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Midkine, a novel neurotrophic factor, is present in senile plaques of Alzheimer disease
O Yasuhara1, H Muramatsu, S U Kim
1Department of Psychiatry, University of British Columbia, Vancouver, Canada.
Abstract:
An affinity purified antibody specific for midkine (MK) stained senile plaques in the brain of Alzheimer disease (AD) patients. After formic acid treatment, plaque staining was dramatically enhanced, and almost all beta-amyloid protein (BAP) deposits were also immunoreactive for MK. MK-immunoreactivity was not observed in normal cellular components nor in other pathological lesions including tangles in AD brain. Control brain sections were not immunoreactive for MK. The presence of MK in AD brain but not in control brain was confirmed by Western blotting. MK appears to be involved in the pathological process leading to senile plaque formation.
Insights
Midkine (MK) is present in Alzheimer disease (AD) brain senile plaques, but not in healthy brains. This finding suggests midkine plays a role in the development of beta-amyloid protein deposits characteristic of AD.
Area of Science:
- Neuroscience
- Biochemistry
- Pathology
Background:
- Alzheimer disease (AD) is characterized by senile plaques, primarily composed of beta-amyloid protein (BAP).
- The specific molecular mechanisms driving senile plaque formation in AD are not fully understood.
Purpose of the Study:
- To investigate the presence and role of midkine (MK) in Alzheimer disease pathology, specifically in relation to senile plaques.
Main Methods:
- Immunohistochemical staining of post-mortem brain tissue from AD patients and controls using an antibody specific for MK.
- Formic acid treatment to enhance antigenicity of BAP deposits.
- Western blotting to confirm the presence of MK in AD brain tissue.
Main Results:
- Midkine (MK) specifically stained senile plaques in Alzheimer disease (AD) brains.
- Formic acid treatment enhanced MK staining, revealing co-localization with almost all beta-amyloid protein (BAP) deposits.
- MK was detected in AD brain tissue but absent in control brain sections, confirmed by Western blotting.
Conclusions:
- Midkine (MK) is present in Alzheimer disease (AD) senile plaques and co-localizes with beta-amyloid protein (BAP) deposits.
- The absence of MK in normal brain components and other pathological lesions suggests a specific role in AD pathogenesis.
- These findings indicate that midkine (MK) is involved in the pathological processes leading to senile plaque formation in Alzheimer disease (AD).