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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'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...
Dementia l: Introduction01:22

Dementia 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...
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: 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...
Dementia01:30

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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.

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Related Experiment Video

Updated: Jun 4, 2026

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

Introduction to Alzheimer's disease.

D Allsop1

  • 1Department of Biological Sciences, University of Lancaster, UK.

Methods in Molecular Medicine
|February 15, 2011
PubMed
Summary
This summary is machine-generated.

Alzheimer's disease (AD) is characterized by neurofibrillary tangles (NFTs) and senile plaques. Research now supports the amyloid cascade hypothesis, highlighting amyloid's central role in AD pathogenesis.

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An Alternative Approach to Study Primary Events in Neurodegeneration Using Ex Vivo Rat Brain Slices
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An Alternative Approach to Study Primary Events in Neurodegeneration Using Ex Vivo Rat Brain Slices

Published on: April 11, 2018

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Last Updated: Jun 4, 2026

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

An Alternative Approach to Study Primary Events in Neurodegeneration Using Ex Vivo Rat Brain Slices
07:57

An Alternative Approach to Study Primary Events in Neurodegeneration Using Ex Vivo Rat Brain Slices

Published on: April 11, 2018

Area of Science:

  • Neuropathology
  • Molecular Genetics
  • Neuroscience

Background:

  • Alzheimer's disease (AD) was first described in 1907, marked by presenile dementia, neurofibrillary tangles (NFTs), and senile plaques.
  • Amyloid was identified in senile plaques, initially thought to be starch-like but now known to comprise various peptides and proteins.
  • The characteristic birefringence of amyloid under polarized light, after Congo red staining, is due to well-ordered fibrils with a β-pleated sheet configuration.

Purpose of the Study:

  • To review the historical and scientific understanding of Alzheimer's disease (AD) pathology.
  • To discuss the evolving role of amyloid in the pathogenesis of AD.
  • To support the amyloid cascade hypothesis in the context of AD.

Main Methods:

  • Historical review of early AD case studies and neuropathological findings.
  • Analysis of histological techniques (Bielschowsky silver stain, Congo red staining) for identifying AD hallmarks.
  • Integration of molecular genetics findings to establish the role of amyloid in AD.

Main Results:

  • The combination of NFTs and senile plaques is a hallmark of Alzheimer's disease (AD).
  • Amyloid forms the core of senile plaques and is composed of diverse protein and peptide components.
  • Molecular genetics has provided strong evidence for amyloid's central role in AD pathogenesis, supporting the amyloid cascade hypothesis.

Conclusions:

  • Alzheimer's disease (AD) pathology involves characteristic neurofibrillary tangles (NFTs) and senile plaques containing amyloid.
  • Amyloid's role in AD pathogenesis is increasingly supported by molecular genetics, aligning with the amyloid cascade hypothesis.
  • While debated by some, the evidence strongly implicates amyloid as a key factor in the development of Alzheimer's disease.