Neuroimmune Crosstalk in Neurological Disorders: Mechanistic Insights to Therapeutic Interventions

A special issue of Brain Sciences (ISSN 2076-3425). This special issue belongs to the section "Molecular and Cellular Neuroscience".

Deadline for manuscript submissions: 31 March 2026 | Viewed by 275

Special Issue Editor


E-Mail Website
Guest Editor
LSUHSC Neuroscience Center, New Orleans, LA, USA
Interests: neuropharmacology and toxicology; molecular neuroscience and neural circuit development; brain insulin resistance and neurodegeneration; preclinical models of Alzheimer’s disease
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The brain has long been considered as an organ that is independent from the immune system, but several studies from last few decades have provided insights into a complex and vital interplay between the central nervous system and the immune system. In addition, cytokine disparity, microglial activation, and immune dysregulation have recently been noted as commonly occurring pathological hallmarks across multiple brain disorders. In this regard, neuroimmune crosstalk has been found to play a critical role in the pathophysiological aspects of numerous neurodegenerative, neurodevelopmental, and neuropsychiatric disorders, including multiple sclerosis, Alzheimer’s disease, Parkinson’s disease, depression, schizophrenia, epilepsy, and autism.

This Special Issue focuses on the mechanisms of neuroimmune interaction and underscores the breakthrough advances made in targeting these pathways as a form of therapeutic intervention. We welcome the submission of original research articles, reviews, and short communications that present novel insights into immune cascades in the brain and their implications for neuronal degeneration, function, therapy, and repair.

Dr. Ansab Akhtar
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 250 words) can be sent to the Editorial Office for assessment.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Brain Sciences is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2200 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • neuroinflammation
  • neuroimmune system
  • glial cell dynamics
  • immune cell trafficking
  • cyto-kine signaling
  • neurological disorders
  • immune modulation

Benefits of Publishing in a Special Issue

  • Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
  • Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • Reprint: MDPI Books provides the opportunity to republish successful Special Issues in book format, both online and in print.

Further information on MDPI's Special Issue policies can be found here.

Published Papers (1 paper)

Order results
Result details
Select all
Export citation of selected articles as:

Review

28 pages, 841 KB  
Review
Neuroimmune Interactions in Neurodegeneration: The Role of Microglia in Alzheimer’s and Parkinson’s Disease Pathogenesis
by Pradeep Goyal, Lalji Baldaniya, Lalit Kumar Tyagi, Kamal Kant Joshi, Suhas Ballal, A. Sabarivani, Subhashree Ray, Deepak Nathiya, Ashish Singh Chauhan, Monica Gulati, Tapan Behl and Ansab Akhtar
Brain Sci. 2026, 16(2), 154; https://doi.org/10.3390/brainsci16020154 - 29 Jan 2026
Viewed by 93
Abstract
Neuroimmune interactions play a critical role in the pathogenesis of neurodegenerative disorders such as Alzheimer’s disease (AD) and Parkinson’s disease (PD), with microglia acting as key mediators of neuroinflammation. Microglia exhibit dual roles, contributing to both neuroprotection and neurotoxicity depending on their activation [...] Read more.
Neuroimmune interactions play a critical role in the pathogenesis of neurodegenerative disorders such as Alzheimer’s disease (AD) and Parkinson’s disease (PD), with microglia acting as key mediators of neuroinflammation. Microglia exhibit dual roles, contributing to both neuroprotection and neurotoxicity depending on their activation state. In AD, amyloid-beta (Aβ) aggregation leads to chronic microglial activation, resulting in excessive pro-inflammatory cytokine release (e.g., TNF-α, IL-1β, IL-6), oxidative stress, and synaptic dysfunction. In PD, α-synuclein aggregation triggers a similar neuroinflammatory cascade, exacerbating dopaminergic neuronal loss in the substantia nigra. Beyond inflammatory responses, microglia regulate synaptic plasticity, phagocytose pathological proteins, and interact with peripheral immune cells, influencing disease progression. Emerging evidence suggests that genetic variants in genes such as TREM2, CD33, and HLA modulate microglial function, thereby altering susceptibility to neurodegeneration. Dysregulated microglial responses, characterized by impaired clearance of protein aggregates and prolonged neuroinflammation, further amplify neuronal damage. Therapeutic strategies targeting microglial activation are under investigation, aiming to balance neuroinflammatory responses and enhance clearance mechanisms. Small-molecule inhibitors, monoclonal antibodies, and modulators of innate immune pathways are being explored to mitigate microglia-driven pathology. Understanding the complex interplay between microglia and neurodegeneration could pave the way for precision medicine approaches, optimizing treatments based on individual immune profiles. Further research is essential to delineate microglial heterogeneity across disease stages and uncover novel targets for therapeutic intervention. Full article
Back to TopTop