Cell death assays for neurodegenerative disease drug discovery
Year: 2019
Type: review
Abstract: Introduction: Neurodegenerative diseases affect millions of people worldwide. Neurodegeneration is gradual over time, characterized by neuronal death that causes deterioration of cognitive or motor functions, ultimately leading to the patient’s death. Currently, there are no treatments that effectively slow the progression of any neurodegenerative disease, but improved microscopy assays and models for neurodegeneration could lead the way to the discovery of disease-modifying therapeutics.Areas covered: Herein, the authors describe cell-based assays used to discover drugs with the potential to slow neurodegeneration, and their associated disease models. They focus on microscopy technologies that can be adapted to a high-throughput screening format that both detect cell death and monitor early signs of neurodegeneration and functional changes to identify drugs that the block early stages of neurodegeneration.Expert opinion: Many different phenotypes have been used in screens for the development of therapeutics towards neurodegenerative disease. The context of each phenotype in relation to neurodegeneration must be established to identify therapeutics likely to successfully target and treat disease. The use of improved models of neurodegeneration, statistical analyses, computational models, and improved markers of neuronal death will help in this pursuit and lead to better screening methods to identify therapeutic compounds against neurodegenerative disease.
Source: Expert Opinion on Drug Discovery
Language: English
Subfield: Cellular and Molecular Neuroscience
Field: Neuroscience
Domain: Life Sciences
Open Access status: green
Awards: Neuron and Glial Cellular Signatures from Normal and Diseased iPS Cells, Discovery of Novel Drugs that Increase Tau Clearance to Treat Alzheimer's Disease, G41133098, Tauopathy in AD and FTD - Molecular Determinants of Phenotypic Diversity, Rare Variant Whole Genome Analysis and iPSC Validation of Putative Genetic Modifiers of Huntington Disease, Dysfunction of the Autophagy-Lysosomal Pathway as a Common Mechanism of Neurodegeneration, EXTRAMULAR RESEARCH FACILITIES CONSTRUCTION, Proteostasis in Aging and Neurodegenerative Disease
OpenAlex ID: W2950163825