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

666
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...
666
Insulin: The Receptor and Signaling Pathways01:28

Insulin: The Receptor and Signaling Pathways

1.5K
Insulin action is mediated through a receptor tyrosine kinase, akin to the IGF-1 receptor. The number of receptors per cell varies significantly, from 40 on erythrocytes to 300,000 on adipocytes and hepatocytes. The insulin receptor consists of linked α/β subunit dimers, forming a heterotetramer glycoprotein with two extracellular α subunits and two β subunits spanning the membrane. The α subunits inhibit the inherent tyrosine kinase activity of the β subunits, but...
1.5K
Alzheimer's Disease: Treatment01:22

Alzheimer's Disease: Treatment

260
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...
260
Psychoneuroimmunology: Diabetes and Cancer01:19

Psychoneuroimmunology: Diabetes and Cancer

62
Chronic stress has been linked to both the onset and progression of serious health conditions, including Type 2 diabetes and cancer. Type 2 diabetes, a widespread chronic illness, is closely associated with obesity and insulin resistance, both of which often worsen under stress. Studies indicate that men experiencing high levels of chronic stress face a 45% higher risk of developing diabetes compared to those with minimal stress. Stress triggers physiological responses that elevate blood...
62
Insulin Secretory Vesicles01:05

Insulin Secretory Vesicles

5.4K
Insulin secretory vesicles release insulin to stimulate blood glucose uptake and regulate carbohydrate metabolism. When the blood glucose levels increase, glucose enters the pancreatic β-islet cells through glucose transporters. Once inside, glucose is metabolized through glycolysis, the citric acid cycle, and the electron transport chain, producing ATP. This increase in ATP concentration closes ATP-sensitive potassium channels, leading to depolarization of the membrane and the opening of...
5.4K
Glucose Homeostasis: Pancreatic Islets and Insulin Secretion01:27

Glucose Homeostasis: Pancreatic Islets and Insulin Secretion

1.4K
The pancreatic islets comprising only 1%-2% of the volume are highly vascularized and innervated mini-organs. They contain five endocrine cell types, including β cells that secrete insulin, which is synthesized as a single polypeptide chain, preproinsulin, processed to proinsulin, and finally to insulin and C-peptide. This process is complex and regulated, involving the Golgi complex, the endoplasmic reticulum, and the secretory granules of the β cell.
Insulin and C-peptide are...
1.4K

You might also read

Related Articles

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

Sort by
Same author

[Preface].

Nihon yakurigaku zasshi. Folia pharmacologica Japonica·2025
Same author

Chronic Neuronal Hyperexcitation Exacerbates Tau Propagation in a Mouse Model of Tauopathy.

International journal of molecular sciences·2024
Same author

Genetic Reduction of Insulin Signaling Mitigates Amyloid-β Deposition by Promoting Expression of Extracellular Matrix Proteins in the Brain.

The Journal of neuroscience : the official journal of the Society for Neuroscience·2023
Same author

Casein kinase 1δ/ε phosphorylates fused in sarcoma (FUS) and ameliorates FUS-mediated neurodegeneration.

The Journal of biological chemistry·2022
Same author

Differential involvement of insulin receptor substrate (IRS)-1 and IRS-2 in brain insulin signaling is associated with the effects on amyloid pathology in a mouse model of Alzheimer's disease.

Neurobiology of disease·2021
Same author

Transmembrane Collagens in Neuromuscular Development and Disorders.

Frontiers in molecular neuroscience·2021

Related Experiment Video

Updated: Sep 9, 2025

Osmotic Minipump Implantation for Increasing Glucose Concentration in Mouse Cerebrospinal Fluid
06:21

Osmotic Minipump Implantation for Increasing Glucose Concentration in Mouse Cerebrospinal Fluid

Published on: April 7, 2023

1.7K

[Insulin signaling and neuropathological changes in Alzheimer's disease].

Tomoko Wakabayashi1

  • 1Department of Pathophysiology, Meiji Pharmaceutical University.

Nihon Yakurigaku Zasshi. Folia Pharmacologica Japonica
|August 31, 2025
PubMed
Summary

Type 2 diabetes and insulin resistance are linked to Alzheimer's disease (AD) progression. Understanding these metabolic factors is key to developing new early interventions for AD.

More Related Videos

Studying the Hypothalamic Insulin Signal to Peripheral Glucose Intolerance with a Continuous Drug Infusion System into the Mouse Brain
08:32

Studying the Hypothalamic Insulin Signal to Peripheral Glucose Intolerance with a Continuous Drug Infusion System into the Mouse Brain

Published on: January 4, 2018

10.4K
Detection of Neuritic Plaques in Alzheimer's Disease Mouse Model
06:02

Detection of Neuritic Plaques in Alzheimer's Disease Mouse Model

Published on: July 26, 2011

36.8K

Related Experiment Videos

Last Updated: Sep 9, 2025

Osmotic Minipump Implantation for Increasing Glucose Concentration in Mouse Cerebrospinal Fluid
06:21

Osmotic Minipump Implantation for Increasing Glucose Concentration in Mouse Cerebrospinal Fluid

Published on: April 7, 2023

1.7K
Studying the Hypothalamic Insulin Signal to Peripheral Glucose Intolerance with a Continuous Drug Infusion System into the Mouse Brain
08:32

Studying the Hypothalamic Insulin Signal to Peripheral Glucose Intolerance with a Continuous Drug Infusion System into the Mouse Brain

Published on: January 4, 2018

10.4K
Detection of Neuritic Plaques in Alzheimer's Disease Mouse Model
06:02

Detection of Neuritic Plaques in Alzheimer's Disease Mouse Model

Published on: July 26, 2011

36.8K

Area of Science:

  • Neuroscience
  • Endocrinology
  • Metabolic Disorders

Background:

  • Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by amyloid-β (Aβ) and tau pathology.
  • Current anti-Aβ therapies show limited efficacy in later stages, emphasizing the need for preclinical interventions.
  • Type 2 diabetes (T2D) and insulin resistance are recognized as acquired risk factors for AD.

Purpose of the Study:

  • To review epidemiological and experimental evidence linking T2D and insulin resistance to AD neuropathology.
  • To clarify the complex relationship between insulin signaling, metabolic disturbances, and Aβ accumulation in AD.
  • To identify potential therapeutic targets for early AD intervention.

Main Methods:

  • Review of epidemiological studies, including postmortem and PET imaging data.
  • Analysis of experimental evidence from animal models of insulin resistance and AD.
  • Synthesis of findings on the dual role of insulin signaling in central and peripheral tissues.

Main Results:

  • Recent PET imaging studies confirm a link between T2D, insulin resistance, and Aβ deposition in the human brain.
  • Animal studies indicate diet-induced insulin resistance exacerbates Aβ accumulation.
  • Genetic disruption of insulin signaling pathways suppresses Aβ pathology, suggesting a protective effect.

Conclusions:

  • Peripheral insulin resistance may accelerate Aβ deposition, while reduced central insulin signaling might inhibit it.
  • The complex interplay between insulin signaling and metabolic health significantly influences AD pathogenesis.
  • Further research into these interactions is vital for novel AD prevention and treatment strategies.