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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'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...
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...
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: May 8, 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

CD33 in Alzheimer's disease.

Teng Jiang1, Jin-Tai Yu, Nan Hu

  • 1Department of Neurology, Qingdao Municipal Hospital, Nanjing Medical University, Nanjing, China.

Molecular Neurobiology
|August 29, 2013
PubMed
Summary

Cluster of differentiation 33 (CD33) is elevated in Alzheimer's disease (AD) brains, impairing amyloid-beta clearance by microglia. Targeting CD33 offers a potential therapeutic strategy for AD.

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Detection of Neuritic Plaques in Alzheimer's Disease Mouse Model
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Detection of Neuritic Plaques in Alzheimer's Disease Mouse Model

Published on: July 26, 2011

Related Experiment Videos

Last Updated: May 8, 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

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

Area of Science:

  • Neuroscience
  • Immunology
  • Genetics

Background:

  • Alzheimer's disease (AD) pathogenesis is increasingly linked to impaired amyloid-beta (Aβ) clearance.
  • Genetic studies identify cluster of differentiation 33 (CD33) as a significant risk locus for AD.
  • CD33 is expressed on microglia, the brain's immune cells, and its levels increase with AD progression.

Purpose of the Study:

  • To review epidemiological findings linking CD33 to AD.
  • To discuss the role of CD33 in AD pathogenesis.
  • To explore CD33 as a therapeutic target for AD.

Main Methods:

  • Review of epidemiological studies on CD33 and AD.
  • Analysis of CD33 expression levels in AD brains.
  • Investigation of CD33's impact on microglial Aβ clearance.

Main Results:

  • Elevated CD33 levels in AD brains correlate with amyloid plaque burden and disease severity.
  • CD33 impairs microglial-mediated clearance of Aβ, contributing to plaque formation.
  • CD33's role in AD pathogenesis is supported by its association with disease progression.

Conclusions:

  • CD33 plays a critical role in AD pathogenesis by hindering Aβ clearance.
  • Targeting CD33 presents a promising therapeutic avenue for Alzheimer's disease.
  • Further research into CD33 modulation could lead to novel AD treatments.