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: Treatment01:22

Alzheimer's Disease: Treatment

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...
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'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...
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...
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...
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

Trem2 R47H mutation shows mild, but functionally divergent alterations in microglial phenotypes compared to Trem2 deficiency in aged App<sup>NL-F</sup> knock-in mice.

Experimental neurology·2026
Same author

Proline-Rich Transmembrane Protein 2 Is Variably Expressed Across Excitatory and Inhibitory Neurons in Mouse Motor Circuits.

The Journal of comparative neurology·2026
Same author

A phase II trial of ramucirumab and docetaxel as second-line treatment for patients with advanced gastric cancer (HGCSG 1903).

Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association·2026
Same author

Gene Expression Profiles Reveal Altered Metabolic Signaling Pathway in Skeletal Muscle With Lipid Sensor Gpr120/Ffar4 Deficiency.

Genes to cells : devoted to molecular & cellular mechanisms·2026
Same author

Cell type- and neuronal differentiation-dependent MME 5'UTR splice variants with distinct translational outputs in human cells.

Journal of biochemistry·2026
Same author

Disruption of the l-DOPA Receptor Gpr143/OA1-Gene in Mice Creates a Unique Mixed Psychosis-Like Phenotype.

Neuropsychopharmacology reports·2026

Related Experiment Video

Updated: Jul 18, 2026

A11-positive &#946;-amyloid Oligomer Preparation and Assessment Using Dot Blotting Analysis
06:17

A11-positive β-amyloid Oligomer Preparation and Assessment Using Dot Blotting Analysis

Published on: May 22, 2018

Berberine alters the processing of Alzheimer's amyloid precursor protein to decrease Abeta secretion.

Masashi Asai1, Nobuhisa Iwata, Ayumu Yoshikawa

  • 1Department of Pharmacology, Faculty of Medicine, Saitama Medical University, 38 Moro-hongo, Iruma-gun, Saitama 350-0495, Japan. asai@saitama-med.ac.jp

Biochemical and Biophysical Research Communications
|November 28, 2006
PubMed
Summary

Berberine, a natural compound, effectively lowers amyloid-beta peptide (Abeta) levels by influencing amyloid precursor protein (APP) processing. This suggests berberine as a potential therapeutic for Alzheimer's disease (AD).

More Related Videos

Preparation of Oligomeric &beta;-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

Imaging the Intracellular Trafficking of APP with Photoactivatable GFP
07:55

Imaging the Intracellular Trafficking of APP with Photoactivatable GFP

Published on: October 17, 2015

Related Experiment Videos

Last Updated: Jul 18, 2026

A11-positive &#946;-amyloid Oligomer Preparation and Assessment Using Dot Blotting Analysis
06:17

A11-positive β-amyloid Oligomer Preparation and Assessment Using Dot Blotting Analysis

Published on: May 22, 2018

Preparation of Oligomeric &beta;-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

Imaging the Intracellular Trafficking of APP with Photoactivatable GFP
07:55

Imaging the Intracellular Trafficking of APP with Photoactivatable GFP

Published on: October 17, 2015

Area of Science:

  • Neuroscience
  • Pharmacology
  • Biochemistry

Background:

  • Berberine, an isoquinoline alkaloid from Coptidis rhizoma, exhibits diverse biological activities.
  • Alzheimer's disease (AD) is characterized by amyloid-beta peptide (Abeta) accumulation, stemming from amyloid precursor protein (APP).
  • Inhibition of Abeta production is a key therapeutic strategy for AD.

Purpose of the Study:

  • To investigate berberine's effect on Abeta production and APP processing.
  • To evaluate berberine's potential as a therapeutic agent for Alzheimer's disease.

Main Methods:

  • Utilized human neuroglioma H4 cells stably expressing the Swedish mutant form of APP.
  • Administered berberine across a range of concentrations.
  • Assessed cellular toxicity and Abeta levels.

Main Results:

  • Berberine significantly reduced Abeta levels in H4 cells.
  • The reduction in Abeta was achieved by modulating APP processing.
  • No cellular toxicity was observed within the effective concentration range.

Conclusions:

  • Berberine modulates APP processing to decrease Abeta levels.
  • Berberine demonstrates potential as a novel therapeutic candidate for Alzheimer's disease treatment.
  • Further research is warranted to explore berberine's efficacy in AD.