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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...
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...
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...
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Pharmacogenomics: Identification of New Drug Targets

Advances in genomics have profoundly influenced drug discovery by increasing both the speed and accuracy of pharmaceutical development. Pharmacogenomics, which examines how genetic variation influences drug response, facilitates the identification of novel therapeutic targets and enables patient stratification for personalized treatment. These strategies contribute to improved drug efficacy, minimized adverse effects, and more efficient clinical trial design.Mapping genetic differences...

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Updated: Jun 7, 2026

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

Alzheimer's disease genetics: current knowledge and future challenges.

Paul Hollingworth1, Denise Harold, Lesley Jones

  • 1Medical Research Council Centre for Neuropsychiatric Genetics and Genomics, Department of Psychological Medicine and Neurology, School of Medicine, Cardiff University, Cardiff, UK. hollingworthp@cardiff.ac.uk

International Journal of Geriatric Psychiatry
|October 20, 2010
PubMed
Summary
This summary is machine-generated.

Recent studies reveal four new Alzheimer's disease (AD) susceptibility genes: CLU, PICALM, CR1, and BIN1. This genetic complexity offers new research avenues for understanding dementia risk.

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Mapping Alzheimer's Disease Variants to Their Target Genes Using Computational Analysis of Chromatin Configuration
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Quantitative 3D In Silico Modeling (q3DISM) of Cerebral Amyloid-beta Phagocytosis in Rodent Models of Alzheimer's Disease

Published on: December 26, 2016

Area of Science:

  • Genetics
  • Neuroscience
  • Molecular Biology

Background:

  • Alzheimer's disease (AD) exhibits high heritability but complex genetic underpinnings.
  • Previous research has identified some genetic risk factors for AD.
  • Advances in large-scale genetic studies are crucial for understanding complex diseases.

Purpose of the Study:

  • To discuss recent breakthroughs in identifying Alzheimer's disease risk genes.
  • To explore the genetic architecture of Alzheimer's disease.
  • To refine understanding of primary disease mechanisms in dementia.

Main Methods:

  • Analysis of three large-scale genome-wide association studies.
  • Combined data from over 43,000 independent individuals.
  • Identification of genetic variants associated with Alzheimer's disease risk.

Main Results:

  • Compelling evidence for association between variants in four novel susceptibility genes (CLU, PICALM, CR1, BIN1) and Alzheimer's disease risk.
  • Substantial progress in disentangling the genetic architecture of Alzheimer's disease.
  • Highlighting the potential for further gene discovery with larger sample sizes.

Conclusions:

  • The identification of CLU, PICALM, CR1, and BIN1 provides new avenues for Alzheimer's disease research.
  • Current findings refine previous ideas about AD pathogenesis.
  • These discoveries are defining new putative primary disease mechanisms for dementia.