Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Alzheimer Disease ll: Pathophysiology

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: Overview

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...

Dementia l: Introduction

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...

Alzheimer Disease l: Introduction

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...

Amyloid Fibrils

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 Fibrils

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...

You might also read

Related Articles

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

Sort by

Same author

Shared brain transcriptomic signature in TDP-43 type A FTLD patients with or without GRN mutations.

Brain : a journal of neurology·2021

Same author

The contribution of behavioral features to caregiver burden in FTLD spectrum disorders.

Alzheimer's & dementia : the journal of the Alzheimer's Association·2021

Same author

Posterior cortical atrophy phenotypic heterogeneity revealed by decoding <sup>18</sup>F-FDG-PET.

Brain communications·2021

Same author

The temporal onset of the core features in dementia with Lewy bodies.

Alzheimer's & dementia : the journal of the Alzheimer's Association·2021

Same author

Rare PSAP Variants and Possible Interaction with GBA in REM Sleep Behavior Disorder.

Journal of Parkinson's disease·2021

Same author

Regional Brain Stiffness Analysis of Dementia with Lewy Bodies.

Journal of magnetic resonance imaging : JMRI·2021

Search research articles

Related Experiment Video

Updated: May 13, 2026

Full- versus Sub-Regional Quantification of Amyloid-Beta Load on Mouse Brain Sections

Full- versus Sub-Regional Quantification of Amyloid-Beta Load on Mouse Brain Sections

Published on: May 19, 2022

Brain β-amyloid load approaches a plateau.

Clifford R Jack¹, Heather J Wiste, Timothy G Lesnick

¹From the Departments of Radiology, Mayo Clinic, Rochester, MN, USA. jack.clifford@mayo.edu

|March 1, 2013

Summary

Researchers modeled beta-amyloid (β-amyloid) accumulation using PET scans. The study identified a 15-year therapeutic window for interventions during the most rapid, linear phase of amyloid buildup.

More Related Videos

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

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

Published on: March 7, 2019

Related Experiment Videos

Last Updated: May 13, 2026

Full- versus Sub-Regional Quantification of Amyloid-Beta Load on Mouse Brain Sections

Full- versus Sub-Regional Quantification of Amyloid-Beta Load on Mouse Brain Sections

Published on: May 19, 2022

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

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

Published on: March 7, 2019

Area of Science:

Neuroimaging
Biomarker Research
Alzheimer's Disease Pathogenesis

Background:

Beta-amyloid (β-amyloid) deposition is a hallmark of Alzheimer's disease.
Serial amyloid positron emission tomography (PET) imaging allows for tracking β-amyloid accumulation over time.
Understanding the temporal dynamics of β-amyloid is crucial for developing effective interventions.

Purpose of the Study:

To develop a model for the temporal trajectory of β-amyloid accumulation using serial amyloid PET imaging.
To identify the relationship between baseline β-amyloid levels and the rate of accumulation.
To determine the time course of β-amyloid progression and its implications for therapeutic timing.

Main Methods:

Utilized data from 260 participants (aged 70-92) from the Mayo Clinic Study of Aging and Mayo Alzheimer's Disease Research Center.
Measured baseline amyloid PET-relative standardized uptake values (SUVR) and estimated annual amyloid accumulation rates.
Employed regression models to analyze the association between baseline SUVR, accumulation rate, and covariates (age, sex, clinical group, APOE).

Main Results:

Amyloid accumulation rates showed an inverted U-shaped relationship with baseline SUVR, peaking around SUVR 2.0 and reaching zero above SUVR 2.7.
Integration of these findings yielded a sigmoid curve describing the relationship between amyloid PET SUVR and time.
The estimated time to progress from SUVR 1.5 to 2.5 was approximately 15 years.

Conclusions:

A roughly 15-year period exhibits the steepest, near-linear increase in amyloid SUVR over time.
This interval represents a significant therapeutic window for secondary preventive interventions in Alzheimer's disease.
Modeling temporal β-amyloid accumulation aids in identifying optimal timing for interventions.