Implication of complement system and its regulators in Alzheimer's disease
Martin V Kolev1, Marieta M Ruseva, Claire L Harris
1Department of Medical Biochemistry and Immunology, School of Medicine, Heath Park, Cardiff University, Cardiff CF14 4XN, UK.
Current Neuropharmacology
|September 2, 2009
Summary
Alzheimer's disease involves amyloid plaques and complement proteins. Targeting complement system regulators may offer new therapeutic strategies for improving cognitive function in patients.
Area of Science:
- Neuroscience
- Immunology
- Pharmacology
Background:
- Alzheimer's disease (AD) is a prevalent neurodegenerative disorder affecting millions globally.
- Neuritic (amyloid) plaques and complement proteins are key pathological hallmarks and risk factors in AD.
- Complement system activation is observed early in amyloid deposition and correlates with dementia symptoms.
Purpose of the Study:
- To review the dual roles of the complement system and its regulators (CRegs) in Alzheimer's disease pathology and progression.
- To highlight evolving strategies for designing complement inhibitors as potential AD therapeutics.
- To explore how restoring complement system balance could improve cognitive performance in AD patients.
Main Methods:
- This is a review article, synthesizing existing research on the complement system in Alzheimer's disease.
- It focuses on the roles of complement proteins and CRegs in AD pathogenesis.
- The review examines current and emerging therapeutic strategies targeting the complement system.
Main Results:
- The complement system plays a significant, dual role in AD pathology and disease progression.
- Complement proteins are integral components of amyloid plaques and are present from early disease stages.
- Dysregulation of the complement system is linked to the clinical manifestation of Alzheimer's dementia.
Conclusions:
- Complement inhibitors represent a promising therapeutic avenue for Alzheimer's disease.
- Restoring the balance of the complement system may help improve cognitive function in AD patients.
- Further development of agents targeting the complement system could lead to effective AD treatments.
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