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Related Concept Videos

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 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...
Human Genetics01:28

Human Genetics

Human genetics provides a profound framework for understanding the interplay between genetic predispositions and human psychology. At the heart of this discipline lies the study of how genes influence physical traits, behaviors, and susceptibility to diseases. Each person carries a unique genetic code that subtly or significantly shapes their psychological and behavioral landscape.
The complex relationship between genetics and psychology is observable through common biological components such...
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...
Genetic Lingo01:11

Genetic Lingo

Overview

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Related Experiment Video

Updated: Jun 24, 2026

Generalized Psychophysiological Interaction (PPI) Analysis of Memory Related Connectivity in Individuals at Genetic Risk for Alzheimer's Disease
09:38

Generalized Psychophysiological Interaction (PPI) Analysis of Memory Related Connectivity in Individuals at Genetic Risk for Alzheimer's Disease

Published on: November 14, 2017

[Genetics and Alzheimer's disease].

S Manzano, J L González, A Marcos

    Neurologia (Barcelona, Spain)
    |March 27, 2009
    PubMed
    Summary

    Alzheimer's disease (AD) genetics are complex, involving early-onset causal genes and late-onset susceptibility genes like APOE. Understanding late-onset AD genetics is crucial for sporadic forms, which are most common.

    Area of Science:

    • Neurogenetics
    • Complex Disease Genetics

    Background:

    • Alzheimer's disease (AD) is the leading cause of dementia, accounting for 60-80% of cases.
    • Early-onset AD involves autosomal dominant genes (APP, PSEN-1, PSEN-2), while late-onset AD is associated with susceptibility genes, notably APOE.

    Discussion:

    • Early-onset AD genes explain only about 5% of total cases.
    • The APOE gene is the only consistently replicated susceptibility gene for late-onset AD.
    • Replication of over 200 other identified genes remains challenging, highlighting genetic complexity.

    Key Insights:

    • Alzheimer's disease exhibits complex inheritance patterns.
    • Early-onset AD genetic research has significantly advanced understanding of disease pathogenesis.
    • Multifactorial models, integrating genetic and environmental factors, best explain common AD phenotypes.

    More Related Videos

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

    Published on: January 9, 2020

    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

    Related Experiment Videos

    Last Updated: Jun 24, 2026

    Generalized Psychophysiological Interaction (PPI) Analysis of Memory Related Connectivity in Individuals at Genetic Risk for Alzheimer's Disease
    09:38

    Generalized Psychophysiological Interaction (PPI) Analysis of Memory Related Connectivity in Individuals at Genetic Risk for Alzheimer's Disease

    Published on: November 14, 2017

    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

    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

    Outlook:

    • Knowledge from late-onset AD forms offers valuable insights into the more prevalent sporadic AD.
    • Further research into complex genetic architectures is essential for developing effective AD therapies.
    • Continued investigation into gene-environment interactions is critical for understanding AD etiology.