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...
Amyloid Fibrils03:03

Amyloid Fibrils

Amyloid fibrils are aggregates of misfolded proteins.  Under most circumstances, misfolded proteins are either refolded by chaperone proteins or degraded by the proteasome. However, in the case of a mutation or a disease, these proteins can accumulate to form large clusters and often further assemble to form elongated fibers, called fibrils. 
Amyloid deposits were observed as early as 1639 in the liver and the spleen.   In 1854, Rudolph Virchow performed iodine staining, normally used to...
Amyloid Fibrils03:03

Amyloid Fibrils

Amyloid fibrils are aggregates of misfolded proteins.  Under most circumstances, misfolded proteins are either refolded by chaperone proteins or degraded by the proteasome. However, in the case of a mutation or a disease, these proteins can accumulate to form large clusters and often further assemble to form elongated fibers, called fibrils. 
Amyloid deposits were observed as early as 1639 in the liver and the spleen.   In 1854, Rudolph Virchow performed iodine staining, normally used to...
Dementia l: Introduction01:22

Dementia l: Introduction

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...

You might also read

Related Articles

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

Sort by
Same author

Unified Brain Surface and Volume Registration.

... International Conference on Learning Representations·2026
Same author

Improving the clinical trial landscape for patients with atypical variants of Alzheimer's disease: a call to action.

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

Learning-based non-linear registration robust to MRI-sequence contrast.

Proceedings of the International Society for Magnetic Resonance in Medicine ... Scientific Meeting and Exhibition. International Society for Magnetic Resonance in Medicine. Scientific Meeting and Exhibition·2026
Same author

Longitudinal FreeSurfer with non-linear subject-specific template improves sensitivity to cortical thinning.

Proceedings of the International Society for Magnetic Resonance in Medicine ... Scientific Meeting and Exhibition. International Society for Magnetic Resonance in Medicine. Scientific Meeting and Exhibition·2026
Same author

Functional network contributions to longitudinal tau spread in Posterior Cortical Atrophy.

NPJ dementia·2026
Same author

Structural connectome analysis using a graph-based deep model for prediction of non-imaging variables.

Frontiers in neuroscience·2026

Related Experiment Video

Updated: Jun 3, 2026

Visualization of Amyloid β Deposits in the Human Brain with Matrix-assisted Laser Desorption/Ionization Imaging Mass Spectrometry
09:31

Visualization of Amyloid β Deposits in the Human Brain with Matrix-assisted Laser Desorption/Ionization Imaging Mass Spectrometry

Published on: March 7, 2019

Amyloid-β associated cortical thinning in clinically normal elderly.

J Alex Becker1, Trey Hedden, Jeremy Carmasin

  • 1Department of Radiology, Martinos Center for Biomedical Imaging, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA.

Annals of Neurology
|March 26, 2011
PubMed
Summary

Alzheimer's disease (AD) biomarker amyloid-β (Aβ) deposition is linked to brain atrophy in cognitively normal individuals. This suggests Aβ accumulation precedes cognitive decline and brain structure changes characteristic of AD.

More Related Videos

How to Measure Cortical Folding from MR Images: a Step-by-Step Tutorial to Compute Local Gyrification Index
09:57

How to Measure Cortical Folding from MR Images: a Step-by-Step Tutorial to Compute Local Gyrification Index

Published on: January 2, 2012

Related Experiment Videos

Last Updated: Jun 3, 2026

Visualization of Amyloid β Deposits in the Human Brain with Matrix-assisted Laser Desorption/Ionization Imaging Mass Spectrometry
09:31

Visualization of Amyloid β Deposits in the Human Brain with Matrix-assisted Laser Desorption/Ionization Imaging Mass Spectrometry

Published on: March 7, 2019

How to Measure Cortical Folding from MR Images: a Step-by-Step Tutorial to Compute Local Gyrification Index
09:57

How to Measure Cortical Folding from MR Images: a Step-by-Step Tutorial to Compute Local Gyrification Index

Published on: January 2, 2012

Area of Science:

  • Neuroscience
  • Neurology
  • Radiology

Background:

  • Alzheimer's disease (AD) is characterized by amyloid-β (Aβ) deposition and brain atrophy.
  • These pathological changes often begin years before clinical symptoms manifest.

Purpose of the Study:

  • To investigate if amyloid-β deposition in cognitively normal (CN) older adults correlates with brain structure changes similar to those in AD.
  • Utilizing Pittsburgh Compound B (PiB) positron emission tomography (PET) and structural magnetic resonance imaging (MRI).

Main Methods:

  • 119 participants (87 CN, 32 mild AD) underwent PiB PET and high-resolution MRI.
  • Regression models analyzed the relationship between PiB retention, cortical thickness, and hippocampal volume.

Main Results:

  • In CN subjects, PiB retention was age-related and associated with reduced cortical thickness in AD-relevant regions (parietal, posterior cingulate, precuneus).
  • This pattern of cortical thinning mirrored that seen in mild AD patients.
  • Hippocampal volume reduction showed a variable association with Aβ deposition.

Conclusions:

  • Amyloid-β deposition is associated with cortical thinning patterns characteristic of Alzheimer's disease even before cognitive impairment is evident.
  • These findings highlight Aβ deposition as an early indicator of AD-related neurodegeneration.