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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...
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Genetic polymorphisms in drug targets have emerged as critical determinants of interindividual variability in drug response and toxicity. Pharmacogenomic investigations increasingly focus on identifying these variations to personalize and optimize therapeutic interventions. A drug target may be a receptor, enzyme, or signaling protein involved in pharmacologic responses or disease-related pathways. While early pharmacogenetic studies focused primarily on drug metabolism, current research...
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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...
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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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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...
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Pharmacogenetic Phenotypes: Alterations in Pharmacokinetics, Drug Targets and Biologic Milieu

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Related Experiment Video

Updated: Jun 8, 2026

Generalized Psychophysiological Interaction (PPI) Analysis of Memory Related Connectivity in Individuals at Genetic Risk for Alzheimer's Disease
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Does apolipoprotein E genotype modify the clinical expression of ALS?

A Jawaid1, M Poon, A M Strutt

  • 1Department of Neurology, Baylor College of Medicine, Houston, TX 77030, USA.

European Journal of Neurology
|October 1, 2010
PubMed
Summary

Apolipoprotein E (ApoE) genotype does not influence the clinical course of amyotrophic lateral sclerosis (ALS). This finding contrasts with ApoE

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09:34

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Published on: April 4, 2018

Area of Science:

  • Neuroscience
  • Genetics
  • Neurology

Background:

  • Apolipoprotein E (ApoE) genotype is linked to earlier onset in Alzheimer's disease (AD) and other neurodegenerative conditions.
  • The role of ApoE in amyotrophic lateral sclerosis (ALS) clinical progression remains unclear.

Purpose of the Study:

  • To investigate the impact of apolipoprotein E (ApoE) genotypes on the clinical course of sporadic amyotrophic lateral sclerosis (ALS).

Main Methods:

  • A cohort of 852 sporadic ALS patients was analyzed.
  • The study examined ApoE genotype's effect on age of onset, disease progression rate, cognitive function, and survival in ALS patients.

Main Results:

  • ApoE genotype frequencies in ALS patients were similar to the general Caucasian population.
  • No significant differences were observed in age of onset, disease progression, cognitive status, or survival among different ApoE genotypes in ALS patients.

Conclusions:

  • Apolipoprotein E (ApoE) genotype does not appear to modify the clinical course of sporadic amyotrophic lateral sclerosis (ALS).
  • This contrasts with the known influence of ApoE genotype on Alzheimer's disease and other neurodegenerative disorders.