglia
Special Issues, Collections and Topics in MDPI journals
Special Issue Information
Dear Colleagues,
The incidence of dementia continues to expand worldwide; however, there are currently no effective therapeutic strategies for this disabling neurocognitive disorder. Therefore, there is an urgent need to elucidate the underlying mechanisms and develop novel therapeutics for the effective treatment of dementia.
Alzheimer’s disease (AD) is one of the main causes of dementia, induced by amyloid-β accumulation and subsequent tau hyperphosphorylation in the brain, which results in neuronal injury and cognitive impairment. Furthermore, cerebrovascular amyloid-β deposition can cause vascular cognitive impairment (VCI). Various mechanisms are involved in eliminating amyloid-β from the brain, and one of them is microglial phagocytosis. Accumulating evidence has further proven the role of microglia in the pathogenesis of these diseases. Amyloid-β accumulation and tau aggregates induce microglial activation, thereby triggering inflammatory responses. Although metabolic diseases such as type 2 diabetes and obesity, as well as aging, also affect microglial function deleteriously and trigger neuroinflammation, the underlying molecular mechanisms are yet to be elucidated. As neuroinflammation is implicated in exacerbating dementia-related brain pathologies, accumulating evidence highlights the need to suppress neuroinflammation to prevent cognitive impairment.
This Special Issue will provide novel insights into the underlying mechanisms, potential targets and/or new agents for suppressing neuroinflammation. Molecular approaches to address the phenotypic shift in microglia from an anti-inflammatory to a proinflammatory state in response to aging or metabolic diseases could allow for a deeper understanding of the pathogenesis of neuroinflammation. Studies on crosstalk between microglia and the other brain cells could also be insightful. Exploring bioactive molecules (e.g., drug repositioning, newly identified substances) that exhibit novel anti-inflammatory effects on microglia should provide significant clues on the regulation of neuroinflammation. We expect this Special Issue to contribute to the development of innovative strategies for preventing and improving AD and related dementias. We welcome original articles and reviews related to this research topic.
Prof. Dr. Masashi Tanaka
Guest Editor
Prof. Dr. Masashi Tanaka
Guest Editor
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Keywords
- Age-related disorders
- Alzheimer’s disease
- Amyloid-
- Bioactive molecules
- Cognitive impairment
- Dementia
- Glial activation
- Microglia
- Neuroinflammation
- Neurological disorders
- Neurotherapeutics
- Tau hyperphosphorylation
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