Title : Characterization of a New molecules’ inhibitor effect on Alzheimer’s Disease Amyloid-Beta Peptides Cascade
Abstract:
Over 50 million people succumbed to Alzheimer’s disease (AD) worldwide. Unless scientists predict effective therapeutic strategies, this number will reach 150 million by 2050. AD is characterized by progressive neurodegeneration associated with Amyloid β (Aβ) plaques constituted by the aggregated Aβ peptides, which are produced from the transmembrane Amyloid precursor protein (APP) after being cleaved by β- and γ-secretases. In the case of the healthy brain, Aβ peptides are in monomeric forms soluble in water and are involved in brain development and protect neurons from excitotoxic cell death. In contrast, in the case of AD-affected brain, the peptides aggregate into soluble oligomers and then insoluble fibrils resulting in the formation of plaques, causing neuronal cell death and cognitive impairment such as memory loss, communication difficulties, and personality changes. Since, Aβ oligomers induced toxicity to neurons, in the present talk, I will discuss an overview of the mechanism of AD development, and how our discovery of molecule assists to improve the cognitive ability of AD mice by employing an array of studies of in-silico, in-vitro and in-vivo studies.
Keywords: Alzheimer’s Disease, Amyloid peptide, drug, and AD mice.
What will the audience learn from your presentation?
- Audience learns the mechanism of Alzheimer’s disease development
- Audience will be benefitted by gaining knowledge of Alzheimer’s disease features and drugs for the treatment of the disease, and why it will affect senior adult populations.
- We characterized new molecules that improve the cognitive ability of AD-affected mice by stopping the killing neurons by Alzheimer’s peptide.