Alzheimer's Disease - Current and Emerging

Summary

This project explores the genetic, biochemical, and therapeutic aspects of Alzheimer's Disease (AD), a progressive neurodegenerative disorder characterized by memory loss, cognitive decline, and brain atrophy. AD primarily affects individuals over 65 years old, with age, genetics, and vascular risks (e.g., smoking, hypertension) as significant contributing factors. Women are at higher risk, partly due to hormonal differences and increased tau protein buildup. The study examines two primary hypotheses for AD pathology: the Amyloid Hypothesis and the Cholinergic Hypothesis. The Amyloid Hypothesis highlights the role of beta-amyloid plaque accumulation, driven by mutations in APP, PSEN1, and PSEN2 genes, which disrupt protein processing and lead to neurotoxicity. The Cholinergic Hypothesis focuses on acetylcholine depletion, impairing memory and cognitive functions. Neuropathological findings indicate amyloid plaques, neurofibrillary tangles, and widespread neuronal loss as key hallmarks. Current treatments target beta-amyloid plaques with drugs like Aducanumab, BAN2401, and Gantenerumab, while BACE inhibitors aim to reduce beta-amyloid production. Genetic research highlights mutations in APP, PSEN1, PSEN2, and the risk gene APOE4, which significantly increase susceptibility. Emerging therapies, including monoclonal antibodies and genetic interventions, hold promise for slowing disease progression.

Alzheimer’s Disease Amyloid Hypothesis (Figure representation created by the author:Prisha Thukral)

Swedish Mutation in APP and APP Domains (Figure representation created by the author:Prisha Thukral)

APP Amyloidogenic and Non-Amyloidogenic Pathways (Figure representation created by the author:Prisha Thukral)

Video Presentation

Impact Statement

Hi, I am Prisha Thukral from Oberoi International School. My research was focused on the Swedish Mutation of the APP Alzheimer's Disease (AD) gene. I looked into the impact of the Swedish Mutation in the BACE1 cleavage at the beta-secretase site. I found that the Swedish Mutation leads to an enhancement in the BACE1 cleavage at the beta-secreatse site which leads to an increase in amyloid-beta production leading to early onset AD. The engaging and informative sessions provided me with various tools and resources to do thorough and in-depth research on my project. Through ERP, I was able to use various scientific databases, access multiple articles and conduct analysis of different genes. The very accommodating, helpful and supportive instructors guided me through my research and made the entire journey fun and informative. I am grateful to the instructors for helping me out with queries and supporting me throughout. ERP provided me with many exciting opportunities and made me feel confident in my research capabilities.

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By: Prisha Thukral. The opinions expressed here are the views of the writer and do not necessarily reflect the views and opinions of Elio Academy.

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