Chapter 9. Post-translational Modifications and Alzheimer's Disease

Polycatechols inhibit ferroptosis and modulate tau liquid–liquid phase separation to mitigate Alzheimer's disease

“…ders, including neurodegeneration. [14][15][16] Post-mortem analysis revealed an abnormal increase in biometal levels such as Cu (5.7 fold), Zn (3.1 fold), and Fe (2.8 fold) in AD brains compared to healthy brains. 17,18 Fe binds to Ab to exacerbate aggregation and the generation of reactive oxygen species (ROS), resulting in biomolecular damage.…”

Multipronged diagnostic and therapeutic strategies for Alzheimer's disease

“…Many kinases that act on tau with glycogen synthase kinase 3 beta (GSK3β) responsible for many tau pathological phosphorylation have been extensively studied. 9,167 Small molecule inhibitors of GSK3β activity were developed and tested for their therapeutic effect to prevent tau pathology (Fig. 8A).…”

Mechanistic Insights for Drug Repurposing and the Design of Hybrid Drugs for Alzheimer’s Disease

“…The quest to identify natural-product-based repurposed drugs for the treatment of AD has led to the exploration of taxanes, which are commonly used in treating cancers. The hyperphosphorylation of τ results in its dissociation from MTs and neurofibrillary degeneration. , As a result, MT-stabilizing agents such as paclitaxel (taxol) have been explored for their protective role against Aβ-induced neuronal cell death and inhibition of τ-hyperphosphorylation by Cdk5 . The MOA behind the therapeutic role of paclitaxel is attributed to its ability to specifically inhibit Aβ-induced Cdk5 activation by blocking the calpain-mediated proteolysis of the early 35 kDa protein (p35).…”