Back to discover
Disease

Brain Ischemia

Late-stage therapeutic developmentActively researchedSteady momentum
25
Publications
12
Clinical trials
10
Related conditions
4
Related proteins
2025
Latest publication
Current focus
Amyloid biologyTau biologyTherapeutic developmentInflammation & immunity
Latest activity
beta

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

Early neurological deterioration in acute lacunar ischemic stroke: Systematic review of incidence, mechanisms, and prospects for treatment.

Research2024-09-05International journal of stroke : official journal of the International Stroke Society

TRPM2 and CaMKII Signaling Drives Excessive GABAergic Synaptic Inhibition Following Ischemia.

Research2024-05-08The Journal of neuroscience : the official journal of the Society for 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
  • 2 clinical trials with recent milestones (1 completed or reporting results).

Clinical trials

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

The current development programme across all trial phases.

Clinical programme
12
All trials
1
Active
7
Late-stage
6
Completed
Late-stage studies
Recently completed

Research activity

25 papers

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

Publications over time
20062025
Most influential

Thrombolysis with alteplase 3 to 4.5 hours after acute ischemic stroke.

The New England journal of medicine · 2008 · 4,724 cites

Endovascular therapy for ischemic stroke with perfusion-imaging selection.

The New England journal of medicine · 2015 · 4,231 cites

A neurovascular niche for neurogenesis after stroke.

The Journal of neuroscience : the official journal of the Society for Neuroscience · 2006 · 659 cites

NMDA receptor subunits have differential roles in mediating excitotoxic neuronal death both in vitro and in vivo.

The Journal of neuroscience : the official journal of the Society for Neuroscience · 2007 · 617 cites
Recent publications
Major themes8
  • Brain Ischemia10
  • Stroke7
  • Ischemic Stroke4
  • Alzheimer Disease2
  • Cardiovascular Diseases2
  • Reperfusion Injury2
  • Adaptive Immunity1
  • Amyloid1
Leading journals6
  • The Journal of neuroscience : the official journal of the Society for Neuroscience6
  • International journal of molecular sciences4
  • The Journal of clinical investigation2
  • The New England journal of medicine2
  • Discovery medicine1
  • European heart journal1
Leading researchers8
  • Pluta R3
  • Xu Y3
  • Biernaskie J2
  • Chen X2
  • Chen Y2
  • Corbett D2
  • Li L2
  • Markus HS2
Affiliations (unnormalised)6
  • Department of Clinical Neurosciences3
  • Medical University of Lublin3
  • Affiliated Drum Tower Hospital2
  • Memorial University of Newfoundland2
  • School of Medicine2
  • 60521 Ege University1

Disease biology

4 matches

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

Related conditions

10 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

Brain ischemia is a localized reduction of blood flow to brain tissue caused by arterial obstruction or systemic hypoperfusion. It often occurs together with brain hypoxia, and if prolonged it can progress to brain infarction and focal tissue death.

Causes

It is caused by arterial obstruction or systemic hypoperfusion. The literature grounding also describes ischemic stroke as resulting from occlusion of major cerebral arteries, small-vessel occlusion, atherosclerosis affecting the cerebral circulation, or embolism with a cardiac origin.

Pathophysiology

Reduced cerebral blood flow triggers ischemic injury that can lead to neuronal death, cerebral tissue death, and brain infarction. The grounding also supports roles for excitotoxicity, oxidative stress, inflammatory responses, neuroinflammation, blood-brain barrier disruption, cerebral edema, hemorrhagic transformation, and ischemia/reperfusion injury, with later phases contributing to tissue repair and functional recovery.

Risk factors

The supplied grounding supports systemic blood pressure as a factor influencing infarct size and neurological severity. It also supports vascular causes of ischemic stroke such as atherosclerosis, small-vessel disease, and cardiac embolism as contributors to risk, but does not provide a broader risk-factor list.

Current standard of care

The grounding supports recanalization-based treatment, including intravenous alteplase and thrombectomy. It also indicates that therapeutic approaches have focused on targeting neuroinflammation and ischemia/reperfusion injury, but does not support more specific standard treatment categories beyond these modalities.

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

Localized reduction of blood flow to brain tissue due to arterial obstruction or systemic hypoperfusion. This frequently occurs in conjunction with brain hypoxia (HYPOXIA, BRAIN). Prolonged ischemia is associated with BRAIN INFARCTION.

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.