Arya Dandawate
Class of 2027Los Gatos, California
About
Projects
- "Amyloid beta versus tau: Therapeutics and biomarker and therapeutics development" with mentor Jobin (Mar. 1, 2025)
Project Portfolio
Amyloid beta versus tau: Therapeutics and biomarker and therapeutics development
Started June 30, 2024
Abstract or project description
Arya will focus on therapeutics and biomarker development in Alzheimer's disease. There are two leading hypotheses for the development of Alzheimer's: amyloid hypothesis and tau hyperphosphorylation. The review will focus on both these hypotheses. She will also look into the genetic basis of Alzheimer's disease. There are various genes that are risk factors for Alzheimer's disease. The review will cover the current state of therapeutics and biomarker development in Alzheimer's disease.
Alzheimer’s disease (AD) is a progressive neurodegenerative disorder characterized by cognitive decline, memory loss, and behavioral changes, primarily caused by the accumulation of amyloid-beta (Aβ) plaques and tau tangles in the brain. The amyloid cascade and tau hypotheses provide insight into the causes of AD, suggesting that Aβ aggregation and tau hyperphosphorylation contribute to neurodegeneration. While current therapies largely focus on Aβ plaques, limited success has been observed in clinical trials, highlighting the need for more comprehensive treatment strategies. This paper explores the process of the amyloid cascade hypothesis and the tau hypothesis, and the potential of synergistic therapies targeting both Aβ and tau, such as agents that inhibit tau hyperphosphorylation combined with therapies preventing Aβ aggregation. Reviewing genetic factors, mouse models, and current therapeutic approaches reveals the challenges and opportunities of dual-target therapies in AD. Specifically, examining the role of genetic risk factors like APOE4, the efficacy of monoclonal antibodies targeting Aβ, and emerging biomarkers such as p-tau217, which could enable better diagnosis and treatment monitoring. The possibility of combining therapeutic strategies for Aβ and tau presents a promising approach for more effective AD management, but further research is needed to determine its feasibility and clinical effectiveness.