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 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 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...
The Effect of Aging on Tissues01:19

The Effect of Aging on Tissues

Several body functions deteriorate with age. The external signs of aging are easily identifiable. For example, the skin becomes dry, less elastic, and thins out, forming wrinkles. The skin of the face begins to appear looser due to a decrease in the levels of elastic and collagen fibers in the connective tissue. Additionally, melanin production in the hair follicle decreases with age, resulting in gray hair. Moreover, the senses of sight and hearing decline, so glasses and hearing aids may...
Aging01:26

Aging

Aging is a complex biological phenomenon influenced by various processes that affect cellular and systemic functions. Several prominent theories attempt to explain its mechanisms, highlighting cellular limitations, oxidative damage, and hormonal changes as central factors in aging.
Cellular Clock Theory
The cellular clock theory posits that the human lifespan is closely tied to the finite capacity of cells to divide, a phenomenon governed by telomeres, which are protective caps at the ends of...
Drugs Affecting Neurotransmitter Synthesis01:29

Drugs Affecting Neurotransmitter Synthesis

Drugs affecting neurotransmitter synthesis can impact the adrenergic neuron and the synthesis of neurotransmitters. For example, α-methyltyrosine and carbidopa target specific enzymes involved in catecholamine synthesis. α-methyltyrosine inhibits the enzyme tyrosine hydroxylase, which converts tyrosine into dopamine. By blocking this enzyme, α-methyltyrosine reduces dopamine production and other catecholamines. Carbidopa, on the other hand, inhibits the enzyme dopa decarboxylase, which converts...
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...

You might also read

Related Articles

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

Sort by
Same author

Using effect biomarker thresholds in regulatory risk assessment: an OECD-based framework for assessing cumulative exposures to chemical mixtures.

Environment international·2026
Same author

Ageing phenotypes and behavioural determinants of health on age acceleration: the Cancer Survivors' Trajectories of Ageing Research (C*STAR) study protocol.

BMJ open·2026
Same author

The Buccal Micronucleus (BMN) Cytome assay: enhancing its applications by addressing challenges and exploring new opportunities.

Mutagenesis·2026
Same author

High-dose vitamin D supplementation and prostate cancer progression: a phase II randomised trial in localised prostate cancer cases with intermediate risk of progression (ProsD).

British journal of cancer·2025
Same author

Comparative Analysis of Aging-related Metabolic and Biological Markers between Cancer Survivors and Healthy Populations: A Systematic Review.

Journal of cancer prevention·2025
Same author

Innovating the buccal micronucleus cytome assay to improve its utility as a biomarker of in vivo genotoxicity.

Mutagenesis·2025

Related Experiment Video

Updated: Jun 15, 2026

Modifying Levels of Maternal Dietary Folic Acid or Choline to Study the Impact of Deficiencies on Offspring Health Outcomes
03:19

Modifying Levels of Maternal Dietary Folic Acid or Choline to Study the Impact of Deficiencies on Offspring Health Outcomes

Published on: June 28, 2024

Folate, DNA damage and the aging brain.

Michael Fenech1

  • 1CSIRO Food and Nutritional Sciences, Nutritional Genomics, Gate 13, Kintore Avenue, PO Box 10041, Adelaide BC, SA 5000, Australia. michael.fenech@csiro.au

Mechanisms of Ageing and Development
|March 12, 2010
PubMed
Summary

Folate deficiency increases DNA damage and accelerates brain aging by impairing DNA synthesis and repair. This review explores folate

Area of Science:

  • Biochemistry and Molecular Biology
  • Neuroscience
  • Genetics and Epigenetics

Background:

  • Folate is crucial as a methyl donor for DNA synthesis (thymine) and cytosine methylation, essential for gene expression and chromatin structure.
  • Folate deficiency leads to increased nuclear and mitochondrial DNA damage and reduced tissue regenerative capacity.
  • Elevated homocysteine, a metabolite linked to folate deficiency, is implicated in various health issues.

Purpose of the Study:

  • To review the evidence linking folate deficiency and its metabolites to accelerated DNA damage and brain aging.
  • To identify knowledge gaps in understanding the role of folate in neurodegeneration.

Main Methods:

  • Literature review of current evidence on folate metabolism, DNA damage, and brain aging.

More Related Videos

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

The Detection of 5-Hydroxymethylcytosine in Neural Stem Cells and Brains of Mice
08:03

The Detection of 5-Hydroxymethylcytosine in Neural Stem Cells and Brains of Mice

Published on: September 19, 2019

Related Experiment Videos

Last Updated: Jun 15, 2026

Modifying Levels of Maternal Dietary Folic Acid or Choline to Study the Impact of Deficiencies on Offspring Health Outcomes
03:19

Modifying Levels of Maternal Dietary Folic Acid or Choline to Study the Impact of Deficiencies on Offspring Health Outcomes

Published on: June 28, 2024

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

The Detection of 5-Hydroxymethylcytosine in Neural Stem Cells and Brains of Mice
08:03

The Detection of 5-Hydroxymethylcytosine in Neural Stem Cells and Brains of Mice

Published on: September 19, 2019

  • Exploration of the mechanisms by which folate deficiency impacts genomic integrity.
  • Analysis of the role of metabolites like homocysteine and uracil incorporation.

    • Main Results:

    • Folate deficiency contributes to DNA damage through uracil misincorporation and increased susceptibility to agents like Aβ42 and ROS.
    • Impaired DNA repair and maintenance due to folate deficiency can accelerate cellular aging.
    • Evidence suggests a correlation between folate deficiency, DNA damage, and neurodegenerative processes.

    Conclusions:

    • Folate deficiency is a significant factor in accelerating DNA damage and brain aging.
    • Further research is needed to fully elucidate the mechanisms and therapeutic implications.
    • Understanding folate's role is critical for addressing DNA damage in neurodegenerative diseases.