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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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Dementia l: Introduction01:22

Dementia l: Introduction

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Dementia is an acquired, progressive syndrome characterized by a decline in multiple cognitive domains severe enough to impair daily functioning and reduce independence. Although memory loss is a central feature, the diagnosis requires additional deficits involving language, executive function, visuospatial skills, judgment, calculation, or abstract reasoning. These cognitive impairments reflect underlying neurodegenerative or vascular processes that gradually disrupt neuronal networks...
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Alzheimer Disease ll: Pathophysiology01:23

Alzheimer Disease ll: Pathophysiology

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Alzheimer disease involves structural changes in the brain that begin long before symptoms appear. The most distinctive features are extracellular neuritic plaques and intracellular neurofibrillary tangles.Neuritic plaques form in the cerebral cortex and around blood vessels. These plaques contain a dense core of beta-amyloid (Aβ)—a toxic protein fragment that clumps outside neurons. The core is surrounded by damaged neuronal extensions, as well as reactive astrocytes and...
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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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Parkinson Disease ll: Pathophysiology01:24

Parkinson Disease ll: Pathophysiology

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Parkinson disease (PD) is a progressive neurodegenerative disorder primarily affecting movement, with additional non-motor features. Its pathophysiology involves complex interactions among genetic susceptibility, environmental exposures, and cellular dysfunction, including dopaminergic neuron loss, protein aggregation, and mitochondrial impairment.Selective NeurodegenerationA key feature is the degeneration of dopaminergic neurons in the substantia nigra pars compacta, leading to reduced...
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Electron Transport Chain: Complex I and II01:46

Electron Transport Chain: Complex I and II

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The mitochondrial electron transport chain (ETC) is the main energy generation system in the eukaryotic cells. However, mitochondria also produce cytotoxic reactive oxygen species (ROS) due to the large electron flow during oxidative phosphorylation. While Complex I is one of the primary sources of superoxide radicals, ROS production by Complex II is uncommon and may only be observed in cancer cells with mutated complexes.
ROS generation is regulated and maintained at moderate levels necessary...
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Updated: May 3, 2026

Evaluation of Bioenergetic Function in Cerebral Vascular Endothelial Cells
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Mitochondrial dysfunction in cerebrovascular diseases.

Fabio Marcheggiani1, Ilaria Nunzi2, Loredana Rao2

  • 1Department of Clinical and Molecular Sciences, Marche Polytechnic University, Ancona, Italy; Department of the Promotion of Human Sciences and Quality of Life, San Raffaele Roma University, Rome, Italy.

Trends in Molecular Medicine
|May 1, 2026
PubMed
Summary
This summary is machine-generated.

Mitochondrial dysfunction is a key factor in cerebrovascular diseases like stroke and aneurysms. Understanding these roles is crucial for developing new treatments and biomarkers for brain blood vessel health.

Keywords:
cerebral malformationsinflammationmitochondriamitochondrial calcium uniporterpermeability transition porestroke

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Area of Science:

  • Neuroscience
  • Cardiovascular Biology
  • Cellular Biology

Background:

  • Mitochondria regulate cerebrovascular health via energy metabolism, calcium (Ca²⁺) homeostasis, and redox signaling.
  • Mitochondrial dysfunction is a common pathogenic mechanism in various cerebrovascular diseases.
  • Dysfunctional mitochondria contribute to neuronal injury, neuroinflammation, and vascular remodeling.

Purpose of the Study:

  • To review the context- and stage-dependent roles of mitochondria in cerebrovascular pathology.
  • To explore the implications of mitochondrial dysfunction for biomarker discovery and therapeutic strategies.

Main Methods:

  • Literature review integrating recent evidence on mitochondria in cerebrovascular diseases.
  • Analysis of mitochondrial roles in ischemic stroke, intracranial aneurysms, atherosclerotic stenosis, and vascular malformations.

Main Results:

  • Mitochondrial failure in ischemic stroke exacerbates neuronal injury and neuroinflammation.
  • Oxidative stress, mitochondrial DNA instability, and metabolic changes drive vascular pathology in conditions beyond stroke.
  • Mitochondrial dynamics and damage-associated molecular patterns significantly impact neuroinflammation.

Conclusions:

  • Mitochondrial dysfunction is a central and convergent mechanism in cerebrovascular diseases.
  • Targeting mitochondria offers potential for novel therapeutic strategies and biomarker development.
  • Further research is needed to translate findings into clinical practice for cerebrovascular disorders.