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
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
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
Long-term Depression01:03

Long-term Depression

2.6K
Long-term depression, or LTD, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTD is the process of synaptic weakening that occurs over time between pre and postsynaptic neuronal connections. The synaptic weakening of LTD works in opposition to synaptic strengthening by long-term potentiation (LTP) and together are the main mechanisms that underlie learning and memory.
Calcium Ion Concentration Mechanism
If over...
2.6K
Long-term Depression01:05

Long-term Depression

27.3K
Long-term depression, or LTD, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTD is the process of synaptic weakening that occurs over time between pre and postsynaptic neuronal connections. The synaptic weakening of LTD works in opposition to synaptic strengthening by long-term potentiation (LTP) and together are the main mechanisms that underlie learning and memory.
27.3K

You might also read

Related Articles

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

Sort by
Same author

Blood biomarkers predict conversion from cognitively stable to mild cognitive impairment or Alzheimer's disease in Down syndrome at 16-month follow-up in ABC-DS.

Alzheimer's & dementia : the journal of the Alzheimer's Association·2026
Same author

Age predicts Alzheimer's in Down syndrome better than MRI, plasma, or cognition.

Alzheimer's & dementia : the journal of the Alzheimer's Association·2026
Same author

Intraindividual cognitive variability predicts amyloid beta, tau PET, and dementia conversion in Down syndrome: a potential marker of cognitive resilience.

Alzheimer's & dementia : the journal of the Alzheimer's Association·2026
Same author

Abdominal adiposity and Alzheimer's disease imaging markers across sex and race at midlife.

Journal of Alzheimer's disease : JAD·2026
Same author

Inflammation Associated With Obesity, Aging, and Amyloid Burden in Adults With Down Syndrome.

Obesity (Silver Spring, Md.)·2026
Same author

Leveraging STRAW +10 criteria to evaluate menopause stage effects on sleep quality.

Climacteric : the journal of the International Menopause Society·2026

Related Experiment Video

Updated: Apr 30, 2026

Application of Granger Causality Analysis of the Directed Functional Connection in Alzheimer's Disease and Mild Cognitive Impairment
08:43

Application of Granger Causality Analysis of the Directed Functional Connection in Alzheimer's Disease and Mild Cognitive Impairment

Published on: August 7, 2017

7.5K

Network dysfunction in Alzheimer's disease: refining the disconnection hypothesis.

Matthew R Brier1, Jewell B Thomas, Beau M Ances

  • 11 Program in Neuroscience, Division of Biological and Biomedical Science, School of Medicine, Washington University in St. Louis , St. Louis, Missouri.

Brain Connectivity
|May 7, 2014
PubMed
Summary

This review explores how resting-state functional connectivity disruptions illuminate Alzheimer's disease (AD) pathophysiology. We examine methods and literature to hypothesize the development and spread of these neural deficits in AD.

Keywords:
Alzheimer's diseasebrain networksresting-state functional connectivity

More Related Videos

Modeling the Functional Network for Spatial Navigation in the Human Brain
05:55

Modeling the Functional Network for Spatial Navigation in the Human Brain

Published on: October 13, 2023

1.7K
Generalized Psychophysiological Interaction PPI Analysis of Memory Related Connectivity in Individuals at Genetic Risk for Alzheimer's Disease
09:38

Generalized Psychophysiological Interaction PPI Analysis of Memory Related Connectivity in Individuals at Genetic Risk for Alzheimer's Disease

Published on: November 14, 2017

14.4K

Related Experiment Videos

Last Updated: Apr 30, 2026

Application of Granger Causality Analysis of the Directed Functional Connection in Alzheimer's Disease and Mild Cognitive Impairment
08:43

Application of Granger Causality Analysis of the Directed Functional Connection in Alzheimer's Disease and Mild Cognitive Impairment

Published on: August 7, 2017

7.5K
Modeling the Functional Network for Spatial Navigation in the Human Brain
05:55

Modeling the Functional Network for Spatial Navigation in the Human Brain

Published on: October 13, 2023

1.7K
Generalized Psychophysiological Interaction PPI Analysis of Memory Related Connectivity in Individuals at Genetic Risk for Alzheimer's Disease
09:38

Generalized Psychophysiological Interaction PPI Analysis of Memory Related Connectivity in Individuals at Genetic Risk for Alzheimer's Disease

Published on: November 14, 2017

14.4K

Area of Science:

  • Neuroscience
  • Neurology
  • Medical Imaging

Background:

  • Alzheimer's disease (AD) significantly impacts neural function, with numerous studies detailing functional impairments.
  • Resting-state functional connectivity (rsFC) is a key tool for investigating these neural changes.
  • Existing research often focuses on rsFC as a biomarker for AD risk, staging, or prognosis.

Purpose of the Study:

  • To critically review how functional connectivity disruptions enhance our understanding of Alzheimer's disease pathophysiology.
  • To examine the rationale and methodological considerations of rsFC studies in AD.
  • To propose a novel hypothesis on the development and spread of functional connectivity deficits in AD.

Main Methods:

  • Comprehensive literature review of studies investigating functional connectivity in Alzheimer's disease.
  • Critical analysis of the rationale and methodologies employed in rsFC research for AD.
  • Synthesis of findings to develop a pathophysiological hypothesis.

Main Results:

  • Functional connectivity disruptions are integral to understanding Alzheimer's disease.
  • Methodological considerations are crucial for accurate interpretation of rsFC data in AD.
  • A review of existing literature provides a foundation for a new hypothesis.

Conclusions:

  • Resting-state functional connectivity offers critical insights into Alzheimer's disease pathophysiology beyond its biomarker potential.
  • A hypothesis is proposed regarding the progression of functional connectivity deficits in AD.
  • Further research integrating rsFC into pathophysiological models is warranted.