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Related Concept Videos

Complement System01:27

Complement System

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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...
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Eukaryotic cells can degrade proteins through several pathways. One of the most important among these is the ubiquitin-proteasome pathway. It helps the cell eliminate the misfolded, damaged, or unwarranted cytoplasmic proteins in a highly specific manner.
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The Extrinsic Apoptotic Pathway01:17

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The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...
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Antibodies, or immunoglobulins, are critical players in the immune system's arsenal against invading pathogens. Produced by B cells and plasma cells, their primary role is to detect and bind to specific antigens, molecules found on the surface of pathogens like bacteria or viruses. Beyond antigen recognition, antibodies perform several vital functions that contribute to immune defense.
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The Intrinsic Apoptotic Pathway01:31

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Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
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Related Experiment Video

Updated: Oct 23, 2025

Exogenous Administration of Microsomes-associated Alpha-synuclein Aggregates to Primary Neurons As a Powerful Cell Model of Fibrils Formation
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Alpha-synuclein activates the classical complement pathway and mediates complement-dependent cell toxicity.

Emil Gregersen1,2, Cristine Betzer1,2, Woojin S Kim3

  • 1DANDRITE, The Danish Research Institute of Translational Neuroscience, Aarhus University, Aarhus C, Denmark.

Journal of Neuroinflammation
|August 17, 2021
PubMed
Summary

Alpha-synuclein activates the complement system, causing cell damage in synucleinopathies like Parkinson's disease. Complement inhibitors reduced this toxicity, suggesting a pro-neurodegenerative role for the complement system.

Keywords:
Complement systemCp20MSANeurodegenerationRaCISH-SY5Yα-Synuclein

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Area of Science:

  • Neuroscience
  • Immunology
  • Cell Biology

Background:

  • Synucleinopathies involve neurodegeneration and alpha-synuclein aggregation.
  • The complement system, involved in CNS functions, mediates synapse loss in Alzheimer's disease.
  • The role of the complement system in alpha-synuclein-associated diseases remains unclear.

Purpose of the Study:

  • Investigate the complement system's pathological role in synucleinopathies.
  • Assess complement-mediated effects on alpha-synuclein expressing cells.
  • Examine direct complement activation by alpha-synuclein.

Main Methods:

  • Assessed complement system effects on alpha-synuclein expressing cell viability.
  • Examined direct complement activation by alpha-synuclein using a plate-based assay.
  • Measured C1q levels in postmortem brain samples from multiple system atrophy (MSA) patients.

Main Results:

  • Alpha-synuclein activates the classical complement pathway.
  • Complement-dependent toxicity in alpha-synuclein expressing cells was demonstrated.
  • Complement inhibitors (RaCI, Cp20) rescued alpha-synuclein-induced cellular toxicity.
  • A trend towards higher C1q levels in MSA brains was observed.

Conclusions:

  • Alpha-synuclein activates the classical complement pathway.
  • The complement system contributes to alpha-synuclein-dependent cytotoxicity.
  • The complement system may play a pro-neurodegenerative role in synucleinopathies.