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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...
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: 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...
Mismatch Repair01:20

Mismatch Repair

Organisms are capable of detecting and fixing nucleotide mismatches that occur during DNA replication. This sophisticated process requires identifying the new strand and replacing the erroneous bases with correct nucleotides. Mismatch repair is coordinated by many proteins in both prokaryotes and eukaryotes.
The Mutator Protein Family Plays a Key Role in DNA Mismatch Repair
The human genome has more than 3 billion base pairs of DNA per cell. Prior to cell division, that vast amount of genetic...
Amyloid Fibrils03:03

Amyloid Fibrils

Amyloid fibrils are aggregates of misfolded proteins.  Under most circumstances, misfolded proteins are either refolded by chaperone proteins or degraded by the proteasome. However, in the case of a mutation or a disease, these proteins can accumulate to form large clusters and often further assemble to form elongated fibers, called fibrils. 
Amyloid deposits were observed as early as 1639 in the liver and the spleen.   In 1854, Rudolph Virchow performed iodine staining, normally used to...

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Related Experiment Video

Updated: May 17, 2026

Detection of Neuritic Plaques in Alzheimer's Disease Mouse Model
06:02

Detection of Neuritic Plaques in Alzheimer's Disease Mouse Model

Published on: July 26, 2011

A protective mutation against Alzheimer disease?

Juliane Proft1, Norbert Weiss

  • 1Hotchkiss Brain Institute; Department of Clinical Neuroscience; Calgary, AB Canada.

Communicative & Integrative Biology
|October 13, 2012
PubMed
Summary

Alzheimer disease (AD) is a common dementia affecting millions globally, characterized by cognitive decline and brain changes like amyloid plaques. This condition is projected to worsen significantly by 2050.

Keywords:
Alzheimer diseaseBACE1amyloid beta (Aβ)amyloid precursor protein (APP)β-secretase

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Saccharomyces cerevisiae Models of Alzheimer's Disease to Screen Genes, Mutations, and Chemicals Affecting Amyloid Beta Production by γ-Secretase

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Quantitative 3D In Silico Modeling (q3DISM) of Cerebral Amyloid-beta Phagocytosis in Rodent Models of Alzheimer's Disease
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Quantitative 3D In Silico Modeling (q3DISM) of Cerebral Amyloid-beta Phagocytosis in Rodent Models of Alzheimer's Disease

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Detection of Neuritic Plaques in Alzheimer's Disease Mouse Model
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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:

  • Neurology
  • Gerontology
  • Pathology

Background:

  • Dementia affects nearly 35.6 million people worldwide, with projections indicating a rise to 115.4 million by 2050.
  • In Western countries, over 5% of individuals aged 60 and above have dementia, with Alzheimer disease accounting for two-thirds of these cases.
  • Alzheimer disease, first identified in 1906, is a progressive neurodegenerative disorder.

Purpose of the Study:

  • To provide an overview of Alzheimer disease (AD) as the most prevalent form of dementia.
  • To highlight the characteristic pathological hallmarks of Alzheimer disease.
  • To underscore the growing global impact and prevalence of dementia and AD.

Main Methods:

  • Review of epidemiological data on dementia prevalence.
  • Historical overview of Alzheimer disease discovery and definition.
  • Description of clinical and pathological features of Alzheimer disease.

Main Results:

  • Alzheimer disease is the leading cause of dementia in individuals over 60.
  • The disease is marked by progressive decline in cognitive functions, behavior, language, and visuospatial skills.
  • Key pathological indicators include intraneuronal tangles and extracellular amyloid plaques in the brain.

Conclusions:

  • Alzheimer disease represents a significant and growing global health challenge.
  • Understanding the characteristic pathological hallmarks is crucial for disease diagnosis and research.
  • The increasing prevalence necessitates urgent attention and research efforts.