HDGFL2 cryptic proteins report presence of TDP-43 pathology in neurodegenerative diseases

Year: 2024

Type: article

Abstract: This letter demonstrates the potential of novel cryptic proteins resulting from TAR DNA-binding protein 43 (TDP-43) dysfunction as markers of TDP-43 pathology in neurodegenerative diseases.

Source: Molecular Neurodegeneration

DOI: 10.1186/s13024-024-00718-8

Institutions: Mayo Clinic in Florida, Mayo Clinic, Stanford Medicine, Stanford University, National Institutes of Health, National Institute of Neurological Disorders and Stroke, National Institute on Aging

Language: English

Topic: Amyotrophic Lateral Sclerosis Research

Subfield: Clinical Neurology

Field: Medicine

Domain: Health Sciences

SDG: Good health and well-being

Open Access status: gold

Estimated APC paid: $2,990

Funders: Johns Hopkins University, Target ALS, National Institutes of Health, National Institute on Aging, National Institute of Neurological Disorders and Stroke, Robert Packard Center for ALS Research, Johns Hopkins University

Awards: G1000301862, G1278310670, G3331013217, G3872162045, Glycogen promotes protein aggregation in ALS and FTD, Pathobiology of Neurodegeneration in C9ORF72 repeat expansion, Understanding the role of TDP-43 in Alzheimer’s disease and FTLD, Stathmin-2 and TDP-43 neurodegeneration in Alzheimer’s and multi-etiology dementias, G7175295568, Expanding insights into FTD disease mechanisms, Innovating Yeast and Human Genetics Approaches to Define Mechanisms of Neurodegenerative Disease, ARTFL LEFFTDS Longitudinal Frontotemporal Lobar Degeneration, Cycle 2 (ALLFTD2), Poly(ADP-ribose) promotes the condensation and toxicity of C9orf72 arginine-rich dipeptide repeat proteins, Discovery of novel TDP-43 splicing targets: the Achilles heel for FTD and towards sensitive biomarkers and therapeutic targets, Stathmin-2 and TDP-43 neurodegeneration in Alzheimer’s and multi-etiology dementias

OpenAlex ID: W4393232817