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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...

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Related Experiment Video

Updated: May 21, 2026

Biomarker Identification for Gender Specificity of Alzheimer's Disease Based on the Glial Transcriptome Profiles
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Biomarker Identification for Gender Specificity of Alzheimer's Disease Based on the Glial Transcriptome Profiles

Published on: May 20, 2024

Cell-specific protein expression in Alzheimer's disease prefrontal cortex.

Maryam Gholampour1,2, Malay K Basu1, Russell H Swerdlow2,3

  • 1Department of Pathology & Laboratory Medicine, University of Kansas Medical Center, Kansas City, Kansas, USA.

Alzheimer'S & Dementia : the Journal of the Alzheimer'S Association
|June 4, 2025
PubMed
Summary
This summary is machine-generated.

This study used the GeoMx Digital Spatial Profiler (DSP) to analyze Alzheimer's disease (AD) brain proteomes. Key proteins like Neprilysin (NEP) were elevated in AD neurons and microglia, offering insights into disease mechanisms.

Keywords:
Alzheimer's diseaseGeoMx DSPbrain cell typesneprilysinspatial proteomics

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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
06:02

Detection of Neuritic Plaques in Alzheimer's Disease Mouse Model

Published on: July 26, 2011

Area of Science:

  • Neuroscience
  • Proteomics
  • Alzheimer's Disease Research

Background:

  • Understanding brain cell type-specific proteomes is crucial for Alzheimer's disease (AD) pathophysiology.
  • Spatial analysis of limited brain cell populations presents significant challenges.

Purpose of the Study:

  • To analyze protein levels in specific brain cell types within Alzheimer's disease (AD) and non-AD brains.
  • To evaluate the efficacy of the GeoMx Digital Spatial Profiler (DSP) platform for cell-specific proteomic analysis in the context of AD.

Main Methods:

  • Utilized the GeoMx Digital Spatial Profiler (DSP) platform on prefrontal cortex tissue from AD and non-AD brains.
  • Interrogated the expression of 76 proteins using immunofluorescence to differentiate between neurons, astrocytes, and microglia.

Main Results:

  • Identified 18 differentially expressed proteins in AD neurons.
  • Observed significantly higher Neprilysin (NEP) levels in AD neurons and microglia, an enzyme involved in amyloid beta degradation.
  • Found elevated Lysosome-associated membrane protein 2A (LAMP2A) in neurons of individuals with AD.
  • Detected increased markers of neuroinflammation (CD11c, CD11b, CD163) in AD neurons.

Conclusions:

  • The GeoMx DSP platform provides effective cell-specific proteomic snapshots of the Alzheimer's disease brain.
  • Findings highlight altered protein expression, including NEP and neuroinflammation markers, in specific brain cells during AD.