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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...
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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...
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...
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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...
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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The progression of dementia is generally gradual.

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Related Experiment Video

Updated: May 26, 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

Alzheimer's - Looking beyond plaques.

W Sue T Griffin1

  • 1Geriatric Research, Education and Clinical Center, Neurobiology, Physiology, and Psychiatry, University of Arkansas for Medical Sciences, and the Geriatrics, Education Clinical Center, Central Arkansas Veterans Healthcare System Little Rock, Arkansas 72205 USA.

F1000 Medicine Reports
|December 14, 2011
PubMed
Summary
This summary is machine-generated.

Inflammation is now understood to be a key driver of Alzheimer's disease. This review details the scientific journey to establish the critical role of chronic interleukin-1 (IL-1) inflammation in the disease's development.

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Last Updated: May 26, 2026

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Published on: April 11, 2018

Area of Science:

  • Neuroscience
  • Immunology
  • Pathology

Background:

  • Historically, inflammation was not considered a factor in Alzheimer's disease (AD).
  • Emerging evidence has shifted this perspective, highlighting inflammation's significant role.
  • Chronic activation of interleukin-1 (IL-1) inflammation is increasingly implicated in AD pathogenesis.

Purpose of the Study:

  • To provide a personal account of the research efforts to demonstrate inflammation's role in Alzheimer's disease.
  • To review the scientific progression from viewing inflammation as irrelevant to recognizing it as a critical factor in AD.

Main Methods:

  • This review synthesizes decades of research findings.
  • It focuses on the evidence linking chronic IL-1 inflammation to AD hallmarks.
  • Personal insights into the scientific quest are included.

Main Results:

  • The scientific community's understanding of inflammation in AD has evolved significantly.
  • Chronic IL-1 inflammation is now recognized as a major contributor to AD pathology.
  • Key hallmarks of Alzheimer's disease are linked to this inflammatory process.

Conclusions:

  • Inflammation, particularly chronic IL-1 activation, is a critical factor in the development of Alzheimer's disease.
  • The scientific journey has established a new paradigm for understanding AD pathogenesis.
  • Further research into anti-inflammatory strategies for AD is warranted.