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

Multiple Sclerosis l: Introduction01:19

Multiple Sclerosis l: Introduction

Multiple sclerosis is a chronic autoimmune disease of the central nervous system (CNS) that affects the brain, spinal cord, and optic nerves. It is an inflammatory demyelinating disorder and a leading cause of neurological disability in young adults.EpidemiologyMS commonly begins between 20 and 40 years of age and is twice as common in women. Its exact cause remains unclear, but genetic susceptibility contributes, with higher risk in first-degree relatives and identical twins. A greater...
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 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'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...
Neural Regulation01:37

Neural Regulation

Digestion begins with a cephalic phase that prepares the digestive system to receive food. When our brain processes visual or olfactory information about food, it triggers impulses in the cranial nerves innervating the salivary glands and stomach to prepare for food.

You might also read

Related Articles

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

Sort by
Same author

Elevated spermidine serum levels in mild cognitive impairment, a potential biomarker of progression to Alzheimer dementia, a pilot study.

Journal of clinical neuroscience : official journal of the Neurosurgical Society of Australasia·2022
Same author

Novel dose escalation to predict treatment with hydroxyurea (NDEPTH): A randomized controlled trial of a dose-prediction equation to determine maximum tolerated dose of hydroxyurea in pediatric sickle cell disease.

American journal of hematology·2020
Same author

Increased free prostate specific antigen serum levels in Alzheimer's disease, correlation with Cognitive Decline.

Journal of the neurological sciences·2019
Same author

Cardiovascular Autonomic Dysfunction: Link Between Multiple Sclerosis Osteoporosis and Neurodegeneration.

Neuromolecular medicine·2018
Same author

Fingolimod anti-inflammatory and neuroprotective effects modulation of RAGE axis in multiple sclerosis patients.

Neuropharmacology·2017
Same author

Serum Hepcidin Levels, Iron Dyshomeostasis and Cognitive Loss in Alzheimer's Disease.

Aging and disease·2017
Same journal

The Emerging Role of Tumor-Associated Neutrophils in Modulating Immune Checkpoint Inhibitor Response and Therapeutic Strategies.

Immunological investigations·2026
Same journal

Immune Reconstitution After Hematopoietic Stem Cell Transplantation: Cellular Dynamics, Clinical Determinants, and Emerging Therapeutic Strategies.

Immunological investigations·2026
Same journal

Riboflavin Modulates Complement Activation, Immune Cell Viability and Activation, and Neutrophil Microbicidal Functions <i>in Vitro</i>.

Immunological investigations·2026
Same journal

Pharmacological Modulation of Immunosenescence and Inflammaging: Senolytics, Senomorphics, and Emerging Therapies.

Immunological investigations·2026
Same journal

Nanoantibodies: A Review of Diagnostic and Therapeutic Applications in Respiratory Diseases.

Immunological investigations·2026
Same journal

TRIM31: A Novel Guardian Against Periodontal Inflammation via Modulation of NLRP3 Inflammasome and Macrophage Polarization.

Immunological investigations·2026
See all related articles

Related Experiment Video

Updated: Jun 6, 2026

Comprehensive Autopsy Program for Individuals with Multiple Sclerosis
09:41

Comprehensive Autopsy Program for Individuals with Multiple Sclerosis

Published on: July 19, 2019

AGE-RAGE in multiple sclerosis brain.

Zohara Sternberg1, Peter Ostrow, Mary Vaughan

  • 1Department of Neurology, Jacobs Neurological Institute, Buffalo, New York 14223, USA. zs2@buffalo.edu

Immunological Investigations
|November 18, 2010
PubMed
Summary
This summary is machine-generated.

Advanced glycation end-products (AGEs) and their receptor (RAGE) were elevated in the brains of multiple sclerosis (MS) patients, similar to Alzheimer's disease (AD) patients. This suggests a potential role for AGEs and RAGE in MS neuropathology.

More Related Videos

Abbiategrasso Brain Bank Protocol for Collecting, Processing and Characterizing Aging Brains
12:28

Abbiategrasso Brain Bank Protocol for Collecting, Processing and Characterizing Aging Brains

Published on: June 3, 2020

Rat Model of Widespread Cerebral Cortical Demyelination Induced by an Intracerebral Injection of Pro-Inflammatory Cytokines
09:46

Rat Model of Widespread Cerebral Cortical Demyelination Induced by an Intracerebral Injection of Pro-Inflammatory Cytokines

Published on: September 21, 2021

Related Experiment Videos

Last Updated: Jun 6, 2026

Comprehensive Autopsy Program for Individuals with Multiple Sclerosis
09:41

Comprehensive Autopsy Program for Individuals with Multiple Sclerosis

Published on: July 19, 2019

Abbiategrasso Brain Bank Protocol for Collecting, Processing and Characterizing Aging Brains
12:28

Abbiategrasso Brain Bank Protocol for Collecting, Processing and Characterizing Aging Brains

Published on: June 3, 2020

Rat Model of Widespread Cerebral Cortical Demyelination Induced by an Intracerebral Injection of Pro-Inflammatory Cytokines
09:46

Rat Model of Widespread Cerebral Cortical Demyelination Induced by an Intracerebral Injection of Pro-Inflammatory Cytokines

Published on: September 21, 2021

Area of Science:

  • Neuroscience
  • Immunohistochemistry
  • Pathology

Background:

  • Advanced glycation end-products (AGEs) are implicated in neurodegenerative diseases.
  • Receptor for AGEs (RAGE) plays a role in inflammatory processes.

Purpose of the Study:

  • To investigate the presence of Nepsilon-(carboxymethyl)lysine (CML), a specific AGE, and RAGE in the hippocampi of multiple sclerosis (MS) patients.
  • To compare CML and RAGE levels in MS patients with those in Alzheimer's disease (AD) patients and age-matched controls.

Main Methods:

  • Pilot study utilizing immunohistochemical techniques.
  • Staining of postmortem hippocampal slides from MS patients, AD patients, and controls.
  • Use of monoclonal antibodies for CML and human RAGE.

Main Results:

  • Increased CML and RAGE immunostaining observed in the hippocampi of MS patients.
  • Similar increases in CML and RAGE were found in AD patients (positive controls).
  • Control subjects showed lower levels of CML and RAGE.

Conclusions:

  • The findings suggest elevated levels of AGEs (specifically CML) and RAGE in the MS brain.
  • These elevations are comparable to those seen in Alzheimer's disease.
  • Further research is warranted to explore the role of CML and RAGE in MS pathogenesis.