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Related Concept Videos

Overview of Transposition and Recombination02:13

Overview of Transposition and Recombination

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...
DNA-only Transposons02:57

DNA-only Transposons

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...
Non-LTR Retrotransposons03:18

Non-LTR Retrotransposons

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...
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...
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...
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...

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Related Experiment Video

Updated: May 11, 2026

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

Cellular insights into transposable elements in Alzheimer's disease.

Vikas Kumar1,2, Samuel Beck1

  • 1Center for Aging Research, Department of Dermatology, Chobanian & Avedisian School of Medicine, Boston University, Boston, MA, United States.

Frontiers in Molecular Biosciences
|January 23, 2026
PubMed
Summary

Transposable elements (TEs) are activated in Alzheimer's disease (AD), particularly in excitatory neurons and oligodendrocytes. This widespread TE dysregulation offers new avenues for understanding AD pathogenesis and developing therapies.

Keywords:
Alzheimer diseasebioinformaticsdifferential expression and marker genessingle-celltransposable elements

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

Mapping Alzheimer's Disease Variants to Their Target Genes Using Computational Analysis of Chromatin Configuration
04:41

Mapping Alzheimer's Disease Variants to Their Target Genes Using Computational Analysis of Chromatin Configuration

Published on: January 9, 2020

Related Experiment Videos

Last Updated: May 11, 2026

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

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

Mapping Alzheimer's Disease Variants to Their Target Genes Using Computational Analysis of Chromatin Configuration
04:41

Mapping Alzheimer's Disease Variants to Their Target Genes Using Computational Analysis of Chromatin Configuration

Published on: January 9, 2020

Area of Science:

  • Genomics
  • Neuroscience
  • Molecular Biology

Background:

  • Alzheimer's disease (AD) is a major neurodegenerative disorder with complex genetic underpinnings.
  • Single-cell technologies have revealed cellular and transcriptional alterations in AD, but the role of transposable elements (TEs) is unclear.

Purpose of the Study:

  • To investigate the cell type-specific landscape of TE expression and regulation in Alzheimer's disease.
  • To identify specific TEs and their regulatory roles in AD pathogenesis.

Main Methods:

  • Integration of single-nucleus RNA sequencing and ATAC-seq data from AD patients and controls.
  • Mapping of cell type-specific TE expression and chromatin accessibility.

Main Results:

  • Identification of 508 differentially expressed TE loci, with 84.3% upregulated in AD.
  • Widespread TE activation observed, predominantly in excitatory neurons and oligodendrocytes.
  • Dysregulated TEs found near key AD-associated genes (e.g., DOC2A, ABCA7, TARDBP).

Conclusions:

  • TE activation is a significant feature of Alzheimer's disease, varying by cell type.
  • TE dysregulation may contribute to AD pathogenesis through regulatory disruption.
  • These findings provide a basis for exploring TEs as therapeutic targets in AD.