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'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...
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

Differential DNA methylation in blood as potential mediator of the association between ambient PM<sub>2.5</sub> and cerebrospinal fluid biomarkers of Alzheimer's disease among a cognitively normal population-based cohort.

Molecular psychiatry·2026
Same author

Mapping cross-domain drivers of Alzheimer's disease risk through integrated network analysis.

Alzheimer's & dementia : the journal of the Alzheimer's Association·2026
Same author

Uncovering lipid biomarkers linked to methylphenidate efficacy in treating apathy in Alzheimer's disease: insights from the ADMET 2 trial.

Alzheimer's research & therapy·2026
Same author

Genetic and Proteomic Investigation of the Smoking-Parkinson's Disease Association.

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

Behavioral and psychological symptoms of dementia: insights from a multivariate and network-based brain proteome-wide study.

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

Visual memory correlates with AD biomarkers in cognitively unimpaired individuals.

Alzheimer's & dementia : the journal of the Alzheimer's Association·2026
Same journal

An intraocular oxygenated emulsion suppresses retinal fibrosis by inhibiting hypoxia-driven bioenergetic shifts and mesenchymal transformation.

Research square·2026
Same journal

Development of Human iPSC-based Microphysiogical Models of Transthyretin Amyloid Cardiomyopathy.

Research square·2026
Same journal

Spatial distribution and density of fibroblasts determine angiogenic response of endothelial cells.

Research square·2026
Same journal

Single-cell gain-of-function mapping reveals latent regulatory programs governing CD8+ T cell fate.

Research square·2026
Same journal

Genetic variability within Triatoma sanguisuga complex in North America and the re- description of Triatoma ambigua (Neiva 1911), with specimens from Florida, USA.

Research square·2026
Same journal

PAD4 deletion in synovial macrophages exacerbates pathology in inflammatory arthritis.

Research square·2026
See all related articles
  1. Home
  3. Development And Application Of Brain Tissue Based Multi-omics Profile Scores For Alzheimer's Disease.
  1. Home
  3. Development And Application Of Brain Tissue Based Multi-omics Profile Scores For Alzheimer's Disease.

Related Experiment Video

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

DEVELOPMENT AND APPLICATION OF BRAIN TISSUE BASED MULTI-OMICS PROFILE SCORES FOR ALZHEIMER'S DISEASE.

Timur Tug1,2, Donghai Liang2,3, Sven Teschke1

  • 1Department of Statistics, TU Dortmund University, Dortmund, Germany.

Research Square
|May 7, 2026

View abstract on PubMed

Summary
This summary is machine-generated.

This study integrated DNA methylation and metabolomics to understand Alzheimer's disease (AD) pathology. Both omics layers converged on lipid metabolism and signal transduction, revealing shared biological mechanisms in AD.

Keywords:
Alzheimer’s diseaseDNA methylationmachine learningmetabolomicsmulti-omicsneuropathologyprofile scores

More Related Videos

A High Throughput, Multiplexed and Targeted Proteomic CSF Assay to Quantify Neurodegenerative Biomarkers and Apolipoprotein E Isoforms Status
07:08

A High Throughput, Multiplexed and Targeted Proteomic CSF Assay to Quantify Neurodegenerative Biomarkers and Apolipoprotein E Isoforms Status

Published on: October 20, 2016

Abbiategrasso Brain Bank Protocol for Collecting, Processing and Characterizing Aging Brains
12:28

Abbiategrasso Brain Bank Protocol for Collecting, Processing and Characterizing Aging Brains

Published on: June 3, 2020

Related Experiment 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

A High Throughput, Multiplexed and Targeted Proteomic CSF Assay to Quantify Neurodegenerative Biomarkers and Apolipoprotein E Isoforms Status
07:08

A High Throughput, Multiplexed and Targeted Proteomic CSF Assay to Quantify Neurodegenerative Biomarkers and Apolipoprotein E Isoforms Status

Published on: October 20, 2016

Abbiategrasso Brain Bank Protocol for Collecting, Processing and Characterizing Aging Brains
12:28

Abbiategrasso Brain Bank Protocol for Collecting, Processing and Characterizing Aging Brains

Published on: June 3, 2020

Area of Science:

  • Neuroscience
  • Genomics
  • Metabolomics

Background:

  • Omics technologies like epigenomics and metabolomics offer insights into Alzheimer's disease (AD) mechanisms.
  • The interaction between different omics layers and AD neuropathology remains poorly understood.

Purpose of the Study:

  • To comprehensively analyze single- and multi-omics data for Alzheimer's disease (AD) pathology.
  • To investigate the interaction of DNA methylation and metabolomics in relation to AD neuropathology.

Main Methods:

  • Integrated genome-wide DNA methylation and high-resolution metabolomics data from 157 frontal cortex samples.
  • Developed novel single- and multi-omics profile scores (PS) for AD pathology using machine learning, regression, and pathway analysis.

Main Results:

  • DNA methylation profile scores outperformed metabolomics scores for the ABC score (median R²: 0.11 vs. 0.04).
  • A multi-omics PS combining both layers yielded a partial R² of 0.15 for the ABC score, independent of covariates.
  • Both omics layers converged on lipid metabolism and signal transduction pathways implicated in AD.

Conclusions:

  • Integrative pathway and network analyses of DNA methylation and metabolomics PS highlight shared biological mechanisms in AD.
  • Multi-omics approaches provide valuable biological insights into Alzheimer's disease, even with limited predictive accuracy gains.