Calpain dysregulation in Alzheimer's disease
1Department of Cell and Molecular Biology, Feinberg School of Medicine, Northwestern University, 303 E. Chicago Avenue, Ward 8-140, Chicago, IL 60611, USA.
ISRN Biochemistry
|May 14, 2015
Summary
Alzheimer's disease involves brain plaques and tangles, linked to calcium imbalance and calpain protease activation. This review explores calpains' role in Alzheimer's neurodegeneration mechanisms.
Area of Science:
- Neuroscience
- Biochemistry
Background:
- Alzheimer's disease (AD) is a prevalent neurodegenerative disorder in aging populations.
- AD pathology includes senile plaques, neurofibrillary tangles, and synaptic loss in the brain.
- Emerging evidence suggests a link between AD hallmarks and disrupted calcium homeostasis.
Purpose of the Study:
- To review the structure and regulation of calpains, a family of calcium-dependent cysteine proteases.
- To summarize the involvement of calpains in the neurodegenerative processes of Alzheimer's disease.
Main Methods:
- Literature review of existing studies on calpains and Alzheimer's disease.
- Analysis of data on calcium homeostasis and its relation to calpain activation in AD.
Main Results:
- Calpains are crucial for various cellular functions, including development and cell death.
- Dysregulation of calcium homeostasis in AD leads to abnormal calpain activation.
- Calpain activation is implicated in the molecular mechanisms underlying AD pathogenesis.
Conclusions:
- Calpains are key players in the neurodegenerative cascade of Alzheimer's disease.
- Understanding calpain's role offers potential therapeutic targets for AD treatment.
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