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Related Concept Videos

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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Alzheimer's Disease: Treatment01:22

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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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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 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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Related Experiment Video

Updated: May 5, 2026

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

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Decoding microglial functions in Alzheimer's disease: insights from human models.

Chandrika Rao1, Stefan Semrau1, Valentina Fossati1

  • 1The New York Stem Cell Foundation Research Institute, New York, NY, USA.

Trends in Immunology
|March 20, 2025
PubMed
Summary

Human cell models reveal unique microglial responses in Alzheimer's disease (AD), offering new therapeutic targets. These advanced models improve our understanding of neuroinflammation and amyloid plaque interactions in AD progression.

Keywords:
Alzheimer's diseasehuman in vitro modelsinduced pluripotent stem cells (iPSCs)microgliasingle-cell technologies

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Obtaining Human Microglia from Adult Human Brain Tissue
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Area of Science:

  • Neuroscience
  • Immunology
  • Stem Cell Biology

Background:

  • Microglia are central to brain immune responses and Alzheimer's disease (AD) pathology.
  • Traditional animal models do not fully replicate human-specific microglial behavior in AD.
  • Advancements in human cell models are crucial for understanding AD.

Purpose of the Study:

  • To review the role of emerging human models in studying microglia in Alzheimer's disease.
  • To highlight human-specific microglial responses to AD pathology.
  • To explore new therapeutic avenues targeting microglia.

Main Methods:

  • Utilizing stem cell-derived microglia and cerebral organoids.
  • Analyzing human-specific microglial responses to amyloid plaques.
  • Investigating the regulation of neuroinflammation in advanced human models.

Main Results:

  • Human models reveal unique microglial responses to amyloid plaques, distinct from animal models.
  • These models elucidate the regulation of neuroinflammation in Alzheimer's disease.
  • Advanced models provide deeper insights into the complex roles of microglia in AD.

Conclusions:

  • Innovative human models are essential for understanding Alzheimer's disease.
  • These models offer new perspectives on microglial function and neuroinflammation.
  • Targeting microglia presents promising therapeutic strategies for AD.