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Relationship between multifunctional protein "clusterin" and Alzheimer disease
1Department of Physiological Chemistry, School of Pharmaceutical Sciences, Showa University, Tokyo, Japan.
Neurobiology of Aging
|September 1, 1996
Summary
Clusterin, a protein found in Alzheimer disease (AD) brains, may worsen neurotoxicity by enhancing beta-amyloid
Area of Science:
- Neuroscience
- Biochemistry
Background:
- Alzheimer disease (AD) brains feature senile plaques with proteins like beta-amyloid (A beta) and cytokines.
- Clusterin, a multifunctional protein, colocalizes with A beta deposits and its levels are elevated in AD brains.
- Cytokines such as TGF beta 1 and interleukin 1 can increase clusterin expression, linking it to AD inflammation.
Purpose of the Study:
- To investigate the role of clusterin in Alzheimer disease pathogenesis.
- To understand how clusterin interacts with beta-amyloid and its impact on neurotoxicity.
Main Methods:
- Analysis of clusterin and A beta interactions in Alzheimer disease models.
- Assessment of clusterin's effects on A beta aggregation and oxidative stress.
Main Results:
- Clusterin levels are increased in Alzheimer disease (AD) brains and colocalize with beta-amyloid (A beta) deposits.
- While clusterin can inhibit A beta aggregation, it paradoxically enhances A beta-induced oxidative stress.
- This enhancement of oxidative stress by clusterin may extend A beta neurotoxicity beyond plaque sites.
Conclusions:
- Clusterin's dual role in Alzheimer disease (AD) involves both potential neuroprotection via A beta aggregation inhibition and neurotoxicity enhancement through oxidative stress.
- Clusterin may contribute to the spread of neurotoxicity in AD by exacerbating A beta's damaging effects.