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Related Concept Videos

Alzheimer Disease ll: Pathophysiology01:23

Alzheimer Disease ll: Pathophysiology

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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...
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Alzheimer Disease l: Introduction01:29

Alzheimer Disease l: Introduction

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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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Alzheimer's Disease: Overview01:26

Alzheimer's Disease: Overview

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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...
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Dementia l: Introduction01:22

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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...
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Alzheimer's Disease: Treatment01:22

Alzheimer's Disease: Treatment

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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...
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Amyloid Fibrils03:03

Amyloid Fibrils

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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,...
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Detection of Neuritic Plaques in Alzheimer's Disease Mouse Model
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What causes alzheimer's disease?

R A Armstrong1

  • 1Dr R. A. Armstrong, Vision Sciences, Aston University, Birmingham B4 7ET, UK, phone: 0121-204-4102, fax: 0121-204-4048,

Folia Neuropathologica
|October 12, 2013
PubMed
Summary
This summary is machine-generated.

Alzheimer's disease (AD) is a complex, multifactorial disorder. Genetic and environmental factors interact, accelerating aging and leading to the accumulation of beta-amyloid (Aβ) and tau proteins, causing AD.

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Area of Science:

  • Neuroscience
  • Genetics
  • Pathology

Background:

  • Alzheimer's disease (AD) etiology has been debated, with theories including aging, pathway degeneration, environmental factors, genetics, mitochondrial dysfunction, blood-brain barrier compromise, immune dysfunction, and infectious agents.
  • Existing theories provide a foundation for understanding the multifaceted nature of AD.

Purpose of the Study:

  • To review and evaluate the evidence for and against various proposed causes of Alzheimer's disease.
  • To synthesize current knowledge on AD pathogenesis, integrating genetic and environmental influences.

Main Methods:

  • Comprehensive literature review of existing theories on Alzheimer's disease etiology.
  • Analysis of evidence supporting or refuting each proposed causal factor for AD.

Main Results:

  • Alzheimer's disease is multifactorial, resulting from interactions between genetic and environmental risk factors that increase "allostatic load" and accelerate aging.
  • Neuronal and vascular degeneration leads to the aggregation of beta-amyloid (Aβ) and tau proteins.
  • Gene mutations cause early-onset familial AD (EO-FAD), while risk factor combinations lead to late-onset sporadic AD (LO-SAD) through slower Aβ and tau accumulation.

Conclusions:

  • AD pathogenesis involves a complex interplay of genetic predisposition and environmental exposures, leading to accelerated aging and protein aggregation.
  • The spread of Aβ and tau via cell-to-cell transfer along neural pathways contributes to the heterogeneity observed in AD clinical presentations.
  • Understanding these multifactorial mechanisms is crucial for developing targeted therapeutic strategies for both familial and sporadic forms of Alzheimer's disease.