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's Disease: Overview01:26

Alzheimer's Disease: Overview

525
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...
525
Alzheimer's Disease: Treatment01:22

Alzheimer's Disease: Treatment

219
Alzheimer's Disease (AD), a neurodegenerative disorder, is pathologically identified by amyloid plaques and neurofibrillary tangles composed of tau protein. AD pharmacotherapy aims to manage cognitive symptoms, delay disease progression, and treat behavioral symptoms. The treatment is primarily symptomatic and palliative, with no definitive disease-modifying therapy available. Cholinesterase inhibitors, including donepezil (Aricept), rivastigmine (Exelon), and galantamine (Razadyne), are...
219
Cognitive Enhancers: Cholinesterase Inhibitors and NMDA Receptor Antagonists01:30

Cognitive Enhancers: Cholinesterase Inhibitors and NMDA Receptor Antagonists

159
Cognitive enhancers, also known as "smart drugs," are substances used to enhance memory, mental alertness, and concentration. These can be natural or synthetic and improve cognition in conditions like Alzheimer's disease (AD) and other neurodegenerative diseases. Some common examples include caffeine, amphetamines, methylphenidate, modafinil, arecoline, donepezil, vortioxetine, and piracetam. These enhancers work on the principle of synaptic plasticity and altered circuit function.
159
Amyloid Fibrils03:03

Amyloid Fibrils

9.6K
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,...
9.6K
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

You might also read

Related Articles

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

Sort by
Same author

Longitudinal associations of epigenetic aging with cognitive aging in Hispanic/Latino adults from the Hispanic Community Health Study/Study of Latinos.

medRxiv : the preprint server for health sciences·2025
Same author

Development and validation of a harmonized memory score for multicenter Alzheimer's disease and related dementia research.

medRxiv : the preprint server for health sciences·2025
Same author

Association of Lp(a) With Stroke and Cerebral Injury on MRI: Insights From the HCHS/SOL (Hispanic Community Health Study/Study of Latinos) and Investigation of Neurocognitive Aging MRI (SOL-INCA MRI).

Stroke·2025
Same author

Amyloid PET predicts longitudinal functional and cognitive trajectories in a heterogeneous cohort.

Alzheimer's & dementia : the journal of the Alzheimer's Association·2025
Same author

Multimodal Associations of Modifiable Risk Factors on White Matter Injury: The SOL-INCA-MRI Study (HCHS/SOL).

Stroke·2025
Same author

Healthy dietary intake diminishes the effect of cerebral small vessel disease on cognitive performance in older adults.

Frontiers in neurology·2025

Related Experiment Video

Updated: Jul 23, 2025

Preparation of Oligomeric β-amyloid1-42 and Induction of Synaptic Plasticity Impairment on Hippocampal Slices
04:41

Preparation of Oligomeric β-amyloid1-42 and Induction of Synaptic Plasticity Impairment on Hippocampal Slices

Published on: July 14, 2010

23.3K

The complex pathway between amyloid β and cognition: implications for therapy.

William J Jagust1, Charlotte E Teunissen2, Charles DeCarli3

  • 1School of Public Health, and Helen Wills Neuroscience Institute, University of California, Berkeley, CA, USA.

The Lancet. Neurology
|July 16, 2023
PubMed
Summary

The amyloid hypothesis for Alzheimer's disease (AD) is being challenged. While targeting amyloid-beta (Aβ) shows some therapeutic promise, it doesn't fully explain cognitive decline, necessitating a multifactorial approach to AD research and treatment.

More Related Videos

Visualizing Axonal Growth Cone Collapse and Early Amyloid β Effects in Cultured Mouse Neurons
06:23

Visualizing Axonal Growth Cone Collapse and Early Amyloid β Effects in Cultured Mouse Neurons

Published on: October 30, 2018

8.0K
Stereotaxic Infusion of Oligomeric Amyloid-beta into the Mouse Hippocampus
08:16

Stereotaxic Infusion of Oligomeric Amyloid-beta into the Mouse Hippocampus

Published on: June 17, 2015

18.3K

Related Experiment Videos

Last Updated: Jul 23, 2025

Preparation of Oligomeric β-amyloid1-42 and Induction of Synaptic Plasticity Impairment on Hippocampal Slices
04:41

Preparation of Oligomeric β-amyloid1-42 and Induction of Synaptic Plasticity Impairment on Hippocampal Slices

Published on: July 14, 2010

23.3K
Visualizing Axonal Growth Cone Collapse and Early Amyloid β Effects in Cultured Mouse Neurons
06:23

Visualizing Axonal Growth Cone Collapse and Early Amyloid β Effects in Cultured Mouse Neurons

Published on: October 30, 2018

8.0K
Stereotaxic Infusion of Oligomeric Amyloid-beta into the Mouse Hippocampus
08:16

Stereotaxic Infusion of Oligomeric Amyloid-beta into the Mouse Hippocampus

Published on: June 17, 2015

18.3K

Area of Science:

  • Neuroscience
  • Neurology
  • Biochemistry

Background:

  • The amyloid-beta (Aβ) cascade hypothesis has long dominated Alzheimer's disease (AD) research.
  • Targeting Aβ has shown emerging therapeutic benefits, but its overall efficacy remains uncertain.

Purpose of the Study:

  • To critically evaluate the sufficiency of the amyloid hypothesis in explaining Alzheimer's disease.
  • To highlight the need for a more comprehensive understanding of cognitive decline.

Main Methods:

  • Review of existing in-vivo biomarker evidence in humans.
  • Analysis of the limitations of the amyloid hypothesis in accounting for disease complexity.

Main Results:

  • Amyloid-lowering drugs show some therapeutic benefit, but their widespread effectiveness is not guaranteed.
  • The amyloid hypothesis alone does not fully explain the multifaceted nature of late-life cognitive impairment.

Conclusions:

  • Alzheimer's disease pathogenesis involves multiple factors beyond amyloid-beta, including brain pathology, inflammation, and host resilience.
  • Future research and treatment strategies must adopt a multifactorial approach to address the complexity of cognitive decline.