FUS Mislocalization Rewires a Cortical Gene Network to Drive 2 Cognitive and Behavioral Impairment in ALS
Posted on: 14 July 2025 , updated on: 11 November 2025
Preprint posted on 14 July 2025
Roughly 50% of individuals with ALS show behavioral and cognitive decline, but it is not known why; this study evaluates a biochemical mechanism underlying these impairments in ALS.
Selected by Taylor Stolberg
Categories: animal behavior and cognition, biochemistry, genetics, molecular biology, neuroscience, pathology
Background
Amyotrophic lateral sclerosis (ALS) is a deadly neurodegenerative disease characterized by progressive muscle atrophy and paralysis. Several mutations, including accumulation of RNA binding proteins within motor neurons, are associated with ALS onset. About 50% of all individuals with ALS develop behavioral or cognitive impairments, including executive function impairments and frontotemporal dementia (FTD). However, the exact mechanisms by which these cognitive and behavioral impairments arise in some but not other individuals, is not known. The researchers in this study used mice behavioral and sequencing experiments to characterize how mislocalization of specific proteins lead to the onset of ALS cognitive impairments.
Findings
1: Mislocalization of the Fus protein alone drives cognitive symptoms of ALS
One protein associated with ALS dementia and executive function problems is the Fus protein, an RNA binding protein important for gene expression. To determine how neurons are affected by Fus activity, the authors created a genetic mouse model with the mouse Fus (Fus) protein accumulated in the cytoplasm of a class of neurons responsible for executive function, known as cortical projection neurons (CPNs). Gene sequencing data revealed that the FUS gene expression was notably lower in CPNs in both genetic mice and ALS patients with cognitive impairments. However, the human Fus mislocalization was absent in ALS patients without cognitive impairments. This indicated that the presence of Fus in the cytoplasm was required to cause cognitive impairments.
2: Fus mislocalization is a genetic risk factor for cognitive and behavioral impairments in ALS
Figure:
Figure 4 (adapted from source and made available under a CC-BY-NC-ND 4.0 International license): 4d: Social interest with new mice in an open chamber; over the course of three times trials, isolated Fus transgenic mice exhibited less interest in social interaction. 4e-f: Social memory and recognition activity of meeting previous mice was impaired in Fus mice. 4g-h: The time to react with other mice and total number of interactions among wild-type (WT) and Fus mice; generally, Fus mice spent less time contacting with new (“intruder”) mice in an open chamber than WT mice. 4i-j: Short and long term memory did not vary much between WT and Fus mice in foreign object recognition tests.
To understand the cognitive and behavioral impacts of Fus mislocalization, the authors ran behavioral tasks of social and learning behavior. Behavioral tests revealed that these genetic mice had deficits in nesting behaviors and reduced social interactions. For example, Fus (ALS) mice spent notably less time interacting with stranger mice in an open chamber compared to WT mice. This suggests these mice exhibit deficits in social behavior as a result of the Fus mutation. Interestingly, there was not much of a difference among short and long-term memory among these mice.
3: Downregulation of the gene FBXO16 is a risk factor for ALS behavioral impairments in humans.
The same sequencing data in humans also revealed that this human FUS gene caused a decrease in expression of related genes, known as the FUS regulon. Within this gene network, variants of a gene known as FBXO16 was correlated with ALS behavioral impairments. These results indicate that carriers of these variants are more likely to develop behavioral ALS impairments,
What I like about this work + relevance:
This preprint makes a direct link between a component of ALS pathology and cognitive impairments. I was excited to learn how the authors utilized both behavioral and immunostaining/sequencing techniques to exemplify that behavioral and cognitive impairments are caused by a specific genetic mutation in ALS. Additionally, the mouse model recapitulated the human ALS without additional, unrelated motor degenerative symptoms, a common problem with genetic knock-in mouse models. Comparing the behavioral deficit data with the genetic sequencing may suggest promise for using Fus as a potential therapeutic target for treating ALS-FTD in humans. Additionally, using the behavioral studies to understand how this mutation causes behavioral or cognitive impairments yields insight into which specific neurons are affected, providing insight into which neurons might be more vulnerable to degeneration. Secondly, these results provide relevance for pathogenesis of other rare neurodegenerative diseases. Several genetic motor diseases, such as Huntington’s, Spinocerebellar ataxias (SCAs), and familiar cases of Parkinson’s are driven by protein dysfunction, but the exact mechanism by which these proteins mutate and induce neuronal deterioration are less understood. Elucidating how mislocalization of proteins within motor neurons in ALS may yield context into how related neurodegenerative diseases induce pathogenesis.
Future directions:
This study confirms that a specific mutation within adult neurons specifically drives pathogenesis of social and cognitive behaviors. I would be interested to see the authors test what specifically controls the FUS gene network. More specifically, I would like to know if other RNA binding proteins also interact with the FUS gene, and how their expression is up/downregulated as a result of Fus mislocalization. If there are other binding proteins that are silenced as a result of the Fus mislocalization, then this could yield insight into how Fus moves to other regions of the cell (specifically the cytoplasm). Secondly, I would like to learn when this mislocalization occurs within the neuron; if there is a critical timing for when this migration of the Fus protein occurs, inhibiting further progression could be used to therapeutically reverse the behavioral and cognitive progression.
Questions for the authors:
- Did these Fus genetic mice have any anxiety phenotypes in the social tests?
- How long does it take for mice to present symptoms after mislocalization of the Fus protein occurs? And is there a critical period by which Fus can be reversed?
- If memory recognition is not shown to be greatly different but social interactions arone, how could these behavioral changes be used as biomarkers in the human population for ALS, is this already tested?
- What are the therapeutic applications for Fus mislocalization?
- Are there gene variants that lead to increased risk factors for cognitive impairments?
Reference:
Cassel, R., Lorenc, F., Bombardier, A., De Tapia, C., Dieterle, S., Gouveia-Roque, C., … & Megat, S. (2025). FUS Mislocalization Rewires a Cortical Gene Network to Drive Cognitive and Behavioral Impairment in ALS. medRxiv, 2025-06.
doi: https://doi.org/10.1242/prelights.41065
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October in preprints – DevBio & Stem cell biology
Each month, preLighters with expertise across developmental and stem cell biology nominate a few recent developmental and stem cell biology (and related) preprints they’re excited about and explain in a single paragraph why. Short, snappy picks from working scientists — a quick way to spot fresh ideas, bold methods and papers worth reading in full. These preprints can all be found in the October preprint list published on the Node.
| List by | Deevitha Balasubramanian et al. |
October in preprints – Cell biology edition
Different preLighters, with expertise across cell biology, have worked together to create this preprint reading list for researchers with an interest in cell biology. This month, most picks fall under (1) Cell organelles and organisation, followed by (2) Mechanosignaling and mechanotransduction, (3) Cell cycle and division and (4) Cell migration
| List by | Matthew Davies et al. |
July in preprints – the CellBio edition
A group of preLighters, with expertise in different areas of cell biology, have worked together to create this preprint reading lists for researchers with an interest in cell biology. This month, categories include: (1) Cell Signalling and Mechanosensing (2) Cell Cycle and Division (3) Cell Migration and Cytoskeleton (4) Cancer Biology (5) Cell Organelles and Organisation
| List by | Girish Kale et al. |
May in preprints – the CellBio edition
A group of preLighters, with expertise in different areas of cell biology, have worked together to create this preprint reading lists for researchers with an interest in cell biology. This month, categories include: 1) Biochemistry/metabolism 2) Cancer cell Biology 3) Cell adhesion, migration and cytoskeleton 4) Cell organelles and organisation 5) Cell signalling and 6) Genetics
| List by | Barbora Knotkova et al. |
April in preprints – the CellBio edition
A group of preLighters, with expertise in different areas of cell biology, have worked together to create this preprint reading lists for researchers with an interest in cell biology. This month, categories include: 1) biochemistry/metabolism 2) cell cycle and division 3) cell organelles and organisation 4) cell signalling and mechanosensing 5) (epi)genetics
| List by | Vibha SINGH et al. |
Biologists @ 100 conference preList
This preList aims to capture all preprints being discussed at the Biologists @100 conference in Liverpool, UK, either as part of the poster sessions or the (flash/short/full-length) talks.
| List by | Reinier Prosee, Jonathan Townson |
2024 Hypothalamus GRC
This 2024 Hypothalamus GRC (Gordon Research Conference) preList offers an overview of cutting-edge research focused on the hypothalamus, a critical brain region involved in regulating homeostasis, behavior, and neuroendocrine functions. The studies included cover a range of topics, including neural circuits, molecular mechanisms, and the role of the hypothalamus in health and disease. This collection highlights some of the latest advances in understanding hypothalamic function, with potential implications for treating disorders such as obesity, stress, and metabolic diseases.
| List by | Nathalie Krauth |
‘In preprints’ from Development 2022-2023
A list of the preprints featured in Development's 'In preprints' articles between 2022-2023
| List by | Alex Eve, Katherine Brown |
CSHL 87th Symposium: Stem Cells
Preprints mentioned by speakers at the #CSHLsymp23
| List by | Alex Eve |
Journal of Cell Science meeting ‘Imaging Cell Dynamics’
This preList highlights the preprints discussed at the JCS meeting 'Imaging Cell Dynamics'. The meeting was held from 14 - 17 May 2023 in Lisbon, Portugal and was organised by Erika Holzbaur, Jennifer Lippincott-Schwartz, Rob Parton and Michael Way.
| List by | Helen Zenner |
FENS 2020
A collection of preprints presented during the virtual meeting of the Federation of European Neuroscience Societies (FENS) in 2020
| List by | Ana Dorrego-Rivas |
ASCB EMBO Annual Meeting 2019
A collection of preprints presented at the 2019 ASCB EMBO Meeting in Washington, DC (December 7-11)
| List by | Madhuja Samaddar et al. |
SDB 78th Annual Meeting 2019
A curation of the preprints presented at the SDB meeting in Boston, July 26-30 2019. The preList will be updated throughout the duration of the meeting.
| List by | Alex Eve |
Autophagy
Preprints on autophagy and lysosomal degradation and its role in neurodegeneration and disease. Includes molecular mechanisms, upstream signalling and regulation as well as studies on pharmaceutical interventions to upregulate the process.
| List by | Sandra Malmgren Hill |
Young Embryologist Network Conference 2019
Preprints presented at the Young Embryologist Network 2019 conference, 13 May, The Francis Crick Institute, London
| List by | Alex Eve |
Also in the pathology category:
October in preprints – DevBio & Stem cell biology
Each month, preLighters with expertise across developmental and stem cell biology nominate a few recent developmental and stem cell biology (and related) preprints they’re excited about and explain in a single paragraph why. Short, snappy picks from working scientists — a quick way to spot fresh ideas, bold methods and papers worth reading in full. These preprints can all be found in the October preprint list published on the Node.
| List by | Deevitha Balasubramanian et al. |
October in preprints – Cell biology edition
Different preLighters, with expertise across cell biology, have worked together to create this preprint reading list for researchers with an interest in cell biology. This month, most picks fall under (1) Cell organelles and organisation, followed by (2) Mechanosignaling and mechanotransduction, (3) Cell cycle and division and (4) Cell migration
| List by | Matthew Davies et al. |
Fibroblasts
The advances in fibroblast biology preList explores the recent discoveries and preprints of the fibroblast world. Get ready to immerse yourself with this list created for fibroblasts aficionados and lovers, and beyond. Here, my goal is to include preprints of fibroblast biology, heterogeneity, fate, extracellular matrix, behavior, topography, single-cell atlases, spatial transcriptomics, and their matrix!
| List by | Osvaldo Contreras |
ECFG15 – Fungal biology
Preprints presented at 15th European Conference on Fungal Genetics 17-20 February 2020 Rome
| List by | Hiral Shah |
COVID-19 / SARS-CoV-2 preprints
List of important preprints dealing with the ongoing coronavirus outbreak. See http://covidpreprints.com for additional resources and timeline, and https://connect.biorxiv.org/relate/content/181 for full list of bioRxiv and medRxiv preprints on this topic
| List by | Dey Lab, Zhang-He Goh |
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Cellular metabolism
A curated list of preprints related to cellular metabolism at Biorxiv by Pablo Ranea Robles from the Prelights community. Special interest on lipid metabolism, peroxisomes and mitochondria.
| List by | Pablo Ranea Robles |