Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Complement System

Complement System

The complement system is a group of approximately 20 plasma proteins that strengthen the body's defenses against infections through opsonization, inflammation, and cell lysis. Opsonization involves coating pathogens with complement proteins, making them more recognizable and facilitating phagocyte engulfment. Certain complement proteins induce inflammation that attracts immune cells to the site of infection. Cell lysis involves the destruction of pathogens through the formation of a...

Alzheimer's Disease: Overview

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...

Alzheimer's Disease: Treatment

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...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by

Same author

Clinical symptoms and surgical outcome of colloid cysts of the third ventricle: A multicenter retrospective study.

Brain & spine·2025

Same author

CHECK: A randomized trial evaluating the efficacy and cost-effectiveness of home visitation in pediatric weight loss treatment.

Contemporary clinical trials·2019

Same author

Factors Influencing Longitudinal Stair Climb Performance from Midlife to Early Late Life: The Study of Women's Health Across the Nation Chicago and Michigan Sites.

The journal of nutrition, health & aging·2019

Same author

Canine IL4-10 fusion protein provides disease modifying activity in a canine model of OA; an exploratory study.

PloS one·2019

Same author

Imputing accelerometer nonwear time in children influences estimates of sedentary time and its associations with cardiometabolic risk.

The international journal of behavioral nutrition and physical activity·2019

Same author

[Cervical spine involvement in rheumatoid arthritis : Diagnostics and treatment of instability due to rheumatism].

Zeitschrift fur Rheumatologie·2018

Search research articles

Related Experiment Video

Updated: Feb 23, 2026

A Model of Epileptogenesis in Rhinal Cortex-Hippocampus Organotypic Slice Cultures

A Model of Epileptogenesis in Rhinal Cortex-Hippocampus Organotypic Slice Cultures

Published on: March 18, 2021

Early complement components in Alzheimer's disease brains

R Veerhuis¹, I Janssen, C E Hack

¹Department of Neuropathology, Free University Hospital, Amsterdam, The Netherlands.

Acta Neuropathologica

|January 1, 1996

Summary

This summary is machine-generated.

Complement activation products are found in Alzheimer's disease (AD) brains, but late components forming the membrane attack complex (MAC) are absent. This suggests AD neurodegeneration involves early complement activation, not MAC-mediated inflammation.

More Related Videos

Establishment of a Valuable Mimic of Alzheimer's Disease in Rat Animal Model by Intracerebroventricular Injection of Composited Amyloid Beta Protein

Establishment of a Valuable Mimic of Alzheimer's Disease in Rat Animal Model by Intracerebroventricular Injection of Composited Amyloid Beta Protein

Published on: July 29, 2018

High-resolution Melting PCR for Complement Receptor 1 Length Polymorphism Genotyping: An Innovative Tool for Alzheimer's Disease Gene Susceptibility Assessment

High-resolution Melting PCR for Complement Receptor 1 Length Polymorphism Genotyping: An Innovative Tool for Alzheimer's Disease Gene Susceptibility Assessment

Published on: July 18, 2017

Related Experiment Videos

Last Updated: Feb 23, 2026

A Model of Epileptogenesis in Rhinal Cortex-Hippocampus Organotypic Slice Cultures

A Model of Epileptogenesis in Rhinal Cortex-Hippocampus Organotypic Slice Cultures

Published on: March 18, 2021

Establishment of a Valuable Mimic of Alzheimer's Disease in Rat Animal Model by Intracerebroventricular Injection of Composited Amyloid Beta Protein

Establishment of a Valuable Mimic of Alzheimer's Disease in Rat Animal Model by Intracerebroventricular Injection of Composited Amyloid Beta Protein

Published on: July 29, 2018

High-resolution Melting PCR for Complement Receptor 1 Length Polymorphism Genotyping: An Innovative Tool for Alzheimer's Disease Gene Susceptibility Assessment

High-resolution Melting PCR for Complement Receptor 1 Length Polymorphism Genotyping: An Innovative Tool for Alzheimer's Disease Gene Susceptibility Assessment

Published on: July 18, 2017

Area of Science:

Neuroscience
Immunology
Biochemistry

Background:

Early complement components (C1, C4, C3) activation products colocalize with beta-amyloid deposits in Alzheimer's disease (AD) brains.
Detection of C1-esterase inhibitor (C1-Inh) and C1 subcomponents (C1s, C1r) in plaques is variable or absent.
Late complement components (C5, C7, C9) and the membrane attack complex (MAC) are not found in beta-amyloid plaques.

Purpose of the Study:

To investigate the role and regulation of complement activation in Alzheimer's disease (AD) brains.
To determine the presence and localization of early and late complement components and C1-Inh in AD.
To elucidate the mechanism of complement-mediated neurodegeneration in AD.

Main Methods:

Immunohistochemistry to detect complement components and C1-Inh in brain tissue.
Reverse transcriptase-polymerase chain reaction (RT-PCR) to assess mRNA expression of complement components.
Monoclonal antibodies specific for different forms of C1-Inh were used.

Main Results:

C1q, C1s, and C1-Inh mRNAs are present in both AD and control brains, suggesting local production.
Inactivated C1-Inh is found in astrocytes surrounding beta-amyloid plaques.
Absence of late complement components (C5, C7, C9) and MAC in plaques indicates they are not formed in situ.

Conclusions:

Complement activation in AD is regulated by C1-Inh within the brain.
The absence of MAC formation suggests that complement does not act as an inflammatory mediator via MAC in AD.
Neurodegeneration in AD likely results from the action of early complement activation products, not MAC formation.