Dementia Big
Alzheimer’s Disease (AD) is classified as a neurodegenerative non-curable disease that affects millions worldwide. Current drugs have side effects that are significant. In AD, the beta-amyloid precursor protein (β-APP) that is critical for normal neuronal growth, survival and repair, is improperly cleaved by specific aspartic proteases, which create fragments that form plaques of amyloid beta. These fragments aggregate outside neurons and create plaques which lead to destruction of neural signaling. The pathophysiology of AD is complex, although there are many approaches to combat the disease. Many studies target PTB domain-containing proteins in order to inhibit binding to β-APP preventing amyloid formation; whereas others target inhibition of specific aspartate proteases required for amyloid plaque formation. The role of GSK-3 is actively being studied in addition to specific inhibitors to this target for AD. Structural examples analyzed include Presenilin Homologue (PSH) protein and Mint1 which are important for the regulation of β-APP.
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