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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...
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'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...

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Related Experiment Video

Updated: Jun 3, 2026

Analysis of Microglia and Monocyte-derived Macrophages from the Central Nervous System by Flow Cytometry
10:43

Analysis of Microglia and Monocyte-derived Macrophages from the Central Nervous System by Flow Cytometry

Published on: June 22, 2017

Monocytes and Alzheimer's disease.

Yu Feng1, Lei Li, Xiao-Hong Sun

  • 1Department of Neurology, The First Affiliated Hospital, China Medical University, Shenyang 110001, China. fengyu_1976@163.com

Neuroscience Bulletin
|March 29, 2011
PubMed
Summary

Monocytes, part of the immune system, may play a dual role in Alzheimer's disease (AD). While they can clear amyloid beta (Aβ), their effectiveness in AD patients is limited, impacting disease progression.

Area of Science:

  • Neuroscience
  • Immunology
  • Pathology

Background:

  • Alzheimer's disease (AD) involves amyloid beta (Aβ) plaques and neurofibrillary tangles.
  • Monocytes are immune cells involved in clearing cellular debris.
  • Aβ may recruit monocytes to the brain in AD models, potentially restricting amyloidosis.

Purpose of the Study:

  • To review the current understanding of monocytes in Alzheimer's disease.
  • To explore the dual role of monocytes in AD pathogenesis.
  • To discuss the implications of monocyte function in AD.

Main Methods:

  • Literature review of studies on monocytes and AD.
  • Analysis of research on monocyte recruitment and function in AD models.
  • Examination of evidence regarding Aβ phagocytosis by monocytes in AD patients.

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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

Published on: December 26, 2016

Quantification of Monocyte Transmigration and Foam Cell Formation from Individuals with Chronic Inflammatory Conditions
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Quantification of Monocyte Transmigration and Foam Cell Formation from Individuals with Chronic Inflammatory Conditions

Published on: October 17, 2017

Related Experiment Videos

Last Updated: Jun 3, 2026

Analysis of Microglia and Monocyte-derived Macrophages from the Central Nervous System by Flow Cytometry
10:43

Analysis of Microglia and Monocyte-derived Macrophages from the Central Nervous System by Flow Cytometry

Published on: June 22, 2017

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

Quantification of Monocyte Transmigration and Foam Cell Formation from Individuals with Chronic Inflammatory Conditions
09:41

Quantification of Monocyte Transmigration and Foam Cell Formation from Individuals with Chronic Inflammatory Conditions

Published on: October 17, 2017

Main Results:

  • Monocytes can be recruited to the brain by Aβ in AD models.
  • Monocytes exhibit a "double-edged sword" effect, with potential beneficial or detrimental roles.
  • Evidence suggests ineffective Aβ phagocytosis by monocytes in human AD.

Conclusions:

  • Monocytes have complex and potentially contradictory roles in Alzheimer's disease.
  • The phagocytic capacity of monocytes for Aβ appears compromised in AD patients.
  • Further research is needed to elucidate the precise involvement of monocytes in AD progression and to explore therapeutic strategies targeting them.