Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Alzheimer's Disease: Treatment01:22

Alzheimer's Disease: Treatment

265
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...
265
Cognitive Enhancers: Cholinesterase Inhibitors and NMDA Receptor Antagonists01:30

Cognitive Enhancers: Cholinesterase Inhibitors and NMDA Receptor Antagonists

214
Cognitive enhancers, also known as "smart drugs," are substances used to enhance memory, mental alertness, and concentration. These can be natural or synthetic and improve cognition in conditions like Alzheimer's disease (AD) and other neurodegenerative diseases. Some common examples include caffeine, amphetamines, methylphenidate, modafinil, arecoline, donepezil, vortioxetine, and piracetam. These enhancers work on the principle of synaptic plasticity and altered circuit function.
214
Complement System01:27

Complement System

2.8K
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...
2.8K
Parkinson's Disease: Overview01:15

Parkinson's Disease: Overview

722
Neurodegenerative disorders are progressive diseases that cause irreversible damage and loss to neurons in specific brain areas. Examples of these disorders include Parkinson's disease, Alzheimer's disease, Multiple Sclerosis (MS), and Amyotrophic Lateral Sclerosis (ALS). These disorders share characteristics such as proteinopathies, selective neuronal vulnerability, and a complex interplay between genetic and environmental factors. The primary therapeutic goal for these conditions is...
722
Alzheimer's Disease: Overview01:26

Alzheimer's Disease: Overview

684
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...
684
Parkinson's Disease: Treatment01:24

Parkinson's Disease: Treatment

391
Neurodegenerative disorders, such as Parkinson's Disease (PD), involve the gradual and irreversible destruction of neurons in particular brain areas. These disorders exhibit standard features like proteinopathies, selective vulnerability of some neurons, and an interaction of intrinsic properties, genetics, and environmental influences in neural injury.
Parkinson's Disease is primarily a result of the loss of dopaminergic neurons in the substantia nigra pars compacta. The cornerstone of...
391

You might also read

Related Articles

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

Sort by
Same author

Shifting From Systemic to Precision-Targeted Complement Therapies: Opportunities and Hurdles.

European journal of immunology·2026
Same author

The TREM2 R47H variant is associated with liver-plasma-brain axis dyshomeostasis in the 5xFAD mouse model of Alzheimer's disease.

Neurobiology of aging·2026
Same author

Abi3<sup>S212F</sup> Alzheimer's disease variant alters plaque structure and disrupts microglia.

Alzheimer's & dementia : the journal of the Alzheimer's Association·2026
Same author

Lymphocyte alterations and elevated complement signaling are key features of refractory myasthenia gravis.

Med (New York, N.Y.)·2026
Same author

Activation of the Lectin Pathway Drives Persistent Complement Dysregulation in Long COVID.

Immunology·2026
Same author

Basic Science and Pathogenesis.

Alzheimer's & dementia : the journal of the Alzheimer's Association·2025
Same journal

WD-3 improves anti-PD-L1 therapy by remodeling the tumor immune microenvironment through gut microbiota.

Immunobiology·2026
Same journal

Interleukin 27 (IL-27) in gastrointestinal cancers: from dual roles in tumor immunity to immunotherapeutic opportunities.

Immunobiology·2026
Same journal

ST2-mediated ERK/JNK/P38/NF-κB signaling: a target of Biminkang mixture in minimal persistent inflammation of allergic rhinitis.

Immunobiology·2026
Same journal

Chronic stress promotes colorectal cancer progression by inducing M2 macrophage polarization and activating the CCL2-CCR2 axis.

Immunobiology·2026
Same journal

Spatial-cellular resolution analysis of ferroptosis-associated immune microenvironment heterogeneity in osteoarthritic cartilage.

Immunobiology·2026
Same journal

Exploring therapeutic targets for neuroinflammation in sepsis-associated encephalopathy: a combined network pharmacology and bioinformatics approach.

Immunobiology·2026
See all related articles

Related Experiment Video

Updated: Sep 18, 2025

High-resolution Melting PCR for Complement Receptor 1 Length Polymorphism Genotyping: An Innovative Tool for Alzheimer's Disease Gene Susceptibility Assessment
07:26

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

11.9K

Complement therapeutics in neurodegenerative diseases.

Wioleta M Zelek1, Andrea J Tenner2

  • 1UK Dementia Research Institute, School of Medicine, CF14 4XN, Cardiff University, UK.

Immunobiology
|June 22, 2025
PubMed
Summary
This summary is machine-generated.

The complement system plays a key role in brain health and neurodegenerative diseases. Targeting this system offers a promising therapeutic strategy for various brain disorders.

Keywords:
BrainComplementNeurodegenerationTherapeutics

More Related Videos

A Model of Epileptogenesis in Rhinal Cortex-Hippocampus Organotypic Slice Cultures
10:05

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

Published on: March 18, 2021

7.1K
A Novel In Vitro Live-imaging Assay of Astrocyte-mediated Phagocytosis Using pH Indicator-conjugated Synaptosomes
06:43

A Novel In Vitro Live-imaging Assay of Astrocyte-mediated Phagocytosis Using pH Indicator-conjugated Synaptosomes

Published on: February 5, 2018

12.3K

Related Experiment Videos

Last Updated: Sep 18, 2025

High-resolution Melting PCR for Complement Receptor 1 Length Polymorphism Genotyping: An Innovative Tool for Alzheimer's Disease Gene Susceptibility Assessment
07:26

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

11.9K
A Model of Epileptogenesis in Rhinal Cortex-Hippocampus Organotypic Slice Cultures
10:05

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

Published on: March 18, 2021

7.1K
A Novel In Vitro Live-imaging Assay of Astrocyte-mediated Phagocytosis Using pH Indicator-conjugated Synaptosomes
06:43

A Novel In Vitro Live-imaging Assay of Astrocyte-mediated Phagocytosis Using pH Indicator-conjugated Synaptosomes

Published on: February 5, 2018

12.3K

Area of Science:

  • Neuroscience
  • Immunology
  • Pharmacology

Background:

  • Neurodegenerative diseases (NDDs) present significant therapeutic challenges, partly due to the necessity for drugs to cross the blood-brain barrier.
  • Inflammation is a critical component of NDDs, with the complement system emerging as a central mediator in the central nervous system (CNS).
  • Dysregulation of the complement system contributes to synaptic loss, chronic inflammation, and neurodegeneration, and is implicated in neurodevelopmental and psychiatric disorders.

Purpose of the Study:

  • To provide a comprehensive overview of the complement system's roles in CNS health and disease.
  • To summarize mechanisms by which complement contributes to neuropathology.
  • To discuss novel therapeutic strategies and challenges in CNS drug development.

Main Methods:

  • Review of existing literature on the complement system in the CNS.
  • Analysis of complement's involvement in neurodegenerative, neurodevelopmental, and neuropsychiatric disorders.
  • Examination of therapeutic approaches and drug delivery challenges for CNS disorders.

Main Results:

  • The complement system is involved in normal brain functions like synaptic pruning and immune surveillance.
  • Aberrant complement activation drives neuroinflammation, synapse loss, and neurodegeneration in NDDs.
  • Complement system overactivation impacts brain development and circuit stability in psychiatric and neurodevelopmental conditions.

Conclusions:

  • The complement system is a critical factor in CNS health and disease.
  • Targeting the complement system presents a novel therapeutic avenue for neurodegenerative and other brain disorders.
  • Overcoming challenges in brain drug delivery and patient stratification is crucial for developing effective complement-based therapies.