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 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...
Dementia l: Introduction01:22

Dementia l: Introduction

Dementia is an acquired, progressive syndrome characterized by a decline in multiple cognitive domains severe enough to impair daily functioning and reduce independence. Although memory loss is a central feature, the diagnosis requires additional deficits involving language, executive function, visuospatial skills, judgment, calculation, or abstract reasoning. These cognitive impairments reflect underlying neurodegenerative or vascular processes that gradually disrupt neuronal networks...
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's Disease: Treatment01:22

Alzheimer's Disease: Treatment

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...

You might also read

Related Articles

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

Sort by
Same author

Antisense Oligonucleotide Tofersen Distribution in the Central Nervous System of SOD1-ALS Autopsy Tissue Donors.

JAMA neurology·2026
Same author

The Target ALS Global Natural History Study: Cross-platform proteomics to accelerate biofluid biomarker and drug target discovery in amyotrophic lateral sclerosis.

medRxiv : the preprint server for health sciences·2026
Same author

A user's guide to calculate return on investment for artificial intelligence algorithms and imaging technologies.

Abdominal radiology (New York)·2026
Same author

Addressing the needs of nano-rare patients: the n-Lorem experience.

Nucleic acids research·2026
Same author

Multimodal analysis of cell-free DNA identifies epigenetic biomarkers for amyotrophic lateral sclerosis diagnosis and progression.

The Journal of clinical investigation·2026
Same author

Multimodal analysis of cell-free DNA identifies epigenetic biomarkers for amyotrophic lateral sclerosis diagnosis and progression.

bioRxiv : the preprint server for biology·2026

Related Experiment Video

Updated: Jul 4, 2026

Biomarker Identification for Gender Specificity of Alzheimer's Disease Based on the Glial Transcriptome Profiles
04:22

Biomarker Identification for Gender Specificity of Alzheimer's Disease Based on the Glial Transcriptome Profiles

Published on: May 20, 2024

TDP-43 subtypes shape transcriptomic signatures in Alzheimer's disease.

Xiaojie Wang, Alyssa C Walker, Madison M Reeves

    Biorxiv : the Preprint Server for Biology
    |July 3, 2026
    PubMed
    Summary

    TAR DNA-binding protein 43 (TDP-43) pathology drives distinct transcriptional changes in Alzheimer's disease (AD) and related dementias. These TDP-43-driven molecular programs are subtype-specific and regionally distinct, offering new insights into neurodegeneration.

    More Related Videos

    DeepOmicsAE: Representing Signaling Modules in Alzheimer's Disease with Deep Learning Analysis of Proteomics, Metabolomics, and Clinical Data
    09:47

    DeepOmicsAE: Representing Signaling Modules in Alzheimer's Disease with Deep Learning Analysis of Proteomics, Metabolomics, and Clinical Data

    Published on: December 15, 2023

    Related Experiment Videos

    Last Updated: Jul 4, 2026

    Biomarker Identification for Gender Specificity of Alzheimer's Disease Based on the Glial Transcriptome Profiles
    04:22

    Biomarker Identification for Gender Specificity of Alzheimer's Disease Based on the Glial Transcriptome Profiles

    Published on: May 20, 2024

    DeepOmicsAE: Representing Signaling Modules in Alzheimer's Disease with Deep Learning Analysis of Proteomics, Metabolomics, and Clinical Data
    09:47

    DeepOmicsAE: Representing Signaling Modules in Alzheimer's Disease with Deep Learning Analysis of Proteomics, Metabolomics, and Clinical Data

    Published on: December 15, 2023

    Area of Science:

    • Neuroscience
    • Genomics
    • Pathology

    Background:

    • TDP-43 pathology often co-occurs with Tau NFTs and amyloid plaques in Alzheimer's disease (AD), complicating understanding of its role.
    • Distinguishing TDP-43's independent molecular programs from Tau-driven neurodegeneration is challenging due to overlapping pathologies.

    Purpose of the Study:

    • To delineate the distinct transcriptomic signatures associated with TDP-43 pathology in AD, AD with limbic-predominant age-related TDP-43 encephalopathy (AD/LATE), and frontotemporal lobar degeneration (FTLD-TDP).
    • To investigate the influence of TDP-43 subtypes and regional differences on transcriptional landscapes in neurodegenerative diseases.

    Main Methods:

    • Generated regionally resolved transcriptomic profiles from control, AD, AD/LATE, and FTLD-TDP cohorts.
    • Integrated transcriptomic data with quantitative measures of phosphorylated TDP-43 (pTDP-43) and Tau (pTau).
    • Stratified analyses by TDP-43 morphological subtypes (α, β for AD/LATE; A, B for FTLD-TDP).

    Main Results:

    • TDP-43 is associated with distinct transcriptomic programs in AD/LATE, independent of Tau burden and differing from FTLD-TDP.
    • Transcriptomic alterations showed regional specificity, with amygdala changes common to both diseases and frontal cortex changes largely specific to FTLD-TDP.
    • Stratification by TDP-43 subtype revealed specific biological trajectories, including immune activation and cellular vulnerabilities, not seen in unstratified groups.

    Conclusions:

    • TDP-43 pathology shapes autonomous, subtype-dependent transcriptional landscapes in AD and related disorders.
    • The findings provide a framework for decoupling mixed proteinopathies and understanding TDP-43's specific contributions to neurodegeneration.
    • Subtype and regional analyses are crucial for uncovering the full spectrum of TDP-43's molecular impact.