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Expression of the complement membrane attack complex and its inhibitors in Pick disease brain
O Yasuhara1, Y Aimi, E G McGeer
1Kinsmen Laboratory of Neurological Research, University of British Columbia, Vancouver, Canada.
Brain Research
|August 1, 1994
Summary
Complement membrane attack complex (MAC) contributes to Pick body formation in Pick disease brains. Clusterin staining suggests it may indicate active neuronal degeneration in affected areas.
Area of Science:
- Neuroscience
- Immunology
- Pathology
Background:
- Pick disease is a neurodegenerative disorder characterized by abnormal tau protein aggregation.
- The complement system, particularly the membrane attack complex (MAC), plays a role in neuroinflammation and neurodegeneration.
- Inhibitors of MAC, such as vitronectin, protectin, and clusterin, modulate complement activity.
Purpose of the Study:
- To investigate the presence and localization of the complement membrane attack complex (MAC) in Pick disease brains.
- To compare the distribution of MAC with its inhibitors: vitronectin, protectin, and clusterin.
- To explore the potential role of clusterin as a marker for neuronal degeneration in Pick disease.
Main Methods:
- Immunohistochemistry was used to detect MAC, vitronectin, protectin, and clusterin in brain tissue samples from patients with Pick disease.
- Specific antibodies were employed to visualize the target proteins within the brain parenchyma.
Main Results:
- Pick bodies showed intense staining for MAC and protectin, and weak staining for vitronectin.
- Clusterin staining was negative in Pick bodies but intensely stained some pyramidal neurons, including ballooned neurons, in affected cortical areas.
- These findings suggest a complement-mediated attack is involved in Pick body formation.
Conclusions:
- Complement-mediated attack is associated with the formation of Pick bodies in Pick disease.
- Clusterin's intense staining of degenerating neurons suggests it may serve as a marker for active neuronal degeneration in this condition.