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

11
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...
11
Dementia l: Introduction01:22

Dementia l: Introduction

29
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...
29
Hemorrhagic Stroke l: Introduction01:17

Hemorrhagic Stroke l: Introduction

16
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...
16
Alzheimer Disease ll: Pathophysiology01:23

Alzheimer Disease ll: Pathophysiology

27
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...
27
Alzheimer's Disease: Overview01:26

Alzheimer's Disease: Overview

1.7K
Alzheimer's Disease (AD) is a continually advancing neurodegenerative disorder, distinguished by escalating memory loss, cognitive dysfunction, and dementia. The disease unfolds in three stages: preclinical, mild cognitive impairment (MCI), and dementia. Its onset is insidious, and the progression gradual, with the cause not well explained by other disorders.
The clinical diagnosis of AD hinges on the presence of memory and other cognitive impairments. Biomarkers, such as changes in Aβ...
1.7K
Cerebral Edema l: Introduction01:19

Cerebral Edema l: Introduction

18
Cerebral edema is a pathological increase in brain water content that disrupts intracranial pressure regulation and impairs neurological function. Because the cranial vault is rigid, even modest increases in tissue volume can compromise cerebral perfusion, distort neural structures, and initiate secondary injury. Cerebral edema develops through four principal mechanisms: vasogenic, cytotoxic, interstitial, and ionic.Vasogenic EdemaVasogenic edema arises from disruption of the blood–brain...
18

You might also read

Related Articles

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

Sort by
Same author

[Transient myoclonic state with asterixis related to COVID-19].

Rinsho shinkeigaku = Clinical neurology·2026
Same author

Salvage robotic-assisted subtotal esophagectomy after chemoradiotherapy for unresectable locally advanced esophageal sarcoma: A case report.

Oncology letters·2026
Same author

[Report of a Case of Unresectable Advanced Gastric Cancer with Long-Term Survival on Chemotherapy Alone].

Gan to kagaku ryoho. Cancer & chemotherapy·2026
Same author

Success rate and efficacy of intentional ipsilateral epidural catheter placement for anterior cruciate ligament reconstruction surgery: a retrospective analysis of 307 consecutive patients.

Journal of anesthesia·2026
Same author

[A Case of Safe Pancreaticoduodenectomy in a 94-Year-Old Patient with Pancreatic Carcinoma].

Gan to kagaku ryoho. Cancer & chemotherapy·2026
Same author

[Report of a Case of Treatment for Unresectable Esophageal Cancer with Esophageal Perforation and Lung Abscess].

Gan to kagaku ryoho. Cancer & chemotherapy·2026

Related Experiment Video

Updated: Apr 27, 2026

Visualization of Amyloid β Deposits in the Human Brain with Matrix-assisted Laser Desorption/Ionization Imaging Mass Spectrometry
09:31

Visualization of Amyloid β Deposits in the Human Brain with Matrix-assisted Laser Desorption/Ionization Imaging Mass Spectrometry

Published on: March 7, 2019

9.6K

[Cerebral amyloid angiopathy].

Kenji Sakai1, Masahito Yamada

  • 1Department of Neurology and Neurobiology of Aging, Kanazawa University Graduate School of Medical Sciences.

Brain and Nerve = Shinkei Kenkyu No Shinpo
|July 8, 2014
PubMed
Summary

Cerebral amyloid angiopathy (CAA) involves amyloid protein buildup in brain blood vessels, causing hemorrhages and dementia. Current treatments are limited, highlighting the need for further research into CAA pathomechanisms and therapies.

Area of Science:

  • Neurology
  • Pathology
  • Vascular Biology

Context:

  • Cerebral amyloid angiopathy (CAA) is a neurological disorder affecting leptomeningeal and cerebral blood vessels.
  • Amyloid protein deposition, including amyloid-beta (Aβ), is a hallmark of CAA.
  • Both sporadic and familial forms of CAA exist, associated with various genetic mutations.

Purpose:

  • To review the pathological characteristics and clinical manifestations of cerebral amyloid angiopathy.
  • To discuss the known and unknown pathomechanisms underlying CAA.
  • To highlight diagnostic challenges and the current lack of curative treatments for CAA.

Summary:

  • CAA is characterized by amyloid protein accumulation in CNS blood vessels, leading to structural damage like 'double-barreled' changes and microaneurysms.

More Related Videos

In Vitro Assays to Assess Blood-brain Barrier Mesh-like Vessel Formation and Disruption
10:36

In Vitro Assays to Assess Blood-brain Barrier Mesh-like Vessel Formation and Disruption

Published on: June 20, 2017

7.7K
Isolation and Cannulation of Cerebral Parenchymal Arterioles
09:49

Isolation and Cannulation of Cerebral Parenchymal Arterioles

Published on: May 23, 2016

11.7K

Related Experiment Videos

Last Updated: Apr 27, 2026

Visualization of Amyloid β Deposits in the Human Brain with Matrix-assisted Laser Desorption/Ionization Imaging Mass Spectrometry
09:31

Visualization of Amyloid β Deposits in the Human Brain with Matrix-assisted Laser Desorption/Ionization Imaging Mass Spectrometry

Published on: March 7, 2019

9.6K
In Vitro Assays to Assess Blood-brain Barrier Mesh-like Vessel Formation and Disruption
10:36

In Vitro Assays to Assess Blood-brain Barrier Mesh-like Vessel Formation and Disruption

Published on: June 20, 2017

7.7K
Isolation and Cannulation of Cerebral Parenchymal Arterioles
09:49

Isolation and Cannulation of Cerebral Parenchymal Arterioles

Published on: May 23, 2016

11.7K
  • Clinical presentations include recurrent hemorrhages, microinfarcts, progressive dementia, and transient neurological symptoms.
  • While imaging aids diagnosis, pathological examination remains definitive; effective treatments are currently unavailable.

    • Impact:

    • Improved understanding of CAA's pathology and clinical spectrum.
    • Highlights the need for further research into CAA pathomechanisms.
    • Emphasizes the current limitations in diagnosing and treating cerebral amyloid angiopathy.