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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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Aging is a complex biological phenomenon influenced by various processes that affect cellular and systemic functions. Several prominent theories attempt to explain its mechanisms, highlighting cellular limitations, oxidative damage, and hormonal changes as central factors in aging.
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Age-related pharmacokinetic changes are extensively documented, but understanding age-related pharmacodynamic alterations is relatively limited. This knowledge gap can be partly attributed to the complexity of developing appropriate measures of drug responses compared to bioanalytical methods for determining drug concentrations.Most information regarding age-related differences in human pharmacodynamics originates from cross-sectional studies. However, these studies assume that observed mean...
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Several body functions deteriorate with age. The external signs of aging are easily identifiable. For example, the skin becomes dry, less elastic, and thins out, forming wrinkles. The skin of the face begins to appear looser due to a decrease in the levels of elastic and collagen fibers in the connective tissue. Additionally, melanin production in the hair follicle decreases with age, resulting in gray hair. Moreover, the senses of sight and hearing decline, so glasses and hearing aids may...
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High-resolution Melting PCR for Complement Receptor 1 Length Polymorphism Genotyping: An Innovative Tool for Alzheimer's Disease Gene Susceptibility Assessment
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Complement C3a receptor-mediated vascular dysfunction: a complex interplay between aging and neurodegeneration.

Kanchan Bhatia1,2, Saif Ahmad1, Adam Kindelin1

  • 1Department of Neurosurgery, Barrow Neurological Institute, St. Joseph's Hospital and Medical Center (SJHMC), Dignity Health, Phoenix, Arizona, USA.

The Journal of Clinical Investigation
|January 4, 2021
PubMed
Summary
This summary is machine-generated.

The complement C3a/C3a receptor (C3a/C3aR) axis drives neurovascular inflammation and blood-brain barrier (BBB) dysfunction in aging and disease. Inhibiting C3aR signaling may protect against age-related cognitive decline and neurodegeneration.

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Area of Science:

  • Neuroscience
  • Immunology
  • Vascular Biology

Background:

  • Vascular dysfunction and compromised blood-brain barrier (BBB) integrity are hallmarks of aging and neurodegenerative diseases.
  • The complement system, particularly the C3a/C3a receptor (C3a/C3aR) axis, plays a role in brain aging and disease, but its specific mechanisms in endothelial cells are unclear.

Purpose of the Study:

  • To investigate the role of endothelial C3a/C3aR signaling in neurovascular inflammation and BBB permeability during normal aging and neurodegeneration.
  • To elucidate the downstream molecular mechanisms linking C3aR signaling to BBB dysfunction.

Main Methods:

  • Utilized normal, aged, and neurodegenerative mouse models.
  • Examined endothelial C3aR signaling, VCAM1 expression, lymphocyte infiltration, and microglial activity.
  • Assessed calcium release, VE-cadherin junction integrity, BBB permeability, and vascular structure.
  • Employed C3aR knockout (C3ar1-/-) mice and C3aR antagonist treatment.

Main Results:

  • Endothelial C3aR signaling promoted age-dependent VCAM1 increases, lymphocyte infiltration, and microglial activation.
  • C3aR signaling induced calcium release, disrupting VE-cadherin junctions and increasing BBB permeability.
  • Loss or inhibition of C3aR attenuated age-related microglial reactivity and neurodegeneration.

Conclusions:

  • Complement-mediated C3aR signaling critically impacts vascular health and BBB function in aging and neurodegenerative conditions.
  • Targeting the C3a/C3aR axis offers a potential therapeutic strategy for cerebral microvascular dysfunction.