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'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...

Bone Disorders

Bone Disorders

Aging and its effect on bone remodeling is the most common cause of bone disorders. In young and healthy people, bone deposition and resorption happen at an equal rate to maintain optimal bone health.
Bone deposition is also affected by the levels of sex hormones like estrogen and testosterone that promote osteoblast activity and bone matrix synthesis. When the level of these hormones decreases due to aging, it causes a reduction in bone deposition. As a result, bone resorption by osteoclasts...

Alzheimer's Disease: Treatment

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...

Modeling in Therapy

Modeling in Therapy

Modeling, a key technique in therapy, uses observational learning to help clients acquire and practice new skills by watching therapists demonstrate desired behaviors. This approach, rooted in Albert Bandura's concept of vicarious learning, plays a significant role in therapeutic interventions for various psychological conditions, including social anxiety, ADHD, and depression.
Participant Modeling
Participant modeling involves therapists demonstrating calm and effective behaviors in...

Bone Remodeling

Bone Remodeling

Bone remodeling is a continuous and balanced process of bone resorption by osteoclasts and bone formation by osteoblasts. In adults, it helps maintain bone mass and calcium homeostasis. While mechanical stress can stimulate turnover as part of the normal maintenance and reparative process, several hormones also regulate bone remodeling.

You might also read

Related Articles

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

Sort by

Same author

Osteoinductivity of Tunable Shape Memory Polymer-Bioglass Composite Scaffolds.

ACS biomaterials science & engineering·2026

Same author

Rapamycin and Suramin Effects on TNF-⍺-Mediated Mast Cell and Brain Microvascular Endothelial Cell Dysfunction.

Biotechnology and bioengineering·2025

Same author

Editorial: The role of glial cells in neurodegeneration.

Frontiers in molecular medicine·2024

Same author

Impact of Suramin on Key Pathological Features of Sporadic Alzheimer's Disease-Derived Forebrain Neurons.

Journal of Alzheimer's disease : JAD·2024

Same author

Trends in bioactivity: inducing and detecting mineralization of regenerative polymeric scaffolds.

Journal of materials chemistry. B·2024

Same author

Effects of Stromal Cell Conditioned Medium and Antipurinergic Treatment on Macrophage Phenotype.

Tissue engineering. Part C, Methods·2022

Search research articles

Related Experiment Video

Updated: Oct 19, 2025

Fabrication of Amyloid-β-Secreting Alginate Microbeads for Use in Modelling Alzheimer's Disease

Fabrication of Amyloid-β-Secreting Alginate Microbeads for Use in Modelling Alzheimer's Disease

Published on: July 6, 2019

Modeling Sympathetic Hyperactivity in Alzheimer's Related Bone Loss.

Robert A Culibrk¹, Ahmad S Arabiyat¹, Carisa A DeKalb¹

¹Hahn Tissue Lab, Department of Biomedical Engineering, Rensselaer Polytechnic Institute, Troy, NY, USA.

Journal of Alzheimer'S Disease : JAD

|September 27, 2021

Summary

Dysregulated sympathetic neurons and mesenchymal stem cells, exacerbated by inflammation, may contribute to bone loss in Alzheimer's disease (AD). This study models these interactions to understand AD-related osteopenia.

Keywords:

Alzheimer’s disease inflammation mesenchymal stem cells osteopenia

More Related Videos

Motor and Hippocampal Dependent Spatial Learning and Reference Memory Assessment in a Transgenic Rat Model of Alzheimer's Disease with Stroke

Motor and Hippocampal Dependent Spatial Learning and Reference Memory Assessment in a Transgenic Rat Model of Alzheimer's Disease with Stroke

Published on: March 22, 2016

Stereotaxic Infusion of Oligomeric Amyloid-beta into the Mouse Hippocampus

Stereotaxic Infusion of Oligomeric Amyloid-beta into the Mouse Hippocampus

Published on: June 17, 2015

Related Experiment Videos

Last Updated: Oct 19, 2025

Fabrication of Amyloid-β-Secreting Alginate Microbeads for Use in Modelling Alzheimer's Disease

Fabrication of Amyloid-β-Secreting Alginate Microbeads for Use in Modelling Alzheimer's Disease

Published on: July 6, 2019

Motor and Hippocampal Dependent Spatial Learning and Reference Memory Assessment in a Transgenic Rat Model of Alzheimer's Disease with Stroke

Motor and Hippocampal Dependent Spatial Learning and Reference Memory Assessment in a Transgenic Rat Model of Alzheimer's Disease with Stroke

Published on: March 22, 2016

Stereotaxic Infusion of Oligomeric Amyloid-beta into the Mouse Hippocampus

Stereotaxic Infusion of Oligomeric Amyloid-beta into the Mouse Hippocampus

Published on: June 17, 2015

Area of Science:

Neuroscience
Bone Biology
Cell Biology

Background:

Alzheimer's disease (AD) patients often have low bone density, increasing fracture risk.
Dysregulated sympathetic neurons (SNs) and chronic immune hyperactivity are implicated in AD-related bone loss.

Purpose of the Study:

Develop an in vitro model to study interactions between SNs and mesenchymal stem cells (MSCs).
Investigate the role of tumor necrosis factor alpha (TNF-α) in AD-related osteopenia.

Main Methods:

PC12 cells (SN-like) and MSCs were cultured in PEGDA hydrogels.
Cells were exposed to TNF-α under mono- and co-culture conditions.

Main Results:

TNF-α induced pro-inflammatory mediators in PC12s and reduced osteopontin (OPN) in MSCs.
Co-culture of TNF-α-activated PC12s and MSCs worsened pathological changes.
MSCs showed reduced osteogenic capacity (decreased OPN and collagen type I alpha I chain).

Conclusions:

TNF-α can induce dysregulated states in both SNs and MSCs, mimicking AD conditions.
Co-culture exacerbates these pathological changes, suggesting a role for SN-MSC interactions in AD.
Dysregulated sympathetic activity may contribute to bone loss in Alzheimer's disease.