Self-attack by the body’s own complement system plays a role in a broad spectrum of human diseases.  Given its complexity and involvement in many physiological processes, it is not surprising that disruption in the balance of complement activation and regulation may have profound physiological consequences.  In recent decades abnormal complement activity has been implicated in a growing number of conditions in a wide variety of clinical areas.


Neurology

    • Amyotrophic Lateral Sclerosis (ALS)
    • Parkinson Disease (PD)
  • Pick’s Disease

Hematology

    • Atypical Hemolytic Uremic Syndrome (aHUS)
  • Paroxysmal Nocturnal Hemoglobinuria (PNH)

Ophthalmology

  • Age-related Macular Degeneration (AMD)

Autoimmune

    • Multiple Sclerosis (MS)
    • Myasthenia Gravis
    • Neuromyelitis Optica
    • Organ transplant
    • Rheumatoid Arthritis (RA)
  • Systemic Lupus Erythematosus (SLE)

Inflammatory

    • Asthma
    • Atherosclerosis
    • Psoriasis
  • Pemphigus

Trauma

    • Burn injuries
    • Ischemia / Reperfusion Injuries (IRI)
  • Neurotrauma / Traumatic Brain Injury (TBI)

Self-attack by the body’s own immune system plays a role in a broad spectrum of human diseases. Targeted inhibition of the Complement system may be sufficient to help rebalance complement activity and thus ameliorate disease symptoms.

An alphabetical list of conditions where abnormal complement activation has been implicated is available on our Role in Disease page.