This issue of Biomedical Information focuses on twelve cutting-edge breakthroughs, covering key fields such as tumor immunology, neuroscience, regenerative medicine, synthetic biology, brain computer interfaces, and medical devices. From Nanjing University intelligent hydrogel to fight against superbacteria, Shandong University to reveal the new mechanism of immune inflammation of Alzheimer’s disease, to the Chinese Academy of Sciences decoding the development of blood brain barrier, Shanghai Jiaotong University synthetic flora intensive immunotherapy, to large-scale proteomics mapping the whole picture of neurodegenerative diseases, many achievements have moved from basic research to clinical transformation, providing new targets, new strategies and new tools for infection, neurodegenerative diseases, stroke, depression, tumors, critical diseases of premature infants, etc., showing huge clinical value and industrial transformation potential.

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1、 Nanjing University team developed intelligent hydrogel to effectively combat superbug infection

On March 16th, Professor Shi Benlong’s team from Nanjing University published an important research result on the treatment of infectious wounds in the internationally renowned journal Advanced Science. The research team designed and constructed a composite intelligent hydrogel system based on allantoin loaded ZIF8 nanoparticles, methacryloylated quaternary ammonium carboxymethyl chitosan and resveratrol（ Alla@ZIF8 – Gel）， This provides an innovative treatment strategy for efficiently combating superbug infections represented by methicillin-resistant Staphylococcus aureus (MRSA).
The hydrogel system shows remarkable intelligent characteristics. Its pH responsiveness enables it to achieve on-demand release of antibacterial components based on changes in acidity in the infectious microenvironment; The adaptive ability of morphology ensures that it can fully fill irregular wounds, achieve tight fit and sustained action. In terms of material design, methacrylated quaternary ammonium salt carboxymethyl chitosan not only provides good biocompatibility, but also has long-lasting antibacterial activity. As the functional core, ZIF8 nanocarrier can intelligently respond to the infectious microenvironment, accurately release the loaded allantoin, and effectively promote angiogenesis and epithelial regeneration. In addition, the integrated resveratrol in the system plays an important role in antioxidant and anti-inflammatory effects, helping to alleviate excessive inflammatory reactions and oxidative stress damage caused by infection, and creating favorable conditions for tissue repair.
Systematic in vivo and in vitro experiments have confirmed that this multifunctional hydrogel can significantly inhibit the proliferation of drug-resistant bacteria such as MRSA, accelerate the closure and healing process of infected wounds, and effectively reduce tissue damage and inflammatory infiltration. This study integrates multiple functions such as intelligent response, antibacterial and anti-inflammatory effects, and active repair promotion, providing a new solution for the management of clinically refractory bacterial infection wounds that combines efficiency and biosafety, demonstrating outstanding clinical translational potential and application prospects.

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2、 Qi Linpengfei’s team from Shandong University reveals a new mechanism of immune inflammation regulation in Alzheimer’s disease

Recently, Professor Lin Pengfei’s team from Qilu Hospital of Shandong University published important research results in the authoritative journal “Journal of Neuroinflammation” in the field of neuroinflammation. For the first time, they systematically elucidated the core regulatory role and molecular mechanism of mammalian Ste20 like kinase 1 (MST1) in the occurrence and development of neuroinflammation in Alzheimer’s disease (AD), providing a highly promising new target and innovative direction for immune intervention therapy of AD.

This study provides an in-depth analysis of the key role of MST1 in the pathological process of AD. Research has found that the activated form of MST1 (p-MST1) is significantly elevated in the brain tissue of AD patients and various AD model mice, and its expression level is significantly positively correlated with the severity of cognitive dysfunction, suggesting that excessive activation of MST1 is one of the important pathological features of AD. Functional experiments further confirmed that mediating MST1 gene knockdown in the AD model can effectively improve cognitive function deficits in mice, significantly reduce pathological deposition of A β and excessive phosphorylation levels of tau protein in the brain, and significantly alleviate neuroinflammatory responses.

At the mechanism level, the research team has made breakthrough discoveries. They revealed that abnormal activation of MST1 specifically inhibits the expression of dipeptidyl peptidase 8 (DPP8). This inhibitory effect further activates the classic cell death pathway dependent on Caspase-1/GSDMD, leading to programmed inflammatory death of neurons and glial cells, and the release of pro-inflammatory factors such as interleukin-1 β (IL-1 β) and interleukin-18 (IL-18) in large quantities, thereby creating a chronic neuroinflammatory environment that continues to amplify and is difficult to regress in the AD brain, accelerating neuronal damage and cognitive decline.
This study innovatively constructed the complete signaling regulatory axis of “MST1/DPP8/Caspase-1/GSDMD”, which not only established the previously unknown core regulatory role of MST1 in AD neuritis, but also revealed a novel AD inflammation amplification pathway. This achievement deepens the academic understanding of the pathogenesis of AD immune inflammation and lays a solid theoretical foundation for the development of novel AD treatment strategies targeting MST1 to regulate neuroinflammation. It has important scientific value and clinical translation prospects.

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3、 Jiao Jianwei’s team reveals the mechanism of neural cell regulation of blood-brain barrier establishment

Jiao Jianwei’s team from the Institute of Zoology of the Chinese Academy of Sciences, together with Dong Ji’s team from Guangzhou National Laboratory and others, published an important research achievement entitled “Decoding the spatiotemporal development of human cortical blood-brain barrier” in the journal Cell Stem Cell on March 23, 2026. This study integrated high-resolution technologies such as single-cell RNA sequencing, spatial transcriptomics, and MERFISH to systematically map the dynamic development of the blood-brain barrier in the cerebral cortex of early human embryos (6-21 weeks of gestation). For the first time, it clarified that human blood-brain barrier like transcriptional features were activated at 8 weeks of gestation, and revealed the dual pathway synergistic mechanism of neural cells as core regulators driving barrier establishment.

The research team found that nerve cells regulate two key components of the blood-brain barrier through two independent and collaborative signaling pathways. On the one hand, neurons interact with CDH2 on the surface of brain endothelial cells through their expressed calcium binding protein-2 (CDH2), specifically activating the β – catenin signaling pathway within endothelial cells, thereby inducing the expression of blood-brain barrier specific transporters and driving the functional characteristics of endothelial cells. On the other hand, neural precursor cells secrete platelet-derived growth factor D (PDGFD) to activate PDGFRB receptors on the surface of parietal cells, directly promoting their proliferation and providing necessary structural support for the maturation and stability of the blood-brain barrier structure.

In addition, the study revealed that with the activation of barrier function, communication signals between endothelial cells and parietal cells were significantly enhanced after 8 weeks of pregnancy. Through cross species comparative analysis, the study confirmed the overall conservation of the blood-brain barrier development between humans and mice, and identified histone variant H2A. Z.1 as a key molecule regulating angiogenesis and barrier formation. This study not only systematically elucidates the development process of the human blood-brain barrier, filling the knowledge gap in this field, but also provides a new theoretical framework and potential targets for understanding the pathological mechanisms of blood-brain barrier related diseases (such as neurodegenerative diseases, brain tumors, etc.) and developing new therapeutic and drug delivery strategies.

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4、 Optimization of pathological microenvironment enhances the efficacy of stem cell extracellular vesicles, providing new strategies for the treatment of intervertebral disc degeneration

Intervertebral disc degeneration is a common pathological basis for chronic back pain, characterized by a decrease in nucleus pulposus cells, degradation of extracellular matrix, and formation of inflammatory microenvironment. The current clinical intervention methods, such as drug analgesia or surgery, mainly focus on symptom relief and are difficult to achieve tissue regeneration and functional reversal. Although stem cell transplantation was once considered a potential regenerative therapy, its efficacy is limited by factors such as low cell survival rates and short-lived paracrine effects after transplantation.
Recently, a research team from the Third Hospital of Hebei Medical University pre treated bone marrow mesenchymal stem cells by simulating the pathological microenvironment of intervertebral disc degeneration, namely hypoxia combined with inflammatory stress conditions, and collected their released apoptotic extracellular vesicles (I-ApoEVs). Research has found that this optimization strategy significantly enhances the biological activity of vesicles: at the cellular level, I-ApoEVs exhibit stronger targeting affinity towards degenerated nucleus pulposus cells, not only promoting cell proliferation and inhibiting apoptosis, but also effectively reducing the expression of aging related biomarkers. Further mechanistic studies have shown that its repair effect is mainly achieved by activating the PGC-1 α/TFAM signaling pathway, which is a key pathway for regulating mitochondrial biosynthesis and functional homeostasis, and helps to restore the energy metabolism and survival ability of degenerated cells.
In animal models, local injection of I-ApoEVs can significantly restore intervertebral disc height and improve tissue morphology, and the effect is better than traditional stem cell transplantation or untreated vesicles. This study suggests that optimizing the function of stem cell derivatives through pathological microenvironment pretreatment can break through the bottleneck of low cell survival rate in existing regenerative medicine and provide new ideas for developing targeted therapies based on extracellular vesicles. Further exploration is needed in the future to determine the optimal preparation parameters, in vivo metabolic kinetics, and long-term safety of I-ApoEVs, in order to promote their clinical translation.

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5、 Liu Yufeng’s team from South China University of Technology reveals a new mechanism of thromboinflammation in necrotizing enterocolitis

On March 19th, Professor Liu Yufeng’s team from South China University of Technology published important research results in Nature Communications, systematically elucidating a key pathogenic mechanism of necrotizing enterocolitis (NEC) that had not been fully understood before. NEC is the most common and life-threatening gastrointestinal emergency in premature infants, with a complex pathogenesis and a lack of specific early diagnostic indicators and effective targeted treatment methods in clinical practice. It has always been a major challenge in the field of neonatal intensive care.

This study, by integrating multi omics analysis, clinical sample validation, and animal model construction, has for the first time clarified that NEC is essentially a thromboinflammatory disease. Research has found that there is a significant occurrence of immune thrombosis in the intestinal tract of NEC patients, with the core driving factor being the massive formation of CD177 neutrophil platelet aggregates. These aggregates activate and release neutrophil extracellular traps, triggering and exacerbating thrombotic inflammatory reactions within intestinal microvessels, directly leading to intestinal mucosal barrier damage, ischemic necrosis, and inflammatory cascade amplification, thereby promoting the occurrence and development of NEC. Mechanism intervention experiments have confirmed that specific blockade of CD177 ⁺ NPA formation can effectively reduce NETosis levels and significantly alleviate intestinal pathological damage in experimental animals.

The clinical translational value of the research is particularly prominent. The team found that the levels of CD177 ⁺ NPA in peripheral blood and intestinal tissue of patients are closely related to the clinical severity, disease progression, and prognosis of NEC, suggesting that it can serve as a highly promising new diagnostic and prognostic biomarker. More noteworthy is that the study proposed innovative treatment strategies: prophylactic use of low molecular weight heparin not only effectively disrupts the stability of NPA, but also significantly reduces NET load, showing a positive trend in improving patient survival rates in clinical observations.

This work not only deepens the understanding of the pathological and physiological nature of NEC, defining it as a thrombotic inflammatory disease, but also proposes a new strategy of joint monitoring and targeted intervention from the entire chain of “mechanism discovery marker identification treatment verification”, laying a solid scientific foundation for early and accurate diagnosis, risk stratification, and development of new anti thrombotic inflammatory therapies for NEC in the future, and is expected to promote the innovation of clinical management mode for this disease.

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6、 New catalyst assists in the synthesis of complex macrocyclic molecules to accelerate drug development

Recently, the Helma Wennemers team at the Swiss Federal Institute of Technology in Zurich reported a groundbreaking catalyst controlled stereoselective “head to tail” macrocyclic method in the journal Science. This study provides innovative solutions to the two long-standing core challenges in the synthesis of chiral macrocyclic compounds: the difficulty of balancing cyclization efficiency and selectivity, and the difficulty of precise control of newly formed stereocenters.

The team designed and developed a bifunctional peptide based organic catalyst, whose core innovation lies in its ability to serve as a template to guide the efficient and precise intramolecular cyclization reaction of the terminal functional groups of linear precursors. This catalytic mechanism effectively suppresses the intermolecular dimerization or oligomerization side reactions that linear molecules are prone to due to their high degree of conformational freedom, thereby preferentially driving the formation of macrocycles thermodynamically and kinetically. In specific applications, only 3 mol% catalyst loading is required to efficiently construct 12 to 18 membered macrolides and lactams. For 13 membered and above ring systems, yields of up to 92-97%, diastereoselectivity exceeding 20:1, and enantioselectivity of 99% can be achieved.

More importantly, the catalytic system exhibits strong stereochemical control capabilities. Even starting from a completely chiral linear precursor, the catalyst can determine the absolute configuration of the newly formed chiral center during the cyclization process. More prominently, when facing linear precursors with chiral centers, this organic catalyst can “cover” the original stereochemical information of the precursor, dominate the three-dimensional spatial configuration of the final macrocyclic product, and achieve predictive synthesis of the product’s stereostructure. This characteristic has been strongly validated in the synthesis of complex natural product core skeletons with biological activity, such as the successful construction of the core structure of robotnikinin, a natural product that can block the cancer-related Sonic Hedgehog signaling pathway.

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7. Study on the mechanism of gender differences in alcohol induced nerve damage reveals the key role of P2X7 receptors

A recent animal study on alcoholic brain injury confirmed significant gender differences in neuroinflammation, blood-brain barrier damage, and spatial memory impairment caused by chronic intermittent ethanol exposure, with male individuals showing higher susceptibility. This study, through systematic analysis of molecular mechanisms, has for the first time clarified the key role of P2X7 receptors in mediating gender specific nerve injury, providing important theoretical basis for the development of differentiated prevention and treatment strategies in clinical practice.

The research team used a chronic intermittent alcohol exposure model to conduct a 3-week intervention experiment on male and female mice. The results showed that under the same exposure conditions, the expression of various pro-inflammatory cytokine genes in the cerebral cortex and hippocampus of male mice was significantly upregulated, including cytokines such as tumor necrosis factor – α (TNF – α) and interleukin-6 (IL-6). It is worth noting that only male individuals exhibit typical damage characteristics of the blood-brain barrier, such as decreased coverage of pericytes and reduced expression of tight junction proteins, accompanied by significant impairment of spatial memory ability. In contrast, female mice only showed a mild increase in interleukin-1 β (IL-1 β) expression, without significant disruption of the blood-brain barrier structure or cognitive impairment.

Mechanism studies have found that the activation level of purinergic receptor P2X7 is significantly higher in male mice after alcohol exposure than in females. This receptor serves as an ATP gated ion channel and plays a central regulatory role in the cascade of neuroinflammation. Experiments have shown that blocking P2X7 receptors with specific inhibitors significantly alleviates neuroinflammatory responses, increased blood-brain barrier permeability, and memory deficits in male mice, while no significant changes were observed in the female intervention group. This suggests that gender specific activation of P2X7 receptors may be a key molecular basis for gender differences in alcohol-related neurological injury.

Further analysis suggests that sex hormones may affect the threshold of neuroinflammation by regulating the expression of P2X7 receptors and downstream signaling pathways. Male hormones may enhance the activation of NLRP3 inflammasome mediated by P2X7 in microglia, while female hormones may exert a protective effect by regulating receptor phosphorylation status. This discovery not only reveals the molecular mechanisms underlying gender differences in alcoholic brain injury, but also provides new directions for developing gender specific neuroprotective strategies targeting P2X7 receptors.

The research team suggests that in the future clinical prevention and treatment of alcohol-related neurological disorders, gender factors should be fully considered. Targeted treatment pathways such as P2X7 receptor antagonists can be explored for male high-risk populations, while prevention strategies for females can focus on early monitoring of inflammation. The research findings have been published in authoritative journals in the field of neuroscience, providing important experimental evidence for understanding the gender biological differences in substance addiction.

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8. Cell Journal Reveals a New Mechanism of Dexmedetomidine in Preventing PTSD: Targeting the Srebf1/Phgdh Pathway in Anterior Lobe Astrocytes

On March 17th, Professor Peng Mian and Professor Li Xiang’s team from Wuhan University published an important study in the Cell Reports, which systematically elucidated the neurobiological mechanism of Dexmedetomidine, a commonly used sedative drug, in preventing post-traumatic stress disorder (PTSD) in clinical practice. This study not only provides a solid theoretical basis for dexmedetomidine as an early intervention strategy for PTSD high-risk populations, but also reveals for the first time a novel signaling pathway centered on astrocytes that regulates fear memory consolidation, indicating potential targets for the development of rapidly acting PTSD preventive drugs.

As a serious post-traumatic stress disorder, the effective prevention and treatment of PTSD remains a major challenge in the field of psychiatry. The existing first-line therapies, such as trauma focused psychotherapy and some medication treatments, generally have bottlenecks such as lengthy treatment courses, limited efficacy, and high recurrence rates. Therefore, effective drug intervention for high-risk individuals in the early stage after trauma exposure to block the consolidation of pathological fear memory has important clinical significance. Previously, clinical observation found that the use of dexmedetomidine in the dose of linen intoxication in the perioperative period can reduce the incidence rate of PTSD, but the exact cellular and molecular mechanisms of the formation of fear memory are still unclear.

Peng Mian and Li Xiang’s team first confirmed by constructing a mouse conditional fear model that administering a dose of dexmedetomidine to mice during the critical time window of traumatic memory formation can significantly and persistently alleviate their fear response, simulating its clinical effect in preventing PTSD. Subsequently, researchers screened key brain regions using high-throughput transcriptome sequencing technology and found that the medial prefrontal cortex (PL) is a sensitive brain area where dexmedetomidine exerts its effects. The expression changes of sterol regulatory element binding protein 1 (Srebf1) in this area are highly correlated with behavioral effects.

In depth mechanism research reveals that the target of dexmedetomidine is not traditional neurons, but astrocytes in the PL region. The drug significantly inhibited the nuclear translocation process of Srebf1 in the cytoplasm of astrocytes by acting on them. Srebf1, as a key transcription factor, its reduced nuclear uptake directly leads to downregulation of the transcription level of downstream target gene, phosphoglycerate dehydrogenase (Phgdh). Phgdh is the rate limiting enzyme in the serine biosynthesis pathway, and serine is a precursor for the synthesis of the important neuroactive substance D-serine, which plays a central role in regulating NMDA receptor function and synaptic plasticity. Therefore, inhibition of this pathway ultimately weakens the neural plasticity foundation required for fear memory consolidation.

In summary, this study has drawn a clear pathway for the preventive effect of dexmedetomidine on PTSD: drug → astrocytes in the medial anterior edge of the prefrontal cortex → inhibition of Srebf1 nuclear translocation → downregulation of Phgdh expression → interference with local serine/D-serine metabolism → inhibition of pathological fear memory consolidation. This discovery breaks through the limitations of previous PTSD research that mainly focused on neurons, highlights the critical role of astrocytes in regulating advanced emotional memory, and establishes Srebf1 and Phgdh as highly promising new targets for drug intervention, bringing a new scientific perspective for revolutionizing PTSD prevention and treatment strategies.

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9. Li Peiying and others from Shanghai Jiao Tong University reveal the “metabolic supply station” in ischemic brain

Ischemic stroke, as a major global health challenge, not only involves neuronal necrosis in the ischemic core, but is also closely related to secondary damage driven by neuroinflammation in the penumbra. Peripheral immune cells, especially the monocyte macrophage system, play a crucial role in the complex regulatory network of post-stroke brain injury and repair. The research conducted by Li Peiying’s team at Shanghai Jiao Tong University, published in the Journal of Experimental Medicine on March 18, 2026, has made a breakthrough contribution to this field by revealing a unique subpopulation of anti-inflammatory immune cells and their key metabolic regulatory mechanisms in the post-stroke brain.

The traditional view is that Ly6C (^ {high}) monocytes mainly differentiate into pro-inflammatory macrophages after stroke, exacerbating neuroinflammation. However, the study identified a class of macrophages derived from Ly6C (^ {high}) and Ly6G (^ {low}) monocytes with anti-inflammatory properties. This discovery challenges previous knowledge, indicating that the same subpopulation of monocytes can exhibit completely opposite functional phenotypes in specific microenvironments, providing a new perspective for understanding the complexity of immune responses after stroke.

The study further elucidates that the maintenance of this anti-inflammatory phenotype relies on a molecule called hypoxia inducible protein 2 (HIG2). HIG2, as a key mediator, upregulates the expression of choline kinase alpha through Hif1 α – dependent transcriptional regulation, thereby promoting the biosynthesis of phosphatidylcholine, an important component of the cell membrane. This metabolic reprogramming process provides the necessary material basis for macrophages to maintain their anti-inflammatory function, forming a bridge connecting hypoxia signaling, cellular metabolism, and immune function. Experimental results have shown that administering recombinant HIG2 protein through intranasal administration can effectively simulate this endogenous protective pathway, significantly improve the neurological function prognosis of stroke model mice, and reduce infarct volume.

The innovation of this study lies in not only discovering a new beneficial subpopulation of immune cells, but also delving deeper into the metabolic mechanisms underlying their functions, namely that the HIG2 driven phospholipid metabolism remodeling serves as a “metabolic supply station” supporting the anti-inflammatory phenotype. This discovery closely links immune regulation with cellular metabolism, proposing a new strategy of “immune metabolism” intervention. Targeting HIG2 or its downstream pathways has the potential to precisely regulate the inflammatory response after stroke, transforming harmful pro-inflammatory environments into anti-inflammatory environments that are conducive to repair. This provides a solid theoretical basis and highly promising drug targets for the development of new therapeutic methods that reduce neuroinflammation and promote brain repair.

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10. Nat Microbiol: Constructing a synthetic microbial community RCom to precisely enhance anti-tumor immune efficacy

On March 9th, the team led by Yang Chen, Wang Ying, and Lu Shun from Shanghai Jiao Tong University published important research results in Nature Microbiology. This study successfully designed and constructed a synthetic microbial community (RCom) consisting of 15 gut bacteria with clear composition. Research has shown that regardless of an individual’s pre-existing gut microbiota background, oral RCom can significantly enhance the efficacy of programmed death receptor-1 (PD-1) antibodies in tumor treatment, and even reverse treatment resistance in some preclinical models. This discovery provides strong experimental evidence and potential translational pathways for improving cancer immunotherapy through precise probiotic intervention strategies.

Immune checkpoint inhibitors (ICIs) have become a key treatment for advanced cancer, but their clinical application faces two core challenges: only some patients can produce persistent responses, and they may trigger immune related adverse events. Recent studies have confirmed that the gut microbiota plays a crucial role in regulating ICIs mediated anti-tumor immune responses, making it a highly promising therapeutic target. Compared to fecal microbiota transplantation (FMT) with complex components and safety risks, or single function probiotic strains, adopting a synthetic microbiota strategy with clear species composition is more advantageous – it ensures the controllability, reproducibility, and safety of treatment. However, how to rationally design and construct a microbial community that combines stable colonization ability and strong immune regulation function has always been a major challenge in this field.

Our research team overcame this challenge by integrating metagenomic data analysis with computational biology prediction models and rationally designed RCom. Subsequent in vitro and in vivo functional validation experiments have consistently shown that RCom can effectively reshape the tumor immune microenvironment, enhance effector T cell function, significantly improve the anti-tumor activity of anti-PD-1 therapy, and limit the development of drug resistance. This study not only confirms the effectiveness of RCom as a potential adjuvant for ICIs treatment, but also demonstrates a “design build test” synthetic microbiome research paradigm, laying a solid foundation for the development of next-generation microbiota based adjuvant therapies for tumor immunotherapy.

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11. Large scale proteomics reveals molecular panorama of neurodegenerative diseases

On March 23rd, Professor Peng Junmin’s team from St. Jude Children’s Research Hospital published an important study in the journal Cell. Through systematic multi-layer proteomic analysis, they constructed a “complete neurodegenerative disease map” covering six major neurodegenerative diseases, including Alzheimer’s disease, Parkinson’s disease, frontotemporal dementia, amyotrophic lateral sclerosis, Huntington’s disease, and Lewy body dementia. This study integrated high-dimensional proteome, phosphoproteome, and transcriptome data from 2279 brain samples, establishing the largest and most complete cross disease proteomics resource library currently available.

The study adopted a cross disease comparison strategy, achieving for the first time a systematic comparative analysis of molecular features between different neurodegenerative diseases. By integrating multi-level omics data, the team not only revealed protein expression patterns unique to various diseases, but also identified common molecular pathway abnormalities that cross disease boundaries. Of particular note, this study identified multiple disease subtypes through machine learning methods, which exhibit unique protein network dysregulation features, providing a molecular basis for understanding clinical heterogeneity of diseases. All data has been made publicly available to the global research community through the PanNDA Portal, which supports multi-dimensional data mining and visualization analysis.

Previously, the team had published two groundbreaking works in Cell in 2025, focusing on the dynamic changes of proteins in specific neurodegenerative diseases. Neurodegenerative diseases have high complexity and pathological heterogeneity, and existing treatment methods are still extremely limited. Large scale proteomics has become a key tool for analyzing the pathogenesis of diseases by systematically capturing changes in protein expression, modification, and interaction networks during the disease process. The map released this time represents the most comprehensive cross disease proteomic analysis in the field to date. It not only deepens the understanding of single disease mechanisms, but also reveals the common patterns and specific pathways of neurodegeneration from a comparative biological perspective.

This resource is expected to drive the development of multiple research directions, including the discovery of novel biomarkers, precise classification of disease subtypes, and identification of cross disease common therapeutic targets. By providing this deeply integrated molecular map for the field, research has laid a key foundation for the ultimate development of novel intervention strategies targeting specific molecular pathways.

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