What is it about?
Small molecule therapeutics for Alzheimer’s disease (AD).
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Why is it important?
Many reports show evidence that p-tau is reported to be an important contributor to the formation of paired helical filaments (PHFs) and neurofibrillary tangles (NFTs) in ad neurons. In the ad, glycogen synthase kinase-3 beta (GSK3β), cyclin-dependent kinase- 5 (CDK5), and dual-specificity tyrosine-phosphorylation-regulated kinase 1A (DYRK1A), are the three important kinases responsible for tau hyperphosphorylation. Currently, there are no drugs and/or small molecules that reduce the toxicity of p-tau in ad.
Perspectives
The long-term goal of our research is to develop hyperphosphorylated tau (p-tau) proteolysis targeting chimeras (PROTAC) based on small molecule therapeutics for Alzheimer’s disease (AD).
Dr., Pradeepkiran Jangampalli Adi
Texas Tech University System
Read the Original
This page is a summary of: Protective effects of a small molecule inhibitor ligand against hyperphosphorylated tau-induced mitochondrial and synaptic toxicities in Alzheimer disease, Human Molecular Genetics, August 2021, Oxford University Press (OUP),
DOI: 10.1093/hmg/ddab244.
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