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'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...
Glial Cells01:04

Glial Cells

Overview
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...

You might also read

Related Articles

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

Sort by
Same author

Combined Adaptive Immune Mechanisms Mediate Cardiac Injury After COVID-19 Vaccination.

Circulation·2025
Same author

Retraction Note: Annexin A1 attenuates microvascular complications through restoration of Akt signalling in a murine model of type 1 diabetes.

Diabetologia·2025
Same author

Biological effects of rapid short pulses of focused ultrasound for drug delivery to the brain.

Journal of controlled release : official journal of the Controlled Release Society·2025
Same author

Publisher Correction: The glucose transporter 2 regulates CD8+ T cell function via environment sensing.

Nature metabolism·2025
Same author

Neuroinflammation in Alzheimer disease.

Nature reviews. Immunology·2024
Same author

EEG hyperexcitability and hyperconnectivity linked to GABAergic inhibitory interneuron loss following traumatic brain injury.

Brain communications·2024

Related Experiment Video

Updated: May 24, 2026

Rapid and Refined CD11b Magnetic Isolation of Primary Microglia with Enhanced Purity and Versatility
07:54

Rapid and Refined CD11b Magnetic Isolation of Primary Microglia with Enhanced Purity and Versatility

Published on: April 13, 2017

Microglia function in Alzheimer's disease.

Egle Solito1, Magdalena Sastre

  • 1Centre for Translational Medicine and Therapeutics, William Harvey Research Institute, Barts and The London, Queen Mary's School of Medicine and Dentistry London, UK.

Frontiers in Pharmacology
|February 25, 2012
PubMed
Summary

Systemic inflammation impacts the brain, affecting microglia, the brain's immune cells. Understanding microglia's dual role in Alzheimer's disease (AD) is crucial for developing new therapies.

Keywords:
Alzheimer’s diseaseNSAIDsamyloid-βannexin A1immunityinflammationmicroglia

More Related Videos

Isolation of Cortical Microglia with Preserved Immunophenotype and Functionality From Murine Neonates
09:12

Isolation of Cortical Microglia with Preserved Immunophenotype and Functionality From Murine Neonates

Published on: January 30, 2014

Related Experiment Videos

Last Updated: May 24, 2026

Rapid and Refined CD11b Magnetic Isolation of Primary Microglia with Enhanced Purity and Versatility
07:54

Rapid and Refined CD11b Magnetic Isolation of Primary Microglia with Enhanced Purity and Versatility

Published on: April 13, 2017

Isolation of Cortical Microglia with Preserved Immunophenotype and Functionality From Murine Neonates
09:12

Isolation of Cortical Microglia with Preserved Immunophenotype and Functionality From Murine Neonates

Published on: January 30, 2014

Area of Science:

  • Neuroimmunology
  • Neuroinflammation
  • Aging Research

Background:

  • Systemic inflammatory responses can affect the brain, influencing microglia, the resident immune cells.
  • Microglia can become hyper-reactive in aging and neurodegenerative diseases, potentially exacerbating neurological conditions like Alzheimer's disease (AD).
  • Aging impairs microglial efficiency, leading to over-activation and potential neurotoxicity.

Purpose of the Study:

  • To investigate the complex role of microglia in Alzheimer's disease (AD) progression.
  • To explore how systemic inflammation influences microglial activation in the context of aging and neurodegeneration.
  • To identify potential biomarkers and therapeutic targets for early AD diagnosis and treatment.

Main Methods:

  • Review of current scientific literature on microglia, inflammation, and AD.
  • Analysis of evidence for both beneficial and detrimental microglial functions in AD.
  • Discussion of potential anti-inflammatory therapies and diagnostic markers.

Main Results:

  • Microglia play a dual role in AD: they can clear amyloid-beta (Aβ) and provide neuroprotection, but also cause neurotoxicity when over-activated.
  • Systemic inflammation, which increases with age, can worsen neurodegenerative conditions by affecting microglial responses.
  • Aging compromises microglia's ability to clear cellular debris and Aβ, while increasing their pro-inflammatory reactions.

Conclusions:

  • Understanding microglia activation states across different AD stages is essential for developing effective anti-inflammatory therapies.
  • Microglia's contribution to AD pathogenesis can be both protective and detrimental, depending on their activation state and age.
  • Further research into microglial function and biomarkers is critical for advancing AD diagnosis and treatment.