Related Experiment Video
Updated: Jun 12, 2026
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
Alzheimer's disease: the quest to understand complexity
Sueli C F Marques1, Catarina R Oliveira, Tiago F Outeiro
1Programa Doutoral em Biologia Experimental e Biomedicina, Centro de Neurociências e Biologia Celular, Coimbra, Portugal.
Journal of Alzheimer'S Disease : JAD
|June 18, 2010
Summary
Epigenetic alterations, including DNA methylation and histone changes, may contribute to Alzheimer's disease (AD) pathogenesis. Understanding these epigenetic changes could reveal new therapeutic targets for neuroprotection.
Area of Science:
- Neuroscience
- Genetics
- Pathology
Background:
- Alzheimer's disease (AD) is a progressive neurodegenerative disorder with increasing global prevalence, linked to population aging.
- While genetics plays a role, the multifactorial etiology of AD involves unknown triggers and disrupted physiological mechanisms.
- Mitochondrial dysfunction and oxidative stress are implicated, but other cellular mechanisms may contribute to sporadic AD.
Purpose of the Study:
- To investigate the potential role of epigenetic modifications in Alzheimer's disease pathophysiology.
- To explore how age-related epigenetic changes might influence neurodegeneration and disease susceptibility.
- To identify novel therapeutic strategies by understanding disrupted epigenetic mechanisms in AD.
Main Methods:
- Review of current evidence on epigenetic modifications in aging and neurodegenerative diseases.
- Analysis of studies investigating DNA methylation abnormalities in AD-related genes and the SAM/HCY cycle.
- Examination of research on global histone acetylation changes in the context of AD.
Main Results:
- Epigenetic modifications, such as DNA methylation and histone acetylation, accumulate with age.
- Disruptions in the SAM/HCY cycle can lead to methylation abnormalities in AD-related genes.
- Altered histone acetylation levels are also suggested to play a role in AD neurodegeneration.
Conclusions:
- Epigenetic alterations are likely significant contributors to the pathophysiology of late-onset Alzheimer's disease.
- Understanding these age-related epigenetic changes is crucial for developing novel neuroprotective strategies.
- Novel global approaches are essential for advancing therapeutic interventions for Alzheimer's disease.
Related Concept Videos
01:23Alzheimer 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...
01:26Alzheimer'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...
The clinical diagnosis of AD hinges on the presence of memory and other cognitive impairments. Biomarkers, such as changes in Aβ and tau...
01:29Alzheimer 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...
01:22Dementia 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...
01:22Alzheimer'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...
01:30Dementia
Dementia is a collective term for cognitive disorders primarily affecting memory, thinking, and reasoning. It is not a specific disease but a syndrome, with Alzheimer's disease being the most common cause, accounting for approximately 60-80% of cases. Other types include vascular dementia, Lewy body dementia, and frontotemporal dementia. Dementia affects millions worldwide, particularly older adults, though it is not a normal part of aging.
The progression of dementia is generally gradual.
The progression of dementia is generally gradual.