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Answer ALS Publication Policy

  1. Original Data vs. Derivatives: You may not publish or claim the original data. However, you’re encouraged to publish derivatives or findings resulting from the data.
  2. Notification of Publications: If you produce publications using AALS samples and datasets, please inform us. We would like to cite your work on other data repository websites.
  3. Acknowledgments and Citations: In your publications and presentations involving Answer ALS Data or Study Materials Results, kindly acknowledge the Answer ALS program, our funders, and the cohorts who contributed data. This recognition is vital for tracking research outputs from our data—a critical measure for our sponsors.
 
 
Below are the general Answer ALS Publications Policy guidelines:
  • You are not permitted to publish or claim the original data. Derivatives or findings from the data, however, can be published.
  • Whenever you use Answer ALS Data or Study Materials in manuscripts and presentations, ensure you acknowledge the Answer ALS program, its funders, and the contributing cohorts with the appropriate language provided below:
Answer ALS Acknowledgement:

“Data used in the preparation of this article were obtained from the ANSWER ALS Data Portal (AALS-01184). For up-to-date information on the study, visit https://dataportal.answerals.org.

To Cite Answer ALS Description Paper:Baxi, E. G. et al. Answer ALS, a large-scale resource for sporadic and familial ALS combining clinical and multi-omics data from induced pluripotent cell lines. Nat Neurosci 1-12 (2022) doi:10.1038/s41593-021-01006-0.

Answer ALS Cohort Acknowledgements:“Clinical data and biosamples used in the preparation of this article were obtained from the Answer ALS Foundation Program, ‘Answer ALS’. For up-to-date information on the program, visit https://www.answerals.org.

Citations Using Answer ALS Resources

2025

  1. Kempthorne, L. et al. Dual-targeting CRISPR-CasRx reduces C9orf72 ALS/FTD sense and antisense repeat RNAs in vitro and in vivo. Nature Communications 16, 459 (2025). doi:10.1038/s41467-024-55550-x.
  2. Sonustun, B. et al. Telmisartan is neuroprotective in a hiPSC-derived spinal microtissue model for C9orf72 ALS via inhibition of neuroinflammation. Stem Cell Reports 20(7), 102535 (2025). doi:10.1016/j.stemcr.2025.102535.
  3. Lester, D.G. et al. A Validated Model to Predict Severe Weight Loss in Amyotrophic Lateral Sclerosis. Annals of Clinical and Translational Neurology 12(9), 1738–1749 (2025). doi:10.1002/acn3.51992. 
  4. Zhang, S. et al. Antisense oligonucleotide depletion of CCDC146 is a broad-spectrum therapeutic strategy for ALS. medRxiv (2025). doi:10.1101/2024.03.30.24305115. 
  5. Dredge, W.H. et al. Meta-analysis of genetic regulation of RNA editing in the human brain identifies new genes underlying neurological disease. medRxiv (2025). doi:10.1101/2025.01.21.2452089. 
  6. Xu, W. et al. Machine learning–based proteomics profiling of ALS identifies downregulation of RPS29 that maintains protein homeostasis and STMN2 level. Communications Biology (2025). doi:10.1038/s42003-025-08578-8. 
  7. Yen, Y.P. et al. The motor neuron m6A repertoire governs neuronal homeostasis and FTO inhibition mitigates ALS symptom manifestation. Nature Communications (2025). doi:10.1038/s41467-025-59117-2. 
  8. Harvey, C. et al. Evaluation of a biomarker for amyotrophic lateral sclerosis derived from a hypomethylated DNA signature of human motor neurons. BMC Medical Genomics 18, 10 (2025). doi:10.1186/s12920-025-02084-w. 
  9. Watanabe, Y. et al. ALS-associated RNA-binding proteins promote UNC13A transcription through REST downregulation. EMBO Journal 44(17), 4745–4771 (2025). doi:10.1038/s44318-025-00506-0.
  10. Réal, A. et al. Mapping genetic effects on splicing in ten thousand post-mortem brain samples reveals novel mediators of neurological disease risk. medRxiv (2025). doi:10.1101/2025.09.25.25336663. 
  11. Cassel, R. et al. FUS Mislocalization Rewires a Cortical Gene Network to Drive Cognitive and Behavioral Impairment in ALS. medRxiv (2025). doi:10.1101/2025.06.16.25329673. 
  12. Krispin, S. et al. Organellomics: AI-driven deep organellar phenotyping reveals novel ALS mechanisms in human neurons. bioRxiv (2025). doi:10.1101/2024.01.31.572110. 

 

2024

  1. Dong, D. et al. Poly-GR repeats associated with ALS/FTD gene C9ORF72 impair translation elongation and induce a ribotoxic stress response in neurons. Science Signaling 17(848) (2024). doi:10.1126/scisignal.adl1030.
  2. Grassano, M. et al. Intermediate HTT CAG repeats worsen disease severity in amyotrophic lateral sclerosis. Journal of Neurology, Neurosurgery & Psychiatry (2024). doi:10.1136/jnnp-2024-333998.
  3. Çelik, M.H. et al. Identifying dysregulated regions in amyotrophic lateral sclerosis through chromatin accessibility outliers. Human Genetics and Genomics Advances 5(3), 100318 (2024). doi:10.1016/j.xhgg.2024.100318.
  4. Swindell, W.R. et al. Meta-analysis of differential gene expression in iPSC-derived motor neuron datasets. Frontiers in Genetics (2024). doi:10.3389/fgene.2024.1385114.
  5. Byrne, R.P. et al. Sex-specific risk loci and modified MEF2C expression in ALS. medRxiv (2024). doi:10.1101/2024.05.25.24307829. 
  6. Tsitkov, S. et al. Disease related changes in ATAC-seq of iPSC-derived motor neuron lines from ALS patients and controls. Nature Communications 15, 3606 (2024). doi:10.1038/s41467-024-47758-8. 
  7. Geraci, J. et al. Machine learning hypothesis-generation for patient stratification and target discovery in rare disease: our experience with Open Science in ALS. Front. Comput. Neurosci. (2024). doi:10.3389/fncom.2023.1199736. 
  8. Grassano, M. et al. Sex Differences in Amyotrophic Lateral Sclerosis Survival and Progression: A Multidimensional Analysis. Ann Neurol. (2024) Jul;96(1):159–169. doi:10.1002/ana.26933. 
  9. Roggenbuck, J. et al. The Answer ALS return of results study: Answering the duty to disclose. Amyotroph Lateral Scler Frontotemporal Degener (2024). doi:10.1080/21678421.2024.2385004.
  10. Cicardi, M.E. et al. The nuclear import receptor Kapβ2 modifies neurotoxicity mediated by poly(GR) in C9orf72-linked ALS/FTD. Communications Biology 7, 376 (2024). doi:10.1038/s42003-024-06071-2. 
  11. Atmaramani, R. et al. Deep Learning Analysis on Images of iPSC-derived Motor Neurons Carrying fALS-genetics Reveals Disease-Relevant Phenotypes. bioRxiv (2024). doi:10.1101/2024.01.04.574270. 
  12. Lehmann, J. et al. Heterozygous knockout of Synaptotagmin13 phenocopies ALS features and TP53 activation in human motor neurons. Cell Death & Disease 15, 560 (2024). doi:10.1038/s41419-024-06957-3.

 

2023

  1. Huber, W. et al. Identification of potential pathways and biomarkers linked to progression in amyotrophic lateral sclerosis. Annals of Clinical and Translational Neurology 10(11), 2270–2285 (2023). doi:10.1002/acn3.51697.
  2. Catanese, A. et al. Multiomics and machine-learning identify novel transcriptional and mutational signatures in amyotrophic lateral sclerosis. Brain (2023). doi:10.1093/brain/awad075.
  3. Kalia, M. et al. Genetic and phenotype analyses of primary lateral sclerosis datasets from international cohorts. medRxiv (2023). doi:10.1101/2023.07.19.23292817. 
  4. Rothstein, J.D. et al. G2C4 targeting antisense oligonucleotides potently mitigate TDP-43 dysfunction in C9orf72 ALS/FTD human neurons. bioRxiv (2023). doi:10.1101/2023.06.26.546581. 
  5. Ziff, O.J. et al. Integrated transcriptome landscape of ALS identifies genome instability linked to TDP-43 pathology. Nat Commun 14, 2176 (2023). doi:10.1038/s41467-023-37630-6. 
  6. Workman, M.J. et al. Large-scale differentiation of iPSC-derived motor neurons from ALS and control subjects. Neuron (2023). doi:10.1016/j.neuron.2023.01.010. 
  7. Megat, S. et al. Integrative genetic analysis illuminates ALS heritability and identifies risk genes. Nat. Commun. 14, 342 (2023). doi:10.1038/s41467-022-35724-1. 
  8. Adey, B.N. et al. Large-scale analyses of CAV1 and CAV2 suggest their expression is higher in post-mortem ALS brain tissue and affects survival. Front. Cell. Neurosci. 17, 1112405 (2023). doi:10.3389/fncel.2023.1112405. 
  9. Chen, Z.S. et al. Mutant GGGGCC RNA prevents YY1 from binding to Fuzzy promoter… Nature Communications 14, 8420 (2023). doi:10.1038/s41467-023-44215-w.

 

2022

  1. Çelik, M.H. et al. Aberrant splicing prediction across human tissues. bioRxiv 2022.06.13.495326 (2022). doi:10.1101/2022.06.13.495326. 
  2. Baxi, E.G. et al. Answer ALS, a large-scale resource for sporadic and familial ALS combining clinical and multi-omics data from induced pluripotent cell lines. Nat Neurosci 1–12 (2022). doi:10.1038/s41593-021-01006-0. 
  3. Fels, J.A. et al. Gene expression profiles in sporadic ALS fibroblasts define disease subtypes and the metabolic effects of the investigational drug EH301. Hum Mol Genet 31, 3458–3477 (2022). doi:10.1093/hmg/ddac072. 
  4. Ma, X.R. et al. TDP-43 represses cryptic exon inclusion in the FTD–ALS gene UNC13A. Nature 603, 124–130 (2022). doi:10.1038/s41586-022-04424-7. 
  5. Zhang, S. et al. Genome-wide identification of the genetic basis of amyotrophic lateral sclerosis. Neuron (2022). doi:10.1016/j.neuron.2021.12.019. 
  6. Pun, F.W. et al. Identification of Therapeutic Targets for Amyotrophic Lateral Sclerosis Using PandaOmics – An AI-Enabled Biological Target Discovery Platform. Front Aging Neurosci 14, 914017 (2022). doi:10.3389/fnagi.2022.914017. 
  7. Ramamoorthy, D. et al. Identifying patterns in amyotrophic lateral sclerosis progression from sparse longitudinal data. Nat Comput Sci 1–12 (2022). doi:10.1038/s43588-022-00299-w. 
  8. Versluys, L. et al. Expanding the TDP-43 Proteinopathy Pathway From Neurons to Muscle: Physiological and Pathophysiological Functions. Front Neurosci. (2022). doi:10.3389/fnins.2022.815765. 
  9. Logan, R. et al. Novel Genetic Signatures Associated With Sporadic Amyotrophic Lateral Sclerosis. Front. Genet. 13, 851496 (2022). doi:10.3389/fgene.2022.851496. 

 

2021

  1. Gilley, J. et al. Enrichment of SARM1 alleles encoding variants with constitutively hyperactive NADase in patients with ALS and other motor nerve disorders. Medrxiv 2021.06.17.21258268 (2021). doi:10.1101/2021.06.17.21258268. 
  2. Consortium, T.N. et al. An integrated multi-omic analysis of iPSC-derived motor neurons from C9ORF72 ALS patients. Iscience 24, 103221 (2021). doi:10.1016/j.isci.2021.103221. 
  3. Coyne, A.N. et al. Nuclear accumulation of CHMP7 initiates nuclear pore complex injury and subsequent TDP-43 dysfunction in sporadic and familial ALS. Sci Transl Med 13, eabe1923 (2021). doi:10.1126/scitranslmed.abe1923. 
  4. Coyne, A. & Rothstein, J.* The ESCRT-III protein VPS4, but not CHMP4B or CHMP2B, is pathologically increased in familial and sporadic ALS neuronal nuclei. Acta Neuropathologica Commun 9, 127 (2021). doi:10.1186/s40478-021-01228-0. 
  5. Coyne, A.N. & Rothstein, J.D.* Nuclear lamina invaginations are not a pathological feature of C9orf72 ALS/FTD. Acta Neuropathologica Commun 9, 45 (2021). doi:10.1186/s40478-021-01150-5. 

 

2020

  1. Ramesh, N. et al. RNA dependent suppression of C9orf72 ALS/FTD associated neurodegeneration by Matrin-3. Acta Neuropathologica Communications 8, 177 (2020). doi:10.1186/s40478-020-01060-y.

 

2019

  1. Agurto, C. et al. Analyzing progression of motor and speech impairment in ALS. 2019 41st Annu Int Conf IEEE Eng Medicine Biology Soc (EMBC) 00, 6097–6102 (2019). doi:NA. 

 

2018

    1. Nicolas, A. et al. Genome-wide Analyses Identify KIF5A as a Novel ALS Gene. Neuron 97, 1268–1283.e6 (2018). doi:10.1016/j.neuron.2018.02.027.