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...
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...

You might also read

Related Articles

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

Sort by
Same author

Progress in the Treatment of Alzheimer's Disease Is Needed - Position Statement of European Alzheimer's Disease Consortium (EADC) Investigators.

The journal of prevention of Alzheimer's disease·2024
Same author

Erratum to: Association between Modifiable Risk Factors and Levels of Blood-Based Biomarkers of Alzheimer's and Related Dementias in the Look AHEAD Cohort.

JAR life·2024
Same author

Association between Modifiable Risk Factors and Levels of Blood-Based Biomarkers of Alzheimer's and Related Dementias in the Look AHEAD Cohort.

JAR life·2024
Same author

Obesity, diabetes and their metabolic correlates in middle-aged adults with Down syndrome.

Journal of intellectual disability research : JIDR·2023
Same author

Metformin in the Prevention of Alzheimer's Disease and Alzheimer's Disease Related Dementias.

The journal of prevention of Alzheimer's disease·2023
Same author

Subjective Cognitive Decline as a predictor of Frailty in older adults: Hellenic Longitudinal Investigation of Aging and Diet study (HELIAD).

The Journal of frailty & aging·2023
Same journal

Factors Associated With Disability Improvement and Worsening Independent of Attacks in Patients With AQP4-IgG+ NMOSD and MOGAD: A Multicenter Cohort Study.

Neurology·2026
Same journal

Cost-Effectiveness of Intracranial Aneurysm Screening: A Systematic Review.

Neurology·2026
Same journal

Rare Eating Epilepsy: Co-Occurrence of Focal Cortical Dysplasia and Gray Matter Heterotopia.

Neurology·2026
Same journal

Spatiotemporal Associations Between Cortical Microinfarcts and Cortical Superficial Siderosis in Cerebral Amyloid Angiopathy.

Neurology·2026
Same journal

Blood-Brain Barrier Disruption Before Interhospital Transfer for Thrombectomy and Clinical Outcome.

Neurology·2026
Same journal

At Death's Door: Cytosolic Dopamine in Patients With Parkinson Disease.

Neurology·2026
See all related articles

Related Experiment Video

Updated: May 22, 2026

Intracerebroventricular Injection of Amyloid-β Peptides in Normal Mice to Acutely Induce Alzheimer-like Cognitive Deficits
08:01

Intracerebroventricular Injection of Amyloid-β Peptides in Normal Mice to Acutely Induce Alzheimer-like Cognitive Deficits

Published on: March 16, 2016

Nutrient intake and plasma β-amyloid.

Y Gu1, N Schupf, S A Cosentino

  • 1Taub Institute for Research in Alzheimer’s Disease and the Aging Brain, Columbia University, New York, NY, USA.

Neurology
|May 4, 2012
PubMed
Summary
This summary is machine-generated.

Higher intake of omega-3 polyunsaturated fatty acids (PUFA) is linked to lower plasma levels of amyloid-beta 42 (Aβ42). This nutrient profile may reduce Alzheimer's disease risk and slow cognitive decline.

More Related Videos

Full- versus Sub-Regional Quantification of Amyloid-Beta Load on Mouse Brain Sections
07:28

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
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

Related Experiment Videos

Last Updated: May 22, 2026

Intracerebroventricular Injection of Amyloid-β Peptides in Normal Mice to Acutely Induce Alzheimer-like Cognitive Deficits
08:01

Intracerebroventricular Injection of Amyloid-β Peptides in Normal Mice to Acutely Induce Alzheimer-like Cognitive Deficits

Published on: March 16, 2016

Full- versus Sub-Regional Quantification of Amyloid-Beta Load on Mouse Brain Sections
07:28

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
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

Area of Science:

  • Neuroscience
  • Nutritional Science
  • Biochemistry

Background:

  • Cognitive decline and Alzheimer's disease (AD) are significant health concerns in aging populations.
  • Nutrient intake is increasingly recognized for its potential role in brain health and AD pathogenesis.
  • Amyloid-beta (Aβ) proteins, specifically Aβ40 and Aβ42, are key biomarkers implicated in AD.

Purpose of the Study:

  • To investigate the association between the dietary intake of various nutrients and plasma levels of Aβ40 and Aβ42.
  • To explore potential nutritional pathways influencing Aβ metabolism in cognitively healthy elderly individuals.

Main Methods:

  • A cross-sectional study involving 1,219 cognitively healthy elderly participants (age >65).
  • Dietary intake data collected approximately 1.2 years prior to plasma Aβ measurements.
  • Linear regression models were used to analyze associations between 10 nutrients and plasma Aβ40/Aβ42, adjusting for multiple covariates.

Main Results:

  • Higher intake of omega-3 polyunsaturated fatty acids (PUFA) was significantly associated with lower plasma Aβ40 and Aβ42 levels in unadjusted models.
  • In adjusted models, omega-3 PUFA intake remained a significant predictor of lower plasma Aβ42 levels (β = -7.31, p = 0.02).
  • No significant associations were found between other examined nutrients and plasma Aβ levels.

Conclusions:

  • Increased dietary intake of omega-3 PUFA is associated with reduced plasma Aβ42 levels.
  • This finding suggests a potential neuroprotective role for omega-3 PUFA in the context of Alzheimer's disease.
  • A higher omega-3 PUFA intake may be linked to a lower risk of developing AD and slower cognitive decline.