Alzheimer's Disease

Alzheimer’s disease, a form of dementia, is a progressive neurological disorder involving loss of memory and cognition. Alzheimer’s disease pathology reveals an excess of aggregated amyloid β protein in amyloid or “senile” plaques. Amyloid β protein is produced via cleavage of the amyloid precursor protein (APP) by β-secretase, yielding soluble APP. The soluble APP is converted to an insoluble amyloid β-peptide prone to aggregation or fibril formation. Although not completely understood, the etiology of Alzheimer’s disease seems to arise from a combination of factors including genetic predisposition, protein trafficking and turnover, glycosphingolipid abnormalities, and inhibition of neurotrophin signaling. Genes that contribute to amyloid β protein generation, clearance, and degradation are involved in the development and progression of Alzheimer’s disease. Genes involved in amyloid β protein signal transduction lead to neuronal toxicity and inflammation, which are additional features of Alzheimer’s disease.

QIAGEN provides a broad range of assay technologies for Alzheimer’s disease research that enables analysis of gene expression and regulation, epigenetic modification, genotyping, and signal transduction pathway activation. Solutions optimized for Alzheimer’s disease studies include PCR array, miRNA, siRNA, mutation analysis, pathway reporter, chromatin IP, DNA methylation, and protein expression products.