Announcing the 2026 Recipients of the Basic Biology Consortia Grant
June 17, 2026 Michael DeChellis-Marks
Target ALS is proud to announce the 2026 awardees of our Basic Biology Consortia program, which supports research to understand the fundamental biology of ALS. Through this program, we seek to accelerate the discovery of novel therapeutic targets and biomarkers by advancing our understanding of the biological mechanisms that drive disease. For the 2026 funding cycle, Target ALS received 122 applications from 366 scientists representing 196 institutions across 26 countries. Following a competitive review process, six consortia were awarded funding.
This year’s program specifically sought proposals to understand the biology of both genetic and sporadic forms of ALS, with the goal of identifying the next generation of therapeutic targets. Target ALS called for multidisciplinary teams employing novel approaches, including convergent multi-omic technologies and applications of artificial intelligence and machine learning.
Key Objectives of the Basic Biology Consortia Program:
The Target ALS Basic Biology Consortia Program aims to:
- Gain a deeper understanding of the biology of the sporadic form of ALS.
- Foster collaborative research that brings together scientists with complementary expertise.
- Encourage the application of new technologies, including AI/ML, to understanding the biology of ALS.
- Engage scientists from outside the ALS research community to participate in collaborative consortia.
2026 Basic Biology Consortia Grantees
- TDP-43 N-terminus driven oligomerization in ALS-TDP subtypes: distinct but converging mechanisms?
- Tatyana Shelkovnikova (University of Sheffield), Antonio Calabrese (University of Leeds), Gareth Write (University of Essex), and Vera Wiersma (University of Amsterdam)
- TDP-43 protein malfunction is a hallmark of 97% of ALS cases, where it moves from its normal location in the nucleus of cells and forms abnormal clumps in the cytoplasm. This consortium is studying how a region of TDP-43, called the N-terminal domain, contributes to abnormal function in ALS. In C9orf72-linked ALS, the most common genetic form of the disease, toxic dipeptide repeat (DPR) polypeptides bind to TDP-43 and disrupt its normal function and causing toxicity. The researchers will study how and when this breakdown begins across genetic and sporadic ALS, using cell models and postmortem tissue. By understanding how these interactions contribute to disease, the project could identify new drugs and antibody-like therapies that restore normal TDP-43 function.
- An AI-driven Multi-omics Platform integrating lipidomics, immune profiling, and inflammatory miRNA signatures to identify actionable therapeutic Targets in ALS (IMPACT-ALS)
- Jessica Mandrioli (Universita’ degli studi di Modena e Reggio Emilia), Laura Brunelli (Istituo di Ricerche Farmacologiche “Mario Negri” IRCCS), Amedeo Amedei (University of Florence), and Luca Marchetti (University of Trento)
- The IMPACT-ALS project seeks to better understand ALS heterogeneity by studying the disease from a new, integrated biological perspective. By combining lipidomics, immunophenotyping, and microRNA profiling, with advanced artificial intelligence and machine learning tools, researchers seek to identify distinct biological subtypes of ALS and uncover the pathways that drive disease progression. These insights could reveal new therapeutic targets and help advance more precise, personalized treatment strategies for people living with ALS.
- Nucleoporin coding variants (NupV) as sporadic ALS disease initiators: Altered nuclear pore structure, function, downstream TDP-43 dysfunction and neurodegeneration
- Jeffrey Rothstein (Johns Hopkins University), Julia Kaye (Gladstone Institute), Andre Hoelz (California Institute of Technology), and Juro Gottweis (Google)
- Mutations in nucleoporins, genes that encode pores that allow molecules to pass through the nuclei of cells, are thought to contribute to TDP-43 mislocalization and to the development of sporadic ALS. Researchers will examine how these protein-coding variants affect transport between the nucleus and cytoplasm and lead to nuclear TDP-43 loss, cytoplasmic TDP-43 aggregation, and loss of function. The potential findings of this project would provide new evidence that nuclear pore dysfunction is a disease-initiative mechanism in sporadic ALS, driving TDP-43 mislocalization, thereby spurring new therapeutic approaches and supporting expanded genetic testing in ALS clinics.
- Lipid Metabolic Vulnerabilities in ALS as a Pathway Toward New Therapeutic Strategies
- Jiou Wang (Johns Hopkins University), Ling Hao (University of Maryland), and Norman Haughey (Tulane University)
- ALS is characterized by the progressive loss of motor neurons, yet the biological changes that contribute to this degeneration remain incompletely understood, especially in the more common sporadic form of the disease. Emerging evidence suggests that disruptions of lipid (fat) regulation in motor neurons play a critical role in ALS. Researchers have identified a direct link between lipid regulation and protein quality control, a process known to be disrupted in ALS. The consortia will determine whether the disruption of lipid metabolism is a shared biological feature between inherited and sporadic forms of ALS, and develop measurable lipid biomarkers to track treatment response, potentially opening new pathways for ALS treatment.
- Characterizing the TDP-43 pathology-driven peripheral immune response and its CNS infiltration in ALS
- Pietro Fratta (University College London), Leonard Petrucelli (University of Miami), Jenny Jiang (University of Pennsylvania), and Sarosh Irani (Mayo Clinic)
- Emerging research is shifting how scientists view the immune system in ALS; it may play an active role in neurodegeneration. This team will study how cryptic peptides, produced as a result of TDP-43 dysfunction, are recognized by T cells in the peripheral and central nervous systems and elicit an immune response. By characterizing the immune system response to mis-spliced RNAs and their peptides, the project could uncover new disease mechanisms, identify novel biomarkers, and inform the development of more targeted therapies for ALS.
- Microglial Autophagy and Proteostasis Mechanisms Driving TDP-43 Pathology in ALS
- Panos Roussos (Mount Sinai), Steve Finkbeiner (University of California at San Francisco), Guo-Cheng Yuan (Mount Sinai), Zhenyu Yue (Mount Sinai)
- While ALS is a disease of motor neurons, new findings suggest that other cells in the brain and spinal cord play active roles in motor neuron degeneration. For example, cells called microglia, which normally help protect and maintain the brain and spinal cord, may become dysfunctional in ALS. These researchers will study how TDP-43 dysfunction in sporadic and C9orf72-associated ALS affects communication between microglia and motor neurons and contributes to disease progression. By mapping these interactions in human tissue and stem cell models, the team aims to identify biological pathways that could serve as targets for future treatments.
About Our Review Process
At Target ALS, we hold fairness and transparency paramount in our review process. The Target ALS Independent Review Committee (IRC) makes all research funding decisions without involvement from the organization’s staff or leadership, ensuring every application receives a fair evaluation. The IRC is comprised of experts across scientific disciplines from both industry and academia, reflecting the evolving nature of ALS research. To avoid any possible conflicts of interest, no member of the IRC can apply for or receive Target ALS funding for their own work. Members on the IRC abide by a comprehensive conflict of interest policy and are all under confidentiality agreements.
Our Vision and Commitment
At Target ALS, our vision is to realize a world where everyone lives. We are driven by a sense of urgency, knowing that every day counts for people diagnosed with ALS. Currently, there are no treatments on the market that promise to make sporadic ALS a manageable disease. We are committed to funding cutting-edge research and fostering collaborations that will bring us closer to effective treatments for all forms of ALS.
Together, we continue to strive for a future where ALS is no longer a life-threatening diagnosis. Thank you to all the applicants for their dedication and hard work. For more detailed information about our grants and the application process, please visit our Basic Biology Consortia Page.
