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

Non-LTR Retrotransposons03:18

Non-LTR Retrotransposons

11.7K
As the name suggests, non-LTR retrotransposons lack the long terminal repeats characteristic of the LTR retrotransposons. Additionally, both LTR and non-LTR retrotransposons use distinct mechanisms of mobilization. Non-LTR retrotransposons are further divided into two classes - Long interspersed nuclear elements (LINEs) and short interspersed nuclear elements (SINEs), both of which occur abundantly in most mammals, including humans. Some of the active non-LTR retrotransposons in humans are L1...
11.7K
Transposons01:24

Transposons

90
Transposons, or "jumping genes," are small mobile genetic elements (MGEs) that range from 700 to 40,000 base pairs in length. They are found in all organisms and can move within the same chromosome or transfer to different chromosomes. In some cases, transposons can also jump between different host DNA molecules, such as plasmids or viruses, contributing to genetic variability.Barbara McClintock first discovered these mobile genetic elements in the 1940s while studying maize genetics, and she...
90
Overview of Transposition and Recombination02:13

Overview of Transposition and Recombination

16.0K
Transposons make up a significant part of genomes of various organisms. Therefore, it is believed that transposition played a major evolutionary role in speciation by changing genome sizes and modifying gene expression patterns. For example, in bacteria, transposition can lead to conferring antibiotic resistance. Movement of transposable elements within the genetic pool of pathogenic bacteria can aid in transfer of antibiotic-resistant genetic elements. In eukaryotes, transposons can carry out...
16.0K
Alzheimer's Disease: Overview01:26

Alzheimer's Disease: Overview

602
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...
602
DNA-only Transposons02:57

DNA-only Transposons

14.6K
DNA-only transposons are called autonomous transposons since they code for the enzyme transposase that is required for the transposition mechanism. Insertion of transposons can alter gene functions in multiple ways. They can mutate the gene, alter gene expression by introducing a novel promoter or insulator sequence, introduce new splice sites, and change the mRNA transcripts produced, or remodel chromatin structure.
The donor site from where the transposon is excised is either degraded or...
14.6K
LTR Retrotransposons03:08

LTR Retrotransposons

17.7K
LTR retrotransposons are class I transposable elements with long terminal repeats flanking an internal coding region. These elements are less abundant in mammals compared to other class I transposable elements. About 8 percent of human genomic DNA comprises LTR retrotransposons. Some of the common examples of LTR retrotransposons are Ty elements in yeast and Copia elements in Drosophila.
The internal coding region of LTR retrotransposons and their mechanism of transposition closely resembles a...
17.7K

You might also read

Related Articles

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

Sort by
Same author

EBV Triggers a Distinct Antiviral Response in HMC3 Cells.

bioRxiv : the preprint server for biology·2026
Same author

Human endogenous retrovirus profiling reveals heterogenous expression in cutaneous melanoma.

Frontiers in oncology·2026
Same author

HIV Nef-mediated WAVE2-ARP2/3 inhibition underlies CD4<sup>+</sup> T-cell lamellipodial abnormalities and immune dysfunction.

mBio·2026
Same author

Multiomic analysis of ART-interruption cohorts identifies cell-extrinsic and -intrinsic mechanisms driving lymphocyte-mediated control of HIV rebound.

Immunity·2026
Same author

CDK9 Inhibition with enitociclib reveals influence on HERV and LINE RNA abundances in whole blood, T-, and B-Cell lines.

BMC medical genomics·2026
Same author

Transcriptional signature of induced neurons differentiates virologically suppressed people with HIV from people without HIV.

JCI insight·2025

Related Experiment Video

Updated: Aug 15, 2025

Motor and Hippocampal Dependent Spatial Learning and Reference Memory Assessment in a Transgenic Rat Model of Alzheimer's Disease with Stroke
09:45

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

10.3K

Transposable elements and Alzheimer's disease pathogenesis.

Teresa H Evering1, Jez L Marston1, Li Gan2

  • 1Division of Infectious Diseases, Department of Medicine, Weill Cornell Medicine, New York, NY, 10021, USA.

Trends in Neurosciences
|January 1, 2023
PubMed
Summary
This summary is machine-generated.

Alzheimer's disease involves amyloid plaques and tau tangles. New research shows that glial cells, like microglia and astrocytes, react to tau by activating transposable elements, linking their dysregulated expression to Alzheimer's disease pathogenesis.

Keywords:
human endogenous retrovirusesinnate immunitylong interspersed nuclear elements type 1neurodegenerationretrotransposontau

More Related Videos

Novel Passive Clearing Methods for the Rapid Production of Optical Transparency in Whole CNS Tissue
06:14

Novel Passive Clearing Methods for the Rapid Production of Optical Transparency in Whole CNS Tissue

Published on: May 8, 2018

8.9K
Quantitative 3D In Silico Modeling q3DISM of Cerebral Amyloid-beta Phagocytosis in Rodent Models of Alzheimer's Disease
09:33

Quantitative 3D In Silico Modeling q3DISM of Cerebral Amyloid-beta Phagocytosis in Rodent Models of Alzheimer's Disease

Published on: December 26, 2016

8.0K

Related Experiment Videos

Last Updated: Aug 15, 2025

Motor and Hippocampal Dependent Spatial Learning and Reference Memory Assessment in a Transgenic Rat Model of Alzheimer's Disease with Stroke
09:45

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

10.3K
Novel Passive Clearing Methods for the Rapid Production of Optical Transparency in Whole CNS Tissue
06:14

Novel Passive Clearing Methods for the Rapid Production of Optical Transparency in Whole CNS Tissue

Published on: May 8, 2018

8.9K
Quantitative 3D In Silico Modeling q3DISM of Cerebral Amyloid-beta Phagocytosis in Rodent Models of Alzheimer's Disease
09:33

Quantitative 3D In Silico Modeling q3DISM of Cerebral Amyloid-beta Phagocytosis in Rodent Models of Alzheimer's Disease

Published on: December 26, 2016

8.0K

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Genetics

Background:

  • Alzheimer's disease (AD) is defined by amyloid-beta (Aβ) plaques and hyperphosphorylated tau tangles.
  • Microglia and astrocytes are key glial cells in the brain's response to AD pathology.

Purpose of the Study:

  • To explore the connection between transposable element (TE) transcription and Alzheimer's disease.
  • To discuss novel data linking aberrant TE expression to AD pathogenesis.

Main Methods:

  • Review of recent studies on glial cell response in AD.
  • Analysis of data on transposable element activity in the context of tau pathology.

Main Results:

  • Tau protein in AD triggers transposable element (TE) transcription in microglia and astrocytes.
  • Dysregulation of TE expression is implicated in the development and progression of Alzheimer's disease.

Conclusions:

  • Transposable element dysregulation represents a novel mechanism in Alzheimer's disease.
  • Targeting TE activity in glial cells may offer new therapeutic strategies for AD.