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

Translation01:31

Translation

Lesson: Translation
Translation is the process of synthesizing proteins from the genetic information carried by messenger RNA (mRNA). Following transcription, it constitutes the final step in the expression of genes. This process is carried out by ribosomes, complexes of protein and specialized RNA molecules. Ribosomes, transfer RNA (tRNA), and other proteins produce a chain of amino acids—the polypeptide—as the end product of translation.
Translation Produces the Building Blocks of Life
Translation01:31

Translation

Lesson: Translation
Translation is the process of synthesizing proteins from the genetic information carried by messenger RNA (mRNA). Following transcription, it constitutes the final step in the expression of genes. This process is carried out by ribosomes, complexes of protein and specialized RNA molecules. Ribosomes, transfer RNA (tRNA), and other proteins produce a chain of amino acids—the polypeptide—as the end product of translation.
Translation Produces the Building Blocks of Life
Factors Affecting Erythropoiesis01:24

Factors Affecting Erythropoiesis

The cardiovascular system regulates the number of erythrocytes in the bloodstream to ensure optimal oxygen transport. It also prevents over-proliferation of these cells, which helps to maintain blood viscosity and flow rate.
Several factors influence the erythrocyte production rate, with tissue oxygen level being among the most critical. Intense exercise or high altitudes can cause tissue hypoxia, which triggers the kidneys to release more erythropoietin (EPO) into the bloodstream.
EPO then...
Pharmacogenetic Phenotypes: Alterations in Pharmacokinetics, Drug Targets and Biologic Milieu01:29

Pharmacogenetic Phenotypes: Alterations in Pharmacokinetics, Drug Targets and Biologic Milieu

Genetic variations significantly influence drug response through pharmacokinetics, receptor interactions, and biologic milieu modifications. Pharmacokinetic alterations impact drug metabolism and clearance, affecting efficacy and toxicity. Variants in drug-metabolizing enzymes, such as CYP2C9 and CYP2C19, alter drug activation and elimination. For example, CYP2C9 loss-of-function variants require lower warfarin doses to prevent excessive bleeding, while CYP2C19 variants reduce clopidogrel...
Human Genetics01:28

Human Genetics

Human genetics provides a profound framework for understanding the interplay between genetic predispositions and human psychology. At the heart of this discipline lies the study of how genes influence physical traits, behaviors, and susceptibility to diseases. Each person carries a unique genetic code that subtly or significantly shapes their psychological and behavioral landscape.
The complex relationship between genetics and psychology is observable through common biological components such...
Genetic Lingo01:11

Genetic Lingo

Overview

You might also read

Related Articles

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

Sort by
Same author

L-DOPA influences transferrin-dependent iron release at the blood-brain barrier.

Fluids and barriers of the CNS·2026
Same author

The role of iron in driving sex-biased differences in cancer.

Cancer metastasis reviews·2026
Same author

Reimagining the contribution of iron in Parkinson's disease.

Neurobiology of disease·2026
Same author

Systemic iron availability differentially shapes tumor and brain iron handling in a sex-dependent manner in glioblastoma.

PloS one·2026
Same author

Tumor-associated macrophages promote ferroptosis resistance in glioblastoma by stimulating iron-loaded extracellular vesicle release.

Journal of neuro-oncology·2026
Same author

Cerebrospinal Fluid from Restless Legs Syndrome Patients Reduces Iron Uptake in Blood-Brain Barrier Endothelial Cells by Disrupting the Regulation of Transferrin Receptors.

Annals of neurology·2026

Related Experiment Video

Updated: Jun 4, 2026

Assessing Iron Deposition in the Brains of 5xFAD Mice by Perls'/DAB Staining
07:32

Assessing Iron Deposition in the Brains of 5xFAD Mice by Perls'/DAB Staining

Published on: May 23, 2025

HFE gene variants affect iron in the brain.

Wint Nandar1, James R Connor

  • 1Department of Neurosurgery, Pennsylvania State University, M. S. Hershey Medical Center, Hershey, PA 17033, USA.

The Journal of Nutrition
|February 25, 2011
PubMed
Summary

The HFE gene variants, particularly H63D, are linked to iron dysregulation and oxidative stress, potentially increasing the risk for neurodegenerative diseases like Alzheimer's and Parkinson's.

Area of Science:

  • Neuroscience
  • Genetics
  • Biochemistry

Background:

  • Iron accumulation and oxidative stress are hallmarks of neurodegenerative diseases.
  • The HFE gene plays a crucial role in iron metabolism, and its variants can lead to iron overload.
  • The HFE gene variants C282Y and H63D are common, with H63D gaining attention for its role in neurodegeneration.

Purpose of the Study:

  • To review the association between HFE gene variants and neurodegenerative diseases.
  • To explore the cellular mechanisms linking HFE variants to neurodegeneration.
  • To challenge the notion that the brain is protected from HFE mutation-associated iron accumulation.

Main Methods:

  • Literature review of studies investigating HFE gene variants and neurodegenerative diseases.

More Related Videos

Measurement of Heme Synthesis Levels in Mammalian Cells
09:43

Measurement of Heme Synthesis Levels in Mammalian Cells

Published on: July 9, 2015

Setup of Capillary Electrophoresis-Inductively Coupled Plasma Mass Spectrometry (CE-ICP-MS) for Quantification of Iron Redox Species (Fe(II), Fe(III))
04:48

Setup of Capillary Electrophoresis-Inductively Coupled Plasma Mass Spectrometry (CE-ICP-MS) for Quantification of Iron Redox Species (Fe(II), Fe(III))

Published on: May 4, 2020

Related Experiment Videos

Last Updated: Jun 4, 2026

Assessing Iron Deposition in the Brains of 5xFAD Mice by Perls'/DAB Staining
07:32

Assessing Iron Deposition in the Brains of 5xFAD Mice by Perls'/DAB Staining

Published on: May 23, 2025

Measurement of Heme Synthesis Levels in Mammalian Cells
09:43

Measurement of Heme Synthesis Levels in Mammalian Cells

Published on: July 9, 2015

Setup of Capillary Electrophoresis-Inductively Coupled Plasma Mass Spectrometry (CE-ICP-MS) for Quantification of Iron Redox Species (Fe(II), Fe(III))
04:48

Setup of Capillary Electrophoresis-Inductively Coupled Plasma Mass Spectrometry (CE-ICP-MS) for Quantification of Iron Redox Species (Fe(II), Fe(III))

Published on: May 4, 2020

  • Analysis of cellular mechanisms involving HFE mutant proteins, iron homeostasis, oxidative stress, and neuroinflammation.
  • Synthesis of current knowledge on HFE variants in amyotrophic lateral sclerosis, Alzheimer's disease, Parkinson's disease, and ischemic stroke.
  • Main Results:

    • HFE gene variants, especially H63D, are associated with iron dyshomeostasis and increased oxidative stress in the brain.
    • Cellular effects of HFE mutant proteins include glutamate release, tau phosphorylation, and altered inflammatory responses.
    • Evidence suggests HFE variants act as genetic modifiers or risk factors for neurodegenerative diseases.

    Conclusions:

    • HFE gene variants are implicated in the pathogenesis of neurodegenerative diseases by disrupting iron balance.
    • The brain is not fully protected from iron accumulation associated with HFE mutations.
    • Further research into HFE variants may reveal new therapeutic targets for neurodegenerative conditions.