Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Cerebral Edema ll: Pathophysiology01:22

Cerebral Edema ll: Pathophysiology

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 barrier loses...
Hemorrhagic Stroke ll: Pathophysiology01:29

Hemorrhagic Stroke ll: Pathophysiology

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...
Alzheimer Disease ll: Pathophysiology01:23

Alzheimer Disease ll: Pathophysiology

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 microglia. Abnormal...
Ischemic Stroke ll: Pathophysiology01:15

Ischemic Stroke ll: Pathophysiology

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...
Encephalitis ll: Pathophysiology01:26

Encephalitis ll: Pathophysiology

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...
Hemorrhagic Stroke l: Introduction01:17

Hemorrhagic Stroke l: Introduction

A hemorrhagic stroke is an acute neurological event that occurs when a weakened cerebral blood vessel ruptures, allowing blood to accumulate within or around the brain. The sudden release of blood forms a focal hematoma that increases intracranial pressure, displaces neural tissue, and can obstruct cerebrospinal fluid pathways. These effects may be compounded by intraventricular extension of the hemorrhage, cerebral edema, or compression of adjacent structures, all of which contribute to...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

IM-MetaLAB: the first digital laboratory for teaching the fundamental concepts of instrumentation and measurement in metaverse.

Scientific reports·2025
Same author

Progressive activation of the astrocyte A1 phenotype underlies microglia-astroglia crosstalk and contributes to neuroinflammation in neuronopathic MPS.

Molecular genetics and metabolism·2025
Same author

Anti-amyloid treatment is broadly effective in neuronopathic mucopolysaccharidoses and synergizes with gene therapy in MPS-IIIA.

Molecular therapy : the journal of the American Society of Gene Therapy·2024
Same author

Fertility specialists' views, behavior, and attitudes towards the use of endometrial scratching in Italy.

BMC women's health·2023
Same author

The Amyloid Inhibitor CLR01 Relieves Autophagy and Ameliorates Neuropathology in a Severe Lysosomal Storage Disease.

Molecular therapy : the journal of the American Society of Gene Therapy·2022
Same author

Use of mineral oil in IVF culture systems: physico-chemical aspects, management, and safety.

Journal of assisted reproduction and genetics·2022

Related Experiment Video

Updated: Jun 8, 2026

Antibody Binding Specificity for Kappa (Vκ) Light Chain-containing Human (IgM) Antibodies: Polysialic Acid (PSA) Attached to NCAM as a Case Study
11:10

Antibody Binding Specificity for Kappa (Vκ) Light Chain-containing Human (IgM) Antibodies: Polysialic Acid (PSA) Attached to NCAM as a Case Study

Published on: June 29, 2016

Polyclonal light chains in cerebrovascular disease.

Patrizia Fiori1, Maria Giannetti Luigi, Linda Iurato

  • 1Central Operative Unit of Neurology (Dir. A Monaco), ASL AV, Civil Hospital of Ariano Irpino, University of Naples, Italy. patriziafiorirmit@alice.it

Neuropsychiatric Disease and Treatment
|September 22, 2010
PubMed
Summary
This summary is machine-generated.

Urinary polyclonal light chains are early markers of kidney dysfunction in cerebrovascular disease, indicating reversible vascular impairment before severe renal failure.

Keywords:
cerebrovascular diseasepolyclonal light chainsrenal failure

More Related Videos

Longitudinal In Vivo Imaging of the Cerebrovasculature: Relevance to CNS Diseases
07:47

Longitudinal In Vivo Imaging of the Cerebrovasculature: Relevance to CNS Diseases

Published on: December 6, 2016

Reliable Isolation of Central Nervous System Microvessels Across Five Vertebrate Groups
10:35

Reliable Isolation of Central Nervous System Microvessels Across Five Vertebrate Groups

Published on: January 12, 2020

Related Experiment Videos

Last Updated: Jun 8, 2026

Antibody Binding Specificity for Kappa (Vκ) Light Chain-containing Human (IgM) Antibodies: Polysialic Acid (PSA) Attached to NCAM as a Case Study
11:10

Antibody Binding Specificity for Kappa (Vκ) Light Chain-containing Human (IgM) Antibodies: Polysialic Acid (PSA) Attached to NCAM as a Case Study

Published on: June 29, 2016

Longitudinal In Vivo Imaging of the Cerebrovasculature: Relevance to CNS Diseases
07:47

Longitudinal In Vivo Imaging of the Cerebrovasculature: Relevance to CNS Diseases

Published on: December 6, 2016

Reliable Isolation of Central Nervous System Microvessels Across Five Vertebrate Groups
10:35

Reliable Isolation of Central Nervous System Microvessels Across Five Vertebrate Groups

Published on: January 12, 2020

Area of Science:

  • Nephrology
  • Neurology
  • Vascular Biology

Background:

  • Altered membrane permeability is a key feature of inflammation and ischemia.
  • Renal dysfunction is a significant risk factor for cardiovascular, cerebrovascular, and metabolic diseases.

Purpose of the Study:

  • To evaluate proteinuria and urinary polyclonal light chains in acute stroke and chronic cerebrovascular disease.
  • To compare these markers with those in other neurologic diseases.

Main Methods:

  • Analysis of urinary polyclonal light chains (κ and λ) and creatininemia.
  • Comparison of marker levels across patient groups: acute stroke, chronic cerebrovascular disease, and other neurologic diseases.
  • Assessment of correlation with blood pressure and other seric parameters.

Main Results:

  • Urinary polyclonal light chains were significantly elevated in cerebrovascular disease patients compared to other neurologic diseases.
  • Urinary polyclonal κ chains were highest in acute stroke, while λ chains were increased in chronic cerebrovascular disease.
  • A decreased polyclonal light chain/creatinemia ratio indicated a shift towards chronic renal failure.

Conclusions:

  • Urinary polyclonal light chains serve as an early indicator of reversible renal dysfunction in cerebrovascular disease.
  • These markers may predict vascular impairment before the onset of irreversible renal failure.
  • Polyclonal light chains show no significant correlation with blood pressure or other seric parameters, highlighting their unique role as early biomarkers.