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Related Concept Videos

Ischemic Stroke ll: Pathophysiology01:15

Ischemic Stroke ll: Pathophysiology

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An ischemic stroke occurs when a cerebral blood vessel becomes obstructed, most often by a thrombus or embolus, interrupting the delivery of oxygen and glucose to brain tissue. Because neurons rely on continuous aerobic metabolism, energy failure begins within minutes of reduced perfusion. The region receiving the least blood flow becomes the infarct core, an area of irreversible cellular death. Surrounding this core lies the penumbra, a zone of hypoperfused but still viable tissue that is...
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Encephalitis ll: Pathophysiology01:26

Encephalitis ll: Pathophysiology

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Encephalitis is inflammation of the brain parenchyma caused by direct viral invasion or immune-mediated mechanisms triggered by infections or tumors. Both processes lead to neuronal injury, disrupted neurotransmission, and diverse neurological symptoms, often with overlapping clinical and pathological features.Autoimmune EncephalitisIn autoimmune encephalitis, antibodies target neuronal antigens on cell surfaces, synapses, or within neurons. A key example is anti-NMDAR encephalitis, which can...
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Hemorrhagic Stroke ll: Pathophysiology01:29

Hemorrhagic Stroke ll: Pathophysiology

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A hemorrhagic stroke develops when a cerebral blood vessel ruptures, allowing blood to escape into the surrounding brain tissue, as in intracerebral hemorrhage (ICH), or into the subarachnoid space, as in subarachnoid hemorrhage (SAH). Because the skull is a rigid compartment, the sudden presence of extravascular blood rapidly increases intracranial pressure and compresses adjacent neural structures, leading to immediate tissue injury and impaired cerebral perfusion.Mass Effect and Primary...
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Ischemic Stroke l: Introduction01:15

Ischemic Stroke l: Introduction

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Ischemic stroke is an acute cerebrovascular condition in which blood flow to a brain region is suddenly interrupted, leading to tissue infarction. Neurons depend on continuous oxygen and glucose supply, so even brief reductions in perfusion cause energy failure, ionic imbalance, and irreversible injury. Ischemic strokes are classified into thrombotic and embolic types based on their underlying mechanisms.Thrombotic MechanismsThrombotic stroke develops when a clot forms within a cerebral artery.
38
Cerebral Edema ll: Pathophysiology01:22

Cerebral Edema ll: Pathophysiology

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Vasogenic edema is a major form of cerebral edema characterized by abnormal accumulation of fluid in the brain’s extracellular space due to disruption of the blood–brain barrier (BBB). The BBB is a specialized structure composed of endothelial cells connected by tight junctions, supported by astrocytic endfeet and a basement membrane. Under normal conditions, it tightly regulates the movement of ions, proteins, and solutes between the bloodstream and brain parenchyma. When this...
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Bacterial Meningitis II: Pathophysiology01:26

Bacterial Meningitis II: Pathophysiology

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Bacterial meningitis typically begins when pathogens such as Neisseria meningitidis and Streptococcus pneumoniae colonize the nasopharynx and invade the bloodstream. This process is facilitated by bacterial virulence factors, such as polysaccharide capsules, which resist phagocytosis and complement-mediated killing. Less commonly, bacteria reach the central nervous system via contiguous spread from infections like otitis media or sinusitis, through congenital or acquired dural defects, or...
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Related Experiment Video

Updated: Apr 29, 2026

AAV Systems and Mouse Models for Investigating Ectopic Expression of Neurod1 in Transduced Cells at Subacute and Chronic Times Post-Ischemic Stroke
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Perivascular SPP1 Drives Microglial Synaptic Engulfment After Ischemic Stroke.

Chenchen Xu1,2,3, Xiaoxiao Li1, Nan Cheng1,3

  • 1Institute of Neurology, Anhui University of Chinese Medicine, Hefei, China.

CNS Neuroscience & Therapeutics
|April 28, 2026
PubMed
Summary

Targeting perivascular SPP1 in ischemic stroke (IS) reduces harmful microglia activity, preserves brain tissue and function, and offers a new therapeutic approach. This study highlights SPP1

Keywords:
barrier integrityglial‐vascular unitischemic strokemicroglia synaptic engulfmentperivascular signaling

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Area of Science:

  • Neuroscience
  • Immunology
  • Vascular Biology

Background:

  • Microglia activation post-ischemic stroke (IS) can exacerbate neuronal damage and blood-brain barrier (BBB) disruption.
  • The specific vascular signals initiating detrimental microglia activity during IS are not fully understood.

Purpose of the Study:

  • To investigate the role of perivascular secreted phosphoprotein 1 (SPP1) in regulating microglia-mediated synaptic engulfment during IS.
  • To determine if SPP1 is a key vascular-derived signal that drives neuroinflammation and synaptic damage after IS.

Main Methods:

  • Mice underwent middle cerebral artery occlusion/reperfusion (MCAO/R) with or without SPP1 silencing (shSpp1).
  • Assessed cerebral perfusion, neuronal injury (Nissl, TUNEL), synaptic remodeling (proteomics, electron microscopy, immunofluorescence), glial-vascular unit (GVU) integrity, and behavioral outcomes.
  • Examined microglial synaptic engulfment in vivo and synaptic protein/mRNA levels in vitro.

Main Results:

  • MCAO/R led to increased microglial synaptic engulfment, synaptic damage, and reduced synaptic proteins in the ischemic penumbra.
  • Proteomic analysis revealed upregulated inflammatory and vascular pathways, with increased SPP1 from perivascular macrophages.
  • SPP1 silencing attenuated neuroinflammation, reduced infarct volume, improved perfusion, preserved GVU integrity, and improved behavioral deficits.

Conclusions:

  • Perivascular SPP1 drives excessive microglia-mediated synaptic engulfment and synaptic damage following IS.
  • Targeting SPP1 suppresses detrimental microglia activity, preserves BBB integrity and synaptic architecture.
  • SPP1 presents a potential therapeutic target for IS, focusing on the glial-vascular unit.