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Disease

Neuroinflammatory Diseases

Active therapeutic pipelineExtensively researchedRising momentum
116
Publications
1
Clinical trials
12
Related conditions
1
Related treatments
10
Related proteins
2025
Latest publication
Current focus
Amyloid beta biologyTau biologyTherapeutic developmentGenetics & risk factorsInflammation & immunityMetabolic & lifestyle factors
Latest activity
beta

Recent clinical, regulatory, research and industry developments relating to this disease.

Neuroinflammation across neurological diseases.

Research2025-06-19Science (New York, N.Y.)

The Role of Cytokines in Postherpetic Neuralgia.

Research2025-04-01Journal of integrative neuroscience

What's happening now

An analyst briefing on current research, clinical, regulatory and industry activity surrounding this disease.

Executive briefingUpdating summary…Momentum: Low
Key developments
  • 1 clinical trial expected to report results, the earliest in Q2 2030.
  • Active recent publication activity.

Research-associated treatments

Drugs and agents co-studied with this disease across the research literature — associative, not necessarily established treatments. Number shows shared papers.

Clinical trials

1 sponsors · 0 new · 0 completed in the last 12 months (net +0)

The current development programme across all trial phases.

Clinical programme
1
All trials
1
Active
0
Late-stage
0
Completed
Recruiting

Research activity

116 papers

Key research shaping understanding of this disease, combining the latest publications with the most influential evidence.

Publications over time
20212025
Most influential

Microglia in neurodegenerative diseases: mechanism and potential therapeutic targets.

Signal transduction and targeted therapy · 2023 · 998 cites

Role of neuroinflammation in neurodegeneration development.

Signal transduction and targeted therapy · 2023 · 904 cites

An Overview of Oxidative Stress, Neuroinflammation, and Neurodegenerative Diseases.

International journal of molecular sciences · 2022 · 672 cites

NAD<sup>+</sup> supplementation reduces neuroinflammation and cell senescence in a transgenic mouse model of Alzheimer's disease via cGAS-STING.

Proceedings of the National Academy of Sciences of the United States of America · 2021 · 387 cites
Recent publications
Major themes8
  • Neuroinflammatory Diseases46
  • Alzheimer Disease27
  • Neurodegenerative Diseases15
  • Microglia12
  • Nervous System Diseases12
  • Gastrointestinal Microbiome11
  • Cognitive Dysfunction8
  • Parkinson Disease8
Leading journals6
  • Journal of neuroinflammation14
  • International journal of molecular sciences11
  • Frontiers in immunology10
  • Cells7
  • Scientific reports3
  • Aging and disease2
Leading researchers8
  • Li Y6
  • Zhang Y5
  • Chen Y4
  • Zhao Y4
  • Li Q3
  • Liu X3
  • Wang Y3
  • Yang J3
Affiliations (unnormalised)6
  • School of Medicine11
  • Harvard Medical School3
  • Johns Hopkins University School of Medicine3
  • Medical School3
  • University of California3
  • Department of Anesthesiology and Center for Shock2

Disease biology

10 matches

Key proteins & gene products studied in this disease. Number shows shared papers.

Related conditions

12 matches

Diseases frequently studied alongside this one. Number shows shared papers.

Disease profile

A grounded synthesis of the condition — overview, causes, mechanism, risk factors and current standard of care.

Overview

Neuroinflammatory diseases are disorders characterized by inflammation of nervous tissue. The literature grounding frames this as a broad category that includes conditions in which central nervous system immune responses are prominent and may contribute to tissue injury and neurodegeneration.

Causes

The grounding supports several causes or triggers, including CNS injury, infection, toxicity, and autoimmunity. It also notes that neuroinflammation can arise from genetic variations in CNS cells or from peripheral immune cell involvement, and that protein aggregates can induce inflammatory responses.

Pathophysiology

The core mechanism is activation and dysregulation of CNS immune cells, especially microglia and astrocytes, with release of cytokines and other inflammatory mediators. The literature also links neuroinflammation with oxidative stress, blood-brain barrier dysfunction, peripheral immune cell infiltration, and impaired clearance or propagation of misfolded protein aggregates. Chronic or excessive inflammation can worsen neuronal injury and contribute to neurodegeneration.

Risk factors

Supported risk factors include CNS injury, infection, toxicity, and autoimmunity. The grounding also indicates susceptibility associated with genetic variation in CNS cells, peripheral immune cell infiltration, aging, oxidative stress, and the presence of misfolded protein aggregates.

Current standard of care

The supplied grounding does not support a single standard treatment for neuroinflammatory diseases as a category. It only indicates that the literature covers drug therapy and therapy broadly, and discusses potential therapeutic targeting of microglia, oxidative stress, and inflammatory pathways rather than a defined class-based standard of care.

AI-generated summary grounded in MeSH and 6 peer-reviewed sources. Informational only — not medical advice. Generated 2026-07-07.

Reference

Authoritative identity, definition & identifiers.

Defined in MeSH

Diseases characterized by inflammation of the nervous tissue.

References & data sources
  • Disease identity & definition — NLM Medical Subject Headings (MeSH), public domain
  • Clinical trials — ClinicalTrials.gov (U.S. National Library of Medicine)
  • Research activity — Europe PMC (EMBL-EBI) + OpenAlex-derived paper links
  • Related entities are derived from literature co-mention (studied together) — associative, not causal.