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

35
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...
35
Alzheimer Disease l: Introduction01:29

Alzheimer Disease l: Introduction

21
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...
21
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
Export of Misfolded Proteins out of the ER01:32

Export of Misfolded Proteins out of the ER

4.3K
After folding, the ER assesses the quality of secretory and membrane proteins. The correctly folded proteins are cleared by the calnexin cycle for transport to their final destination, while misfolded proteins are held back in the ER lumen. The ER chaperones attempt to unfold and refold the misfolded proteins but sometimes fail to achieve the correct native conformation. Such terminally misfolded proteins are then exported to the cytosol by ER-associated degradation or ERAD pathway for...
4.3K
Role of ER in the Secretory Pathway01:17

Role of ER in the Secretory Pathway

6.3K
Eukaryotic cells have a special pathway that enables communication between various intracellular membrane-bound compartments and also with the extracellular environment. This pathway is termed as the secretory pathway.
Components of the secretory pathway
About a third of proteins synthesized in the cell are sorted via the secretory route. They shuffle between different compartments in membrane-bound vesicles until they reach their final destination. The main intracellular compartments involved...
6.3K
Dementia l: Introduction01:22

Dementia l: Introduction

35
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...
35

You might also read

Related Articles

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

Sort by
Same author

Baseline plasma p-tau217/Aβ42 as a sensitive marker for the severity of Alzheimer's disease continuum.

Journal of translational medicine·2026
Same author

An artificial intelligence accelerated ab initio molecular dynamics dataset for electrochemical interfaces.

Scientific data·2025
Same author

Exploring the links among peripheral immunity, biomarkers, cognition, and neuroimaging in Alzheimer's disease.

Alzheimer's & dementia (Amsterdam, Netherlands)·2023
Same author

Disease trajectories in older adults with non-AD pathologic change and comparison with Alzheimer's disease pathophysiology: A longitudinal study.

Neurobiology of aging·2023
Same author

Associations Between TREML2 Gene Variants and Alzheimer's Disease: Biomarkers, Neuroimage, and Cognition.

Journal of Alzheimer's disease : JAD·2023
Same author

Epstein-Barr virus infection with non-tumor-associated Anti-N-Methyl-D-Aspartate receptor encephalitis: a case report and review of literature.

Neurocase·2023

Related Experiment Video

Updated: May 1, 2026

Quantitative Analysis of Mitochondria-Associated Endoplasmic Reticulum Membrane (MAM) Stabilization in a Neural Model of Alzheimer's Disease (AD)
06:41

Quantitative Analysis of Mitochondria-Associated Endoplasmic Reticulum Membrane (MAM) Stabilization in a Neural Model of Alzheimer's Disease (AD)

Published on: January 10, 2025

1.3K

Endoplasmic reticulum dysfunction in Alzheimer's disease.

Jie-Qiong Li1, Jin-Tai Yu, Teng Jiang

  • 1Department of Neurology, Qingdao Municipal Hospital, School of Medicine, Qingdao University, Qingdao, China.

Molecular Neurobiology
|April 10, 2014
PubMed
Summary

Endoplasmic reticulum (ER) stress and the unfolded protein response are implicated in Alzheimer's disease (AD) pathogenesis. Targeting these pathways may offer novel therapeutic strategies for AD.

More Related Videos

Visualization of Endoplasmic Reticulum Subdomains in Cultured Cells
16:43

Visualization of Endoplasmic Reticulum Subdomains in Cultured Cells

Published on: February 18, 2014

12.8K
Imaging the Intracellular Trafficking of APP with Photoactivatable GFP
07:55

Imaging the Intracellular Trafficking of APP with Photoactivatable GFP

Published on: October 17, 2015

10.7K

Related Experiment Videos

Last Updated: May 1, 2026

Quantitative Analysis of Mitochondria-Associated Endoplasmic Reticulum Membrane (MAM) Stabilization in a Neural Model of Alzheimer's Disease (AD)
06:41

Quantitative Analysis of Mitochondria-Associated Endoplasmic Reticulum Membrane (MAM) Stabilization in a Neural Model of Alzheimer's Disease (AD)

Published on: January 10, 2025

1.3K
Visualization of Endoplasmic Reticulum Subdomains in Cultured Cells
16:43

Visualization of Endoplasmic Reticulum Subdomains in Cultured Cells

Published on: February 18, 2014

12.8K
Imaging the Intracellular Trafficking of APP with Photoactivatable GFP
07:55

Imaging the Intracellular Trafficking of APP with Photoactivatable GFP

Published on: October 17, 2015

10.7K

Area of Science:

  • Cellular Biology
  • Neuroscience
  • Pathology

Background:

  • The endoplasmic reticulum (ER) is vital for cellular functions.
  • ER stress occurs when misfolded proteins accumulate, activating the unfolded protein response (UPR).
  • UPR is mediated by stress sensors IRE1, PERK, and ATF6.

Purpose of the Study:

  • To review the role of ER stress in Alzheimer's disease (AD) pathogenesis.
  • To explore the association between ER dysfunction and AD pathology.
  • To identify ER stress and UPR as potential therapeutic targets for AD.

Main Methods:

  • Literature review of medical reports and studies.
  • Analysis of ER stress markers in postmortem AD brains, animal models, and in vitro models.
  • Examination of the link between ER stress and key AD pathological hallmarks.

Main Results:

  • ER stress is evident in AD brains and models.
  • ER stress is linked to presenilin gene mutations, abnormal mRNA processing, beta-amyloid production, tau phosphorylation, and cell death in AD.
  • ER dysfunction is a significant contributor to AD pathogenesis.

Conclusions:

  • ER stress and UPR are integral to the development of Alzheimer's disease.
  • The mechanisms of ER stress and UPR in AD pathology provide a basis for therapeutic interventions.
  • Targeting ER stress and UPR pathways holds promise for novel AD treatments.