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

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...
Alzheimer Disease l: Introduction01:29

Alzheimer Disease l: Introduction

Alzheimer disease is a chronic, progressive, and irreversible neurodegenerative disorder and the most common cause of dementia in older adults. It leads to gradual neuronal loss, causing cognitive decline, behavioral changes, and loss of functional independence.Risk Factors and EtiologyThe disease is multifactorial. Age is the strongest risk factor, with prevalence doubling every 5 years after age 65. Genetic factors include mutations in genes such as APP, PSEN1, and PSEN2, which are associated...
Alzheimer's Disease: Treatment01:22

Alzheimer's Disease: Treatment

Alzheimer's Disease (AD), a neurodegenerative disorder, is pathologically identified by amyloid plaques and neurofibrillary tangles composed of tau protein. AD pharmacotherapy aims to manage cognitive symptoms, delay disease progression, and treat behavioral symptoms. The treatment is primarily symptomatic and palliative, with no definitive disease-modifying therapy available. Cholinesterase inhibitors, including donepezil (Aricept), rivastigmine (Exelon), and galantamine (Razadyne), are...
Alzheimer's Disease: Overview01:26

Alzheimer's Disease: Overview

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 and tau...
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...
Ischemic Stroke l: Introduction01:15

Ischemic Stroke l: Introduction

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.

You might also read

Related Articles

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

Sort by
Same author

[Experimental study of the eyelid reconstruction in situ with the acellular xenogeneic dermal matrix].

Zhonghua zheng xing wai ke za zhi = Zhonghua zhengxing waike zazhi = Chinese journal of plastic surgery·2007
Same author

[Mutation analysis of GCH1 gene in Chinese patients with dopa responsive dystonia].

Zhonghua yi xue yi chuan xue za zhi = Zhonghua yixue yichuanxue zazhi = Chinese journal of medical genetics·2007
Same author

[Screening and characterization of marine bacteria with antibacterial and cytotoxic activities, and existence of PKS I and NRPS genes in bioactive strains].

Wei sheng wu xue bao = Acta microbiologica Sinica·2007
Same author

[Collateral supply in patients with severe carotid stenosis].

Zhonghua yi xue za zhi·2007
Same author

[Changes of sleep architecture in patients with narcolepsy].

Zhonghua yi xue za zhi·2007
Same author

[Combined anterior and posterior approach for cervical fracture-dislocation with ankylosing spondylitis].

Zhonghua wai ke za zhi [Chinese journal of surgery]·2007

Related Experiment Video

Updated: May 16, 2026

A High Throughput, Multiplexed and Targeted Proteomic CSF Assay to Quantify Neurodegenerative Biomarkers and Apolipoprotein E Isoforms Status
07:08

A High Throughput, Multiplexed and Targeted Proteomic CSF Assay to Quantify Neurodegenerative Biomarkers and Apolipoprotein E Isoforms Status

Published on: October 20, 2016

Aberrant apolipoprotein E expression and cognitive dysfunction in patients with poststroke depression.

Zhaohui Zhang1, Junlin Mu, Jing Li

  • 1Department of Psychosomatic Medicine, The Second Affiliated Hospital of Xinxiang Medical University, Xinxiang, China.

Genetic Testing and Molecular Biomarkers
|November 23, 2012
PubMed
Summary
This summary is machine-generated.

Apolipoprotein E (ApoE) levels and event-related potentials (ERPs) may help identify post-stroke depression (PSD) risk. Aberrant serum ApoE and altered ERPs could serve as diagnostic markers for PSD.

More Related Videos

A Middle Cerebral Artery Occlusion Technique for Inducing Post-stroke Depression in Rats
04:38

A Middle Cerebral Artery Occlusion Technique for Inducing Post-stroke Depression in Rats

Published on: May 22, 2019

Motor and Hippocampal Dependent Spatial Learning and Reference Memory Assessment in a Transgenic Rat Model of Alzheimer's Disease with Stroke
09:45

Motor and Hippocampal Dependent Spatial Learning and Reference Memory Assessment in a Transgenic Rat Model of Alzheimer's Disease with Stroke

Published on: March 22, 2016

Related Experiment Videos

Last Updated: May 16, 2026

A High Throughput, Multiplexed and Targeted Proteomic CSF Assay to Quantify Neurodegenerative Biomarkers and Apolipoprotein E Isoforms Status
07:08

A High Throughput, Multiplexed and Targeted Proteomic CSF Assay to Quantify Neurodegenerative Biomarkers and Apolipoprotein E Isoforms Status

Published on: October 20, 2016

A Middle Cerebral Artery Occlusion Technique for Inducing Post-stroke Depression in Rats
04:38

A Middle Cerebral Artery Occlusion Technique for Inducing Post-stroke Depression in Rats

Published on: May 22, 2019

Motor and Hippocampal Dependent Spatial Learning and Reference Memory Assessment in a Transgenic Rat Model of Alzheimer's Disease with Stroke
09:45

Motor and Hippocampal Dependent Spatial Learning and Reference Memory Assessment in a Transgenic Rat Model of Alzheimer's Disease with Stroke

Published on: March 22, 2016

Area of Science:

  • Neuroscience
  • Genetics
  • Psychiatry

Background:

  • Apolipoprotein E (ApoE) is implicated in cognitive disorders.
  • Understanding ApoE's role in post-stroke depression (PSD) is crucial.

Purpose of the Study:

  • To investigate the influence of ApoE on PSD risk.
  • To identify objective biomarkers for PSD diagnosis.

Main Methods:

  • Compared cognitive function, serum ApoE, and ApoE mRNA in PSD patients, stroke controls, and healthy volunteers.
  • Utilized event-related potentials (ERPs) for cognitive evaluation.
  • Measured serum ApoE and ApoE mRNA expression via ELISA and RT-qPCR.

Main Results:

  • PSD patients exhibited prolonged ERP latencies (N2, P3) and reduced P3 amplitude.
  • No significant correlation found between P3 amplitude, ApoE mRNA, and serum ApoE in PSD patients.
  • PSD group showed lower peripheral ApoE mRNA and higher serum ApoE compared to stroke controls.

Conclusions:

  • Aberrant serum ApoE levels and specific ERP abnormalities may serve as potential biomarkers for PSD risk assessment.
  • These findings suggest objective markers for the clinical diagnosis of PSD.