Astrocytes, the star-shaped glial cells that provide structural and metabolic support to neurons, have been the subject of intense investigation due to their critical influence on synaptic function and neuroinflammation. This study meticulously delineates the morphological, molecular, and functional aberrations in cerebellar astrocytes detected in depressive phenotypes, potentially redefining the cellular targets in depression pathology. Employing state-of-the-art imaging and transcriptomic analysis, the research team led by Hercher et al. reports distinctive astrocytic remodeling that correlates strongly with depressive symptomatology.

The cerebellum, often underestimated in mood disorders research, houses a rich population of astrocytes which modulate neurotransmitter dynamics, maintain ion homeostasis, and regulate the blood-brain barrier integrity. Altered astrocytic function could therefore drastically impact neuronal circuit stability and information processing within this brain territory. The study’s findings revealed significant reductions in astrocytic density and complexity in key cerebellar subregions, indicating an impaired glial microenvironment that might contribute to the aberrant neural coding associated with depression.

One of the most compelling aspects of the study is the demonstration of disrupted astrocyte-neuron communication. Astrocytes engage in bidirectional signaling with neurons, shaping synaptic plasticity and transmission efficacy. Researchers identified downregulation of crucial astrocytic glutamate transporters, which are imperative for preventing excitotoxic neuronal damage and maintaining optimal excitatory neurotransmission balance. This dysregulation may underpin excessive or imbalanced glutamatergic signaling pathways often implicated in depressive disorders.

Moreover, neuroinflammatory processes, which astrocytes orchestrate through cytokine release and immune modulation, appear to be aberrantly activated in the depressive cerebellum. The study documents elevated markers of astrocytic reactivity, suggestive of a chronic, low-grade inflammatory state that could exacerbate neuronal vulnerability and hinder synaptic repair mechanisms. This aligns with broader hypotheses positioning neuroinflammation as a pivotal component in the etiology of depression, implicating astroglial cells as both initiators and perpetuators of pathological states.

Another important innovation of the study was the use of single-cell RNA sequencing to characterize heterogeneity among cerebellar astrocyte populations in depression. The results unveiled distinct subtypes exhibiting divergent molecular signatures, some of which are enriched in genes related to oxidative stress responses, cell cycle regulation, and metabolic pathways. Such heterogeneity may reflect compartmentalized functions of astrocytes within cerebellar circuits, indicating that targeted interventions need to consider this cellular diversity to achieve therapeutic efficacy.

The research also explores how stress-induced depression models in rodents parallel human pathological findings, reinforcing the translational relevance of cerebellar astrocytic changes. Chronic stress paradigms resulted in astrocytic atrophy and diminished synaptic support capacity analogous to observations in postmortem human cerebellar samples from depressive patients. This consistency across species underlines the importance of astroglial health in maintaining mood stability and resilience to environmental stressors.

Importantly, the authors discuss how these astrocytic alterations may perturb cerebellar outputs to limbic and prefrontal networks, which are heavily implicated in mood regulation. Dysfunctional cerebellar connectivity could contribute to maladaptive emotional processing and cognitive impairments observed in depressive disorders, linking glial biology directly with higher-order neurocognitive symptoms. This paradigm shift invites a reevaluation of cerebellar involvement in psychiatric illnesses beyond its classical motor domain.

Therapeutically, these findings open exciting avenues for novel interventions targeting astrocyte function. Existing antidepressant strategies primarily focus on monoaminergic systems; however, modulating astroglial health and neuroinflammation represents a promising complementary approach. Pharmacologic agents aimed at restoring astrocyte glutamate uptake, reducing oxidative stress, or normalizing cytokine profiles may help to reestablish cerebellar homeostasis and alleviate depressive symptoms.

Furthermore, the study emphasizes the potential utility of astrocyte-derived biomarkers for early diagnosis and treatment monitoring. Altered expression patterns of astrocytic genes or proteins detectable in cerebrospinal fluid or peripheral circulation could provide objective measures of disease progression or treatment response, addressing long-standing challenges in psychiatric practice. These biomarkers could herald a new era of precision medicine focused on glial-neuronal interplay.

The intricate relationship between astrocytes and neurovascular coupling is also highlighted, illustrating how cerebellar blood flow regulation is disrupted in depression. Since astrocytes are central to maintaining cerebral microcirculation, their dysfunction may contribute to neurovascular impairments, further linking vascular health and mood disorders. This multifactorial perspective underscores the complexity of depressive pathology, necessitating holistic research approaches.

While this study primarily concentrates on cerebellar astrocytes, it prompts broader questions regarding glial involvement throughout the central nervous system. The orchestration of neural networks by glial cells, encompassing oligodendrocytes, microglia, and astrocytes, represents a rich terrain for future exploration. Understanding how these cells coordinate to maintain neuropsychiatric health promises to revolutionize diagnostic and therapeutic frameworks.

The use of cutting-edge methodologies, from high-resolution microscopy to transcriptomics and in vivo modeling, sets a new standard for neuroscience research into mood disorders. Hercher et al. have demonstrated the essential role of advanced technological integration in unraveling the cellular intricacies underpinning depression, bridging molecular biology with behavioral neuroscience.

In conclusion, this seminal research recasts the cerebellum not merely as a motor coordinator but as a crucial hub in depression neuropathology via astrocytic dynamics. It challenges entrenched paradigms, elevates the importance of glial cells, and paves the way for pioneering interventions. As the scientific community continues to decipher the neurobiology of depression, incorporating astrocytic functions in cerebellar contexts will be indispensable for comprehensive understanding and more effective treatments.

The implications extend beyond depression, hinting at potential astrocyte-centered mechanisms in other neuropsychiatric conditions involving cerebellar circuits, such as bipolar disorder, anxiety, and schizophrenia. This discovery places astrocytes prominently on the map of brain research, heralding a paradigm shift toward glia-inspired neuroscience.

Hercher et al.’s work embodies a paradigm of translational psychiatry, demonstrating how dissecting cellular and molecular substrates within nontraditional brain structures informs clinical practice and drug development. The future of depression research lies in expanding this integrative framework to include multifaceted brain regions and their cellular constituents, promising hope for millions suffering worldwide.

Subject of Research: Cerebellar astrocytic alterations in depression

Article Title: Cerebellar astrocytic alterations in depression

Article References:
Hercher, C., Abajian, G., Davoli, M.A. et al. Cerebellar astrocytic alterations in depression. Transl Psychiatry (2026). https://doi.org/10.1038/s41398-026-03866-1

Image Credits: AI Generated

DOI: https://doi.org/10.1038/s41398-026-03866-1

The multifaceted immune response following ischemic brain injury involves a rapid mobilization of various immune subsets including T cells, monocytes, and neutrophils. Neutrophils, often considered first responders to tissue injury, can exacerbate neuronal damage through excessive production of reactive oxygen species (ROS). The study’s rigorous profiling demonstrated that Hspa8 expression surged specifically in neutrophils during the acute phase, suggesting a targeted immunomodulatory function. Intriguingly, Hspa8’s influence extended beyond mere expression levels—it modulated neutrophil behavior and ROS generation, processes integral to secondary injury amplification.

Employing gene silencing techniques both in vitro and in vivo, the researchers elegantly demonstrated that downregulation of Hspa8 markedly attenuated neutrophil accumulation within the ischemic brain. This decrease in neutrophil infiltration correlated closely with diminished ROS levels, mitigating the oxidative damage that traditionally exacerbates ischemic injury. The neurological deficits commonly observed post-stroke were substantially reduced in animal models with Hspa8 knockdown, underscoring the protein’s potential as a neuroprotective target.

The authors leveraged a comprehensive protein-protein interaction (PPI) network analysis to elucidate the mechanistic underpinnings of Hspa8’s role in immune regulation. The interaction map revealed that Hspa8 occupies a strategic node interfacing with key immune signaling molecules, facilitating crosstalk between disparate immune cell populations. This positioning affirms Hspa8 as a central modulator of inflammatory cascades rather than a passive bystander, cementing its relevance in the pathophysiology of ischemic brain injury.

Beyond the immediate implications for stroke pathology, these findings expand our understanding of heat shock proteins in neuroinflammation. While the chaperone functions of Hspa8 in protein folding and cellular homeostasis are well-documented, its immunomodulatory capacity in the context of brain ischemia uncovers a novel facet of the protein’s biology. This dual functionality positions Hspa8 as a compelling molecular target, offering dual benefits of proteostasis maintenance and immune response tempering.

The study’s integration of single-cell RNA sequencing provided unprecedented resolution in characterizing the immune landscape after ischemia. This approach uncovered heterogeneous immune cell subpopulations exhibiting distinct transcriptional profiles influenced by Hspa8 activity. Notably, the shift in neutrophil phenotypes toward a less pro-inflammatory state upon Hspa8 suppression highlights potential pathways for therapeutic intervention. Modulating such granular immune responses could pave the way for tailored immunotherapies that prevent collateral damage while preserving essential immune defense.

In parallel, the research underscored the value of bulk RNA sequencing and flow cytometry as complementary modalities, affirming changes at both the cellular and population levels. The convergence of these data sets fortifies the conclusion that Hspa8 is a linchpin in the neuroimmune dialogue following ischemic injury, mediating both cell recruitment and functional states within the inflammatory milieu. This multidimensional insight bridges molecular mechanisms with observable physiological outcomes.

A particularly compelling aspect of the research involved detailed assessments of reactive oxygen species production. Excess ROS generation is a notorious driver of oxidative stress and subsequent neuronal apoptosis in ischemia-reperfusion injury. By demonstrating that Hspa8 silencing curtails ROS output, the authors highlight a mechanistic nexus where protein chaperones intersect with oxidative stress pathways. Targeting this interface may yield novel antioxidant strategies specifically tailored to the ischemic brain’s unique environment.

Furthermore, the translational relevance of these findings is notable. The reduction in neurological impairments observed in rodent models post-Hspa8 silencing points to the protein as not just a biomarker but an actionable target in clinical therapeutics. Given the limited efficacy of current interventions for ischemic stroke, innovative approaches that modulate immune responses carry substantial promise. Manipulating Hspa8 activity could complement reperfusion strategies, potentially improving long-term recovery and reducing stroke-related disabilities.

The study also raises intriguing questions about the temporal dynamics of immune modulation in brain injury. Since immune responses evolve rapidly post-ischemia, pinpointing optimal windows for Hspa8-targeted interventions could maximize therapeutic benefit while minimizing risks. Future investigations probing temporal expression patterns and downstream effects may further refine clinical applicability, offering personalized treatment regimens based on immune profiling.

Complementing molecular and immunological insights, the work provides a framework for integrating multi-omic data in neuroinflammation research. This holistic methodology enhances mechanistic clarity and identifies convergence points amenable to drug development. As the field evolves toward precision medicine, studies such as this exemplify how detailed immune profiling informs rational therapeutic design, fostering new avenues for combating complex neurological disorders.

Importantly, this research also underscores the complexity of immune responses in the ischemic brain, challenging oversimplified paradigms that categorize immune cells merely as “damaging” or “protective.” Hspa8 emerges as a nuanced regulator capable of fine-tuning immune cell function to balance injury and repair. Harnessing such molecular regulators opens new horizons in neuroimmunology, promising interventions that support the brain’s intrinsic capacity for recovery.

In conclusion, the work by Wu and colleagues marks a significant advance in our understanding of the immune mechanisms driving ischemic brain injury. By unveiling Hspa8’s central role in modulating neutrophil-driven inflammation and oxidative damage, this study positions the heat shock protein as a potent therapeutic target. These insights hold the potential to revolutionize stroke management through targeted immunomodulation, ultimately improving neurological outcomes and quality of life for millions affected worldwide.

The identification of Hspa8 as a critical mediator encourages further exploration into heat shock proteins within various neurodegenerative and neuroinflammatory conditions. The broader applicability of these findings may extend to disorders characterized by aberrant immune activation and oxidative stress, positioning Hspa8-targeting approaches at the forefront of next-generation neurotherapeutics. As research progresses, harnessing molecular chaperones to recalibrate immune environments represents a promising frontier in brain injury treatment.

This study exemplifies the power of interdisciplinary approaches combining genomics, immunology, and neurobiology, fostering innovation at the intersection of these fields. By illuminating novel pathways and therapeutic targets, it inspires future research aimed at decoding the complex dialogue between the immune system and the injured brain. Such endeavors are vital for the development of effective therapies to combat the devastating impact of ischemic strokes and related neurological insults.

Subject of Research: The modulation of immune responses by heat shock protein A8 (Hspa8) and its impact on ischemic brain injury.

Article Title: Hspa8 modulation of immune responses mitigates ischemic brain injury.

Article References:
Wu, X., Wu, Z., Yan, H. et al. Hspa8 modulation of immune responses mitigates ischemic brain injury. Genes Immun (2025). https://doi.org/10.1038/s41435-025-00359-x

Image Credits: AI Generated

DOI: https://doi.org/10.1038/s41435-025-00359-x

Fear extinction—the gradual reduction of a conditioned fear response—is vital for adaptive behavior and mental health. Deficits in this process are implicated in conditions such as PTSD, anxiety disorders, and phobias. While prior studies have identified broad neural circuits involved in fear extinction, the biological factors influencing individual variability remain poorly understood. The study by Ten-Blanco and colleagues addresses this gap by exploring how endocrine, microbial, and genetic factors converge to influence extinction capacity differently across sexes.

Central to their investigation is the hypothalamic-pituitary-adrenal (HPA) axis, a neuroendocrine system that governs stress responses through the release of glucocorticoids like corticosterone in rodents. The authors measured HPA axis activity during fear extinction sessions, revealing that male and female mice exhibit distinct patterns of hormone secretion. These differences corresponded to varying extinction rates, suggesting that the timing and magnitude of corticosterone release modulate how effectively fear memories are diminished.

Beyond hormonal influences, the study harnessed the burgeoning field of microbiome research to examine gut bacterial populations, which have emerged as critical players in brain function via the gut-brain axis. Detailed microbial community profiling revealed sex-specific signatures correlating with fear extinction proficiency. Notably, certain bacterial taxa that produce neuroactive metabolites were more abundant in individuals exhibiting robust extinction, implicating gut microbes as modulators of neural plasticity underlying fear learning.

To deepen the mechanistic understanding, the researchers employed transcriptomic analyses of brain regions implicated in fear processing, such as the amygdala and prefrontal cortex. By sequencing RNA transcripts, they identified gene expression patterns linked to extinction success. Strikingly, gene networks involved in synaptic transmission, neuroinflammation, and stress hormone signaling displayed sex-dependent regulation. This genomic perspective illuminated how males and females mobilize distinct molecular pathways to achieve fear attenuation.

The integrative approach of this study exemplifies modern neuroscience’s shift toward systems biology, where multiple physiological layers are analyzed concurrently to capture the complexity of behavior. By bridging endocrinology, microbiology, and genomics, Ten-Blanco et al. provide a multidimensional map of fear extinction biology. Their findings underscore that any effective therapeutic strategy for anxiety disorders must consider these intertwined factors and sex differences to enhance treatment efficacy.

Moreover, this research highlights the importance of studying both male and female subjects, as most prior fear extinction studies predominantly used male animals, potentially overlooking fundamental sex-specific variables. The documented variations in HPA axis dynamics, microbial composition, and gene expression profiles between sexes contribute to the growing recognition that biological sex profoundly influences brain function and mental health outcomes.

The implications of this work extend into clinical realms. Understanding the mechanisms driving individual differences in fear extinction can inform personalized medicine approaches, including the development of microbiota-targeting interventions or hormone modulation therapies. For example, manipulating gut bacteria through probiotics or diet could offer novel anxiolytic strategies tailored to one’s biological sex and stress hormone profile.

Furthermore, the study opens avenues for biomarker discovery. Molecular signatures uncovered in the transcriptomic data might serve as predictive markers for extinction capacity, which could guide clinicians in identifying patients at risk for chronic fear-related disorders or those likely to respond to cognitive-behavioral therapies that rely on extinction principles.

On a broader scale, the interplay between the HPA axis, gut microbiota, and brain gene expression exemplifies the emerging paradigm of psychoneuroimmunology and neuroendocrinology intersecting with microbial ecology. This holistic view prompts researchers to move beyond reductionist models and appreciate the body’s interconnected systems as dynamic contributors to mental health and disease.

In delineating these biological pathways, the authors also emphasize future directions, suggesting longitudinal studies tracking how these factors evolve across development and in response to environmental challenges. This temporal dimension is crucial as plasticity in stress systems and microbiota composition can profoundly influence lifelong trajectories of emotional regulation.

Technological advances, such as single-cell RNA sequencing and metagenomics, promise to add further granularity by identifying specific cell types involved in fear circuits and pinpointing microbe-host interactions at molecular resolution. Incorporating such methods will refine our understanding of the cellular and microbial actors orchestrating fear extinction.

The interdisciplinary nature of this research spotlights the need for collaborative efforts spanning neuroscience, endocrinology, microbiology, and computational biology. Such synergies will accelerate the translation of basic science findings into clinical applications, ultimately improving outcomes for individuals suffering from debilitating anxiety disorders.

Ten-Blanco et al.’s study stands as a testament to the power of multifaceted inquiry to decode the biological complexity of behavior. By elucidating the sex-specific mechanisms that govern fear extinction through integrated analysis of the HPA axis, gut microbiota, and transcriptomics, they lay a foundation for innovative, personalized treatments that acknowledge individual biological identities.

As anxiety and trauma-related disorders continue to rise globally, insights from this research offer hope for more effective interventions that harness the body’s natural regulatory systems. The convergence of hormonal, microbial, and genetic factors presents a rich tapestry upon which the future of psychiatric neuroscience will be woven, promising breakthroughs that resonate well beyond the laboratory.

Subject of Research: Individual differences in fear extinction mechanisms in male and female mice, focusing on HPA axis function, gut microbiota, and transcriptomic profiles.

Article Title: Exploring individual differences in fear extinction in male and female mice: insights from HPA axis, microbiota, and transcriptomics.

Article References:
Ten-Blanco, M., Ponce-Renilla, M., Pereda-Pérez, I. et al. Exploring individual differences in fear extinction in male and female mice: insights from HPA axis, microbiota, and transcriptomics. Transl Psychiatry 15, 195 (2025). https://doi.org/10.1038/s41398-025-03400-9

Image Credits: AI Generated

DOI: https://doi.org/10.1038/s41398-025-03400-9

The study delves deeply into the epitranscriptomic modifications—chemical alterations on RNA molecules that impact their function without changing the genetic code—that fine-tune gene expression in neurons. Among these, N6-methyladenosine (m6A) methylation has emerged as a critical regulator of RNA metabolism. While m6A has gained recognition for its widespread prevalence in the nervous system, its specific role in motor neurons, the nerve cells responsible for voluntary muscle movements, remained elusive until now. Using state-of-the-art transcriptomic and molecular biology approaches, the researchers charted the m6A “repertoire” in motor neurons, pinpointing how these modifications regulate the stability, translation, and localization of key neuronal transcripts critical for cellular homeostasis.

Motor neurons are uniquely vulnerable cells whose degeneration leads to ALS, a fatal disease characterized by muscle weakness, paralysis, and eventual respiratory failure. Despite decades of research, effective treatments remain elusive due to the disease’s complex pathology. This new research illuminates how the precise balance of m6A methylation and demethylation controls the expression of proteins essential for neuronal survival and function. The authors identified that dysregulation of m6A patterns caused by aberrant activity of the fat mass and obesity-associated protein (FTO), a well-known m6A demethylase, disrupts neuronal homeostasis, contributing to ALS pathogenesis.

To unravel this intricate regulatory network, the team employed cutting-edge single-cell RNA sequencing coupled with m6A-seq techniques, enabling them to map m6A marks across the entire transcriptome of motor neurons derived from both healthy and ALS model mice. This comprehensive profiling unveiled that m6A landscapes are dynamically remodeled in disease states, with notable losses of methyl marks on transcripts involved in synaptic transmission, mitochondrial function, and cytoskeletal integrity. These modifications have profound effects on RNA fate, thereby triggering cascading disruptions in neuronal function and viability.

Crucially, the study explored pharmacological interventions targeting FTO, which actively removes m6A marks and thereby modulates RNA activity. Using selective FTO inhibitors, the researchers demonstrated a remarkable attenuation of ALS-like symptoms in mouse models, including improved motor performance and delayed neurodegeneration. This therapeutic effect is believed to stem from restored m6A homeostasis, which stabilizes vital mRNAs and rescues protein expression patterns that are otherwise perturbed in ALS pathology. These findings underscore the therapeutic potential of modulating RNA modifications to combat neurodegenerative diseases.

Beyond offering hope for ALS patients, the implications of this study resonate broadly within the neuroscience community. The epitranscriptomic regulation by m6A and its controllers such as FTO may represent a universal mechanism for maintaining neuronal health and responding to cellular stress. Given that FTO was originally identified in metabolic disorders, its newly discovered role in neural homeostasis paints a complex picture of cross-talk between metabolism and neurodegeneration, underscoring the need for multidisciplinary research strategies.

Understanding how m6A modifications fine-tune neuronal gene expression involves integrating insights from molecular neuroscience, epigenetics, and RNA biology. The dynamic addition and removal of methyl groups on adenosine bases influence the recruitment of reader proteins, translation machinery, and RNA decay factors, thereby controlling timing and localization of protein synthesis critical for synaptic plasticity and cell survival. By decoding these modifications in motor neurons, the study provides a molecular scaffold to interpret how environmental and genetic factors might disrupt the epitranscriptomic landscape in ALS.

An intriguing facet of the paper is the demonstration that FTO inhibition does not merely suppress disease progression but also promotes neuronal resilience. This was evidenced by enhanced mitochondrial function and reduced markers of neuroinflammation in treated models. Mitochondria, essential for energy production, are notoriously compromised in ALS, linking m6A regulation to cellular energetics. Furthermore, modulation of RNA methylation appears to influence glial cell responses, which are increasingly recognized as active participants in ALS pathophysiology rather than passive bystanders.

The translational potential of these findings reaches beyond preclinical models. Targeted FTO inhibitors present an appealing drug development opportunity, especially as small molecules capable of crossing the blood-brain barrier are in active pipelines. The study also highlights the delicate balance required, as both hypo- and hypermethylation of m6A can be detrimental, emphasizing that precise modulation rather than wholesale suppression of FTO activity will be key in future therapeutic designs.

Notably, the research places motor neuron-specific m6A dynamics front and center, challenging the previous notion that m6A regulation is uniform across neural subtypes. The evidence shows a highly specialized epitranscriptomic signature unique to motor neurons, likely reflecting their distinct functional demands and vulnerability. This specificity advocates for the development of cell-type targeted epitranscriptomic therapies, a frontier area combining neuronal biology with precision medicine.

This deeper understanding of the molecular choreography governing neuronal stability extends to potential biomarker discovery as well. Aberrant m6A profiles in accessible patient-derived samples might serve as early indicators of disease progression or treatment response. Coupled with advanced RNA mapping technologies, such biomarkers could revolutionize diagnostic paradigms in ALS and related neurodegenerative disorders.

Moreover, the intersection of m6A RNA methylation with other cellular stress pathways evokes fundamental questions about the adaptability and failure of neuronal networks. The study posits that m6A acts as a molecular rheostat, calibrating neuronal gene expression in response to physiological and pathological stimuli. Dissecting this calibration mechanism holds promise not only for ALS but for other conditions, including spinal muscular atrophy and frontotemporal dementia, where motor neuron dysfunction is central.

As the field of epitranscriptomics rapidly evolves, this study exemplifies how integrative approaches combining molecular profiling, genetic models, and pharmacological interventions can unlock the complexity of neurodegenerative diseases. The identification of FTO as both a modulator and potential therapeutic target in ALS expands our conceptual toolkit, moving beyond genetic mutations to encompass dynamic RNA regulation as a critical axis of disease biology.

Intriguingly, the work also raises the possibility of leveraging m6A modulation beyond neuroprotection, potentially enhancing neuronal regeneration or plasticity. The reversible nature of RNA methylation renders it an attractive target for interventions aiming to restore lost functions or promote repair mechanisms in injured nervous systems.

In summary, the pioneering research by Yen and colleagues heralds a paradigm shift in neurodegeneration research through elucidation of the motor neuron m6A methylome and its modulation by FTO. By bridging fundamental molecular insights with translational potential, their findings chart a hopeful path toward novel ALS therapies rooted in epitranscriptomic regulation. Continued efforts in this exciting domain promise to unlock further secrets of neuronal resilience and pave the way to overcoming devastating diseases of the nervous system.

Subject of Research: The role of motor neuron m6A RNA methylation and FTO enzyme activity in neuronal homeostasis and ALS symptom mitigation.

Article Title: The motor neuron m6A repertoire governs neuronal homeostasis and FTO inhibition mitigates ALS symptom manifestation.

Article References:
Yen, YP., Lung, TH., Liau, E.S. et al. The motor neuron m6A repertoire governs neuronal homeostasis and FTO inhibition mitigates ALS symptom manifestation. Nat Commun 16, 4063 (2025). https://doi.org/10.1038/s41467-025-59117-2

Image Credits: AI Generated