Protein Kinases in Alzheimer’s Disease: Pioneering Insights intoPathogenesis and Therapeutic Breakthroughs

Alzheimer's Disease (AD) is an exhausting neurodegenerative condition marked by the build-up of abnormal protein aggregates in the brain and a progressive loss of cognitive function. The complicated role that protein kinases play in the pathophysiology of AD has come to light more and more in recent years. The symptoms of AD include memory loss, cognitive impairment, and neuronal malfunction. Many cellular processes, including synaptic plasticity, neuronal survival, and protein homeostasis, have been linked to protein kinases, a class of enzymes that control phosphorylation. The etiology of AD has been closely related to the dysregulation of protein kinases, including those implicated in the phosphorylation of tau and the formation of amyloid-beta. GSK-3, also known as glycogen synthase kinase, is one of the most studied protein kinases in Alzheimer's disease. It is known that GSK-3 phosphorylates tau protein, causing it to clump together and create neurofibrillary tangles. Moreover, GSK-3 activation increases the development of amyloid-beta, which furthers the disease's progression. Additional protein kinases, including Cyclin-Dependent Kinase 5 (CDK5) and calcium/calmodulin-dependent protein kinase II (CaMKII), have also been connected to tau phosphorylation and synaptic dysfunction in AD. Protein kinases play a crucial role in the pathophysiology of AD, extending beyond tau phosphorylation. Research has shown that Amyloid Precursor Protein (APP) processing is regulated by Protein Kinases A (PKA) and C (PKC), which affects the production and clearance of amyloid-beta. Furthermore, AD etiology involves oxidative stress, neuroinflammation, and mitochondrial dysfunction, all of which are regulated by protein kinases. This study will cover the effects of protein kinases in AD, focusing on their role in tau phosphorylation, an attribute of the disease. We will also address the role of protein kinase in the development of amyloid-beta, synaptic malfunction, and neuroinflammation.