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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

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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 (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.
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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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Related Experiment Video

Updated: May 3, 2026

Correlative Light and Electron Microscopy to Study Microglial Interactions with β-Amyloid Plaques
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Microglial dysfunction in brain aging and Alzheimer's disease.

Kira Irving Mosher1, Tony Wyss-Coray2

  • 1Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, California 94305, USA; Neuroscience IDP Program, Stanford University School of Medicine, Stanford, California 94305, USA.

Biochemical Pharmacology
|January 22, 2014
PubMed
Summary

Microglia, the brain's immune cells, show similar changes in Alzheimer's disease (AD) and aging. This review details six microglial functions affected by both conditions to guide future research.

Keywords:
AgingAlzheimer's diseaseMicrogliaNeurodegenerationNeuroinflammation

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Area of Science:

  • Neuroscience
  • Immunology
  • Pathology

Background:

  • Microglia are central nervous system immune cells implicated in Alzheimer's disease (AD) pathophysiology.
  • Recent genetic studies highlight the significance of microglial molecules in AD.
  • Microglia in aging and AD brains share phenotypes, but their combined impact is understudied.

Purpose of the Study:

  • To review the distinct functions of microglia.
  • To discuss the specific effects of aging and Alzheimer's disease on these functions.
  • To identify commonalities between aging and AD states in microglia to inspire new research.

Main Methods:

  • Literature review and synthesis of existing research on microglia.
  • Enumeration of six distinct microglial functions.
  • Comparative analysis of microglial phenotypes in aging and AD.

Main Results:

  • Microglia exhibit altered functions in both aging and AD.
  • Commonalities exist in microglial responses to aging and AD.
  • The concepts of microglial "activation" and "neuroinflammation" are complex and encompass multiple processes.

Conclusions:

  • Understanding shared microglial mechanisms in aging and AD is crucial.
  • This review provides a framework for dissecting microglial functions in neurodegeneration.
  • New research approaches can be inspired by considering aging and AD impacts on microglia together.