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

1.9K
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...
1.9K
Amyloid Fibrils03:03

Amyloid Fibrils

12.7K
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,...
12.7K
Amyloid Fibrils03:03

Amyloid Fibrils

6.9K
6.9K
Role of Neurotransmitters in Memory01:23

Role of Neurotransmitters in Memory

2.8K
Neurotransmitters are integral to the brain's communication system, enabling neurons to transmit signals across synapses. This chemical exchange underpins various cognitive functions, including memory processes. The role of neurotransmitters in memory is multifaceted, influencing the encoding, consolidation, and retrieval of memories through their action on different neural circuits.
 Glutamate and Synaptic Plasticity
Glutamate, the brain's main excitatory neurotransmitter, is...
2.8K
Alzheimer's Disease: Treatment01:22

Alzheimer's Disease: Treatment

1.1K
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...
1.1K
Long-term Depression01:03

Long-term Depression

3.5K
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...
3.5K

You might also read

Related Articles

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

Sort by
Same author

Glial molecular signatures as a liquid biopsy marker in Alzheimer's disease diagnosis.

International review of neurobiology·2026
Same author

Why diabetes matters in dementia studies: Excluding diabetes status masks regional mitochondrial DNA copy number changes in human hippocampus, amygdala, and cerebellum in Alzheimer's disease.

bioRxiv : the preprint server for biology·2026
Same author

Pathology and Genetics in a Global Cohort of Parkinsonian Disorders.

JAMA neurology·2026
Same author

Validation of Factors Associated with Difficult Emergency Transport in Tokyo Before and After COVID-19 Pandemic: A Retrospective Observational Study.

Juntendo medical journal·2026
Same author

DNA methylation profiling in Huntington's disease reveals disease associated changes in the striatum.

Clinical epigenetics·2026
Same author

Relationships between leader behaviors, employee well-being, and profit target achievement: evidence from a company-wide survey in Japan.

Scientific reports·2026

Related Experiment Video

Updated: Mar 16, 2026

In Vitro Aggregation Assays Using Hyperphosphorylated Tau Protein
09:22

In Vitro Aggregation Assays Using Hyperphosphorylated Tau Protein

Published on: January 2, 2015

19.1K

Alzheimer-related decrease in CYFIP2 links amyloid production to tau hyperphosphorylation and memory loss.

Sachin Suresh Tiwari1, Keiko Mizuno1, Anshua Ghosh1

  • 11 Department of Basic and Clinical Neuroscience, Institute of Psychiatry, Psychology and Neuroscience, King's College London, 125 Coldharbour Lane, London, SE5 9NU, UK.

Brain : a Journal of Neurology
|August 16, 2016
PubMed
Summary

Reduced expression of Cytoplasmic FMR1 interacting protein 2 (CYFIP2) is linked to Alzheimer's disease progression, causing memory loss, amyloid plaque formation, and tau hyperphosphorylation. Targeting CYFIP2 may offer a new therapeutic strategy for Alzheimer's disease.

Keywords:
BACE1amyloid betamRNA translationspatial memorytau phosphorylation

More Related Videos

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

24.1K
Assay for Phosphorylation and Microtubule Binding Along with Localization of Tau Protein in Colorectal Cancer Cells
12:55

Assay for Phosphorylation and Microtubule Binding Along with Localization of Tau Protein in Colorectal Cancer Cells

Published on: October 10, 2017

9.5K

Related Experiment Videos

Last Updated: Mar 16, 2026

In Vitro Aggregation Assays Using Hyperphosphorylated Tau Protein
09:22

In Vitro Aggregation Assays Using Hyperphosphorylated Tau Protein

Published on: January 2, 2015

19.1K
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

24.1K
Assay for Phosphorylation and Microtubule Binding Along with Localization of Tau Protein in Colorectal Cancer Cells
12:55

Assay for Phosphorylation and Microtubule Binding Along with Localization of Tau Protein in Colorectal Cancer Cells

Published on: October 10, 2017

9.5K

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Pathology

Background:

  • Alzheimer's disease (AD) is characterized by memory loss, amyloid precursor protein (APP) processing abnormalities, and hyperphosphorylated tau.
  • The molecular links between these pathological hallmarks remain unclear.
  • Cytoplasmic FMR1 interacting protein 2 (CYFIP2) regulates synaptic translation and actin polymerization, processes crucial for memory.

Purpose of the Study:

  • To investigate the hypothesis that reduced CYFIP2 expression contributes to Alzheimer's disease pathogenesis.
  • To explore the role of CYFIP2 in APP processing, tau phosphorylation, and synaptic function in AD models.

Main Methods:

  • Analysis of CYFIP2 expression in post-mortem human brain tissue from Alzheimer's patients.
  • Assessment of CYFIP2 levels in young and old Tg2576 transgenic mice, an AD model.
  • Evaluation of APP, BACE1, tau phosphorylation, synaptic structure, and memory in CYFIP2 heterozygous null mutant mice.

Main Results:

  • CYFIP2 expression was significantly reduced in severe Alzheimer's hippocampus and temporal gyrus, with a trend in mild AD.
  • Reduced CYFIP2 expression in mice led to increased APP and BACE1 protein levels, elevated amyloid-β42 production, and increased alpha-calcium/calmodulin-dependent kinase II (CaMKII) protein.
  • This reduction also caused tau hyperphosphorylation, impaired dendritic spine maturity, and deficits in spatial memory retention.

Conclusions:

  • Reduced CYFIP2 expression is a key factor initiating a cascade of Alzheimer's-like pathology, including amyloidogenesis, tauopathy, and memory impairment.
  • CYFIP2 represents a potential therapeutic target for Alzheimer's disease.
  • Restoring CYFIP2 levels could mitigate multiple pathological features of Alzheimer's disease.