Journal Article

DZNE-2025-00034

http://join2-wiki.gsi.de/foswiki/pub/Main/Artwork/join2_logo100x88.png A dataset profiling the multiomic landscape of the prefrontal cortex in amyotrophic lateral sclerosis.

Hausmann, F. ; Caldi Gomes, L. ; Hänzelmann, S. ; Khatri, R. ; Oller, S. ; Gebelin, M. ; Parvaz, M. ; Tzeplaeff, L. ; Pasetto, L. ; Zhou, Q.DZNE* ; Zelina, P. ; Edbauer, D.DZNE* ; Pasterkamp, R. J. ; Rehrauer, H. ; Schlapbach, R. ; Carapito, C. ; Bonetto, V. ; Bonn, S. ; Lingor, P. (Last author)DZNE*

2024
Oxford University Press Oxford

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Please use a persistent id in citations: doi:10.1093/gigascience/giae100

Abstract: Amyotrophic lateral sclerosis (ALS) is the most common motor neuron disease, which still lacks effective disease-modifying therapies. Similar to other neurodegenerative disorders, such as Alzheimer and Parkinson disease, ALS pathology is presumed to propagate over time, originating from the motor cortex and spreading to other cortical regions. Exploring early disease stages is crucial to understand the causative molecular changes underlying the pathology. For this, we sampled human postmortem prefrontal cortex (PFC) tissue from Brodmann area 6, an area that exhibits only moderate pathology at the time of death, and performed a multiomic analysis of 51 patients with sporadic ALS and 50 control subjects. To compare sporadic disease to genetic ALS, we additionally analyzed PFC tissue from 4 transgenic ALS mouse models (C9orf72-, SOD1-, TDP-43-, and FUS-ALS) using the same methods. This multiomic data resource includes transcriptome, small RNAome, and proteome data from female and male samples, aimed at elucidating early and sex-specific ALS mechanisms, biomarkers, and drug targets.

Keyword(s): Amyotrophic Lateral Sclerosis: genetics (MeSH) ; Amyotrophic Lateral Sclerosis: metabolism (MeSH) ; Prefrontal Cortex: metabolism (MeSH) ; Prefrontal Cortex: pathology (MeSH) ; Humans (MeSH) ; Female (MeSH) ; Mice (MeSH) ; Male (MeSH) ; Animals (MeSH) ; Mice, Transgenic (MeSH) ; Transcriptome (MeSH) ; Proteome (MeSH) ; Disease Models, Animal (MeSH) ; Aged (MeSH) ; Gene Expression Profiling: methods (MeSH) ; Middle Aged (MeSH) ; amyotrophic lateral sclerosis ; early disease mechanisms ; multiomics analysis ; neurodegeneration ; prefrontal cortex ; Proteome

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Contributing Institute(s):

1. Clinical Research (Munich) (Clinical Research (Munich))
2. Adaptive Immunity in Neurodegeneration (AG Zhou)
3. Cell Biology of Neurodegeneration (AG Edbauer)

Research Program(s):

1. 353 - Clinical and Health Care Research (POF4-353) (POF4-353)
2. 352 - Disease Mechanisms (POF4-352) (POF4-352)

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