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: 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...

You might also read

Related Articles

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

Sort by
Same author

Five-year prognosis of transient ischemic attack and transient global amnesia in a Finnish population.

Neuroepidemiology·2026
Same author

Overproduction of 42 Amino Acids Long Amyloid Beta Leads to Activation of Secretory Autophagy and Development of Drusen-Like Structures Originating From Retinal Pigment Epithelium.

FASEB journal : official publication of the Federation of American Societies for Experimental Biology·2026
Same author

Functional MRI following sensory stimulation in rat monosodium iodoacetate model of osteoarthritis pain as a tool for drug therapy discovery.

NeuroImage·2025
Same author

Refined Division of Sleep Stages in the Mouse Based on Distributed Deep Electrodes and Underlying Infra-Slow Oscillation.

Journal of sleep research·2025
Same author

Whole-brain responses to visual and auditory stimuli in anesthetized and minimally restrained awake mice using quiet zero echo time fMRI.

Imaging neuroscience (Cambridge, Mass.)·2025
Same author

Whisker pad stimulation with different frequencies reveals non-uniform modulation of functional MRI signal across sensory systems in awake rats.

Cerebral cortex (New York, N.Y. : 1991)·2025

Related Experiment Video

Updated: Jul 19, 2026

Brain Imaging Investigation of the Memory-Enhancing Effect of Emotion
15:57

Brain Imaging Investigation of the Memory-Enhancing Effect of Emotion

Published on: May 4, 2011

Increased fMRI responses during encoding in mild cognitive impairment.

Anne Hämäläinen1, Maija Pihlajamäki, Heikki Tanila

  • 1Department of Neuroscience and Neurology, University of Kuopio, P.O. Box 1627, FIN-70211 Kuopio, Finland.

Neurobiology of Aging
|September 26, 2006
PubMed
Summary

Mild cognitive impairment (MCI) shows increased brain activation in specific regions, potentially compensating for early Alzheimer's disease (AD) related atrophy. This compensatory mechanism involves functional magnetic resonance imaging (fMRI) and structural changes.

More Related Videos

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

Examining the Characteristics of Episodic Memory using Event-related Potentials in Patients with Alzheimer's Disease
11:01

Examining the Characteristics of Episodic Memory using Event-related Potentials in Patients with Alzheimer's Disease

Published on: August 30, 2011

Related Experiment Videos

Last Updated: Jul 19, 2026

Brain Imaging Investigation of the Memory-Enhancing Effect of Emotion
15:57

Brain Imaging Investigation of the Memory-Enhancing Effect of Emotion

Published on: May 4, 2011

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

Examining the Characteristics of Episodic Memory using Event-related Potentials in Patients with Alzheimer's Disease
11:01

Examining the Characteristics of Episodic Memory using Event-related Potentials in Patients with Alzheimer's Disease

Published on: August 30, 2011

Area of Science:

  • Neuroimaging
  • Cognitive Neuroscience
  • Neurology

Background:

  • Mild cognitive impairment (MCI) is a transitional stage between normal aging and Alzheimer's disease (AD).
  • Understanding the neural mechanisms underlying MCI is crucial for early diagnosis and intervention.
  • Structural and functional brain changes may occur early in the disease process.

Purpose of the Study:

  • To investigate changes in functional magnetic resonance imaging (fMRI) activation in relation to structural atrophy in individuals with MCI and mild AD.
  • To explore the compensatory mechanisms in the brain during the progression of cognitive decline.

Main Methods:

  • Structural and functional magnetic resonance imaging (fMRI) was conducted on healthy elderly controls, subjects with MCI, and patients with mild AD.
  • Associative encoding of novel picture-word pairs was used as the fMRI paradigm.
  • Voxel-based morphometry (VBM) and hippocampal volumetry were employed for structural analysis.

Main Results:

  • MCI subjects showed increased fMRI responses in posterior hippocampal, parahippocampal, and fusiform regions compared to controls.
  • VBM revealed greater atrophy in the anterior left hippocampus in MCI subjects.
  • A negative correlation between hippocampal volume and parahippocampal activation was observed in MCI, but not in controls or AD patients.

Conclusions:

  • Increased fMRI activation in medial temporal and fusiform regions in MCI may represent a compensatory response to incipient anterior medial temporal lobe atrophy.
  • These findings highlight the complex interplay between structural degeneration and functional adaptation in early Alzheimer's disease.