Translational Neurodegeneration最新文献

{"title":"Bacteroides coprocola protects dopaminergic neurons in rotenone-induced Parkinson's disease mouse model by modulating gut microbiota dysbiosis and inhibiting the NLRP3 signaling pathway.","authors":"Zixian Liu, Jiabei Nie, Yimei Li, Maoxin Huang, Ziluo Chen, Shushang Yu, Jiaqi Zheng, Yuyan Tan, Shengdi Chen","doi":"10.1186/s40035-026-00542-8","DOIUrl":"10.1186/s40035-026-00542-8","url":null,"abstract":"<p><strong>Background: </strong>Parkinson's disease (PD) is a prevalent neurodegenerative disease and its pathogenesis is still unclear. Emerging evidence supports the gut-origin hypothesis, highlighting gut microbiota dysbiosis as a contributing factor in PD pathogenesis. Our previous clinical study showed that Bacteroides coprocola (B. coprocola), a gut bacterium producing short-chain fatty acids (SCFAs), was significantly reduced in PD patients. This study was aimed to investigate the potential of B. coprocola in ameliorating PD pathology and explore the underlying mechanisms in a rotenone-induced PD mouse model.</p><p><strong>Methods: </strong>The rotenone-induced PD mouse model was treated by orally administering B. coprocola for three weeks. Immunofluorescence, Western blotting, flow cytometry, 16S rRNA sequencing, and metabolomics were performed to assess midbrain and intestinal changes, NLRP3 inflammasome activation, macrophage polarization, gut microbiota, and SCFA levels. In vitro, LPS-stimulated bone marrow-derived macrophages were used to validate the role of NLRP3 signaling in macrophage polarization following sodium acetate and sodium butyrate treatment via siRNA and molecular assays.</p><p><strong>Results: </strong>B. coprocola treatment alleviated PD-related motor deficits, neuroinflammation, gut microbiota dysbiosis, and intestinal barrier permeability in the rotenone-induced PD mouse model. Mechanistically, B. coprocola reshaped the gut microbiota composition and modulated macrophage polarization, which were associated with the inhibition of the NLRP3 inflammasome signaling pathway. Furthermore, in vitro experiments confirmed that the acetate and butyrate-key metabolites of B. coprocola-attenuated the inflammatory responses and promoted M2-like macrophage polarization via free fatty acid receptor (FFAR) 2/3 receptors, thereby suppressing NLRP3 activation.</p><p><strong>Conclusions: </strong>In conclusion, B. coprocola treatment can improve motor deficits, neuroinflammation, and intestinal function in the rotenone-induced PD mouse model. The effects are associated with microbiota remodeling, regulation of macrophage polarization, and inhibition of the NLRP3 inflammasome pathway. Acetate and butyrate, key metabolites of B. coprocola, might play an important role in promoting M2 macrophage polarization through FFAR2/3 receptors.</p>","PeriodicalId":23269,"journal":{"name":"Translational Neurodegeneration","volume":"15 1","pages":""},"PeriodicalIF":19.1,"publicationDate":"2026-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12949511/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147318356","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction: LRRK2 G2019S mutation contributes to mitochondrial transfer dysfunction in a Drp1-STX17-dependent manner.","authors":"Mei Ding, Fen Wang, Lan-Lan Jiang, Chao Ma, Yu-Wan Qi, Jun-Yi Liu, Juan Li, Mei-Xia Wang, Hong Jin, Jin-Ru Zhang, Cheng-Jie Mao, Xiao-Kang Li, Chun-Feng Liu, Xiao-Yu Cheng","doi":"10.1186/s40035-025-00533-1","DOIUrl":"10.1186/s40035-025-00533-1","url":null,"abstract":"","PeriodicalId":23269,"journal":{"name":"Translational Neurodegeneration","volume":"15 1","pages":"6"},"PeriodicalIF":15.2,"publicationDate":"2026-02-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12905968/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146198141","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mitochondrial DNA: a molecular switch driving sterile neuroinflammation.","authors":"Abhishek Jauhari, Tanisha Singh, Diane L Carlisle, Robert M Friedlander","doi":"10.1186/s40035-026-00540-w","DOIUrl":"10.1186/s40035-026-00540-w","url":null,"abstract":"<p><p>Mitochondrial DNA (mtDNA) plays a pivotal role in the regulation of neuroinflammation, acting as a potent trigger of innate immune responses when released into the cytoplasm or extracellular space. mtDNA is structurally similar to bacterial DNA, containing unmethylated CpG motifs that are readily recognized by immune sensors. Under conditions of cellular stress, injury, or mitochondrial dysfunction, mtDNA can escape into the cytoplasm, where it activates the cGAS (cyclic GMP-AMP synthase)-STING (stimulator of interferon genes) signaling pathway, or it can be detected extracellularly by Toll-like receptors on immune cells. These signaling events lead to the production of pro-inflammatory cytokines and type I interferons, amplifying neuroinflammatory responses. In the central nervous system, this process contributes to the pathogenesis of various neurodegenerative and inflammatory conditions, such as Alzheimer's disease (AD), Parkinson's disease (PD), Huntington's disease (HD), etc.. The dual role of mtDNA as both a damage-associated molecular pattern and a signaling molecule underscores its importance as a therapeutic target for modulating neuroinflammation and protecting against progressive neuronal damage. In this review, we will discuss the implications of mtDNA-mediated neuroinflammation in neurodegenerative diseases, including AD, PD, and HD, highlighting its potential as a diagnostic biomarker and therapeutic target.</p>","PeriodicalId":23269,"journal":{"name":"Translational Neurodegeneration","volume":"15 1","pages":"5"},"PeriodicalIF":19.1,"publicationDate":"2026-02-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12903234/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146195664","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Implications of virus-induced stress granules in tauopathies.","authors":"Snigdda Sharma, Alex Vandenakker, Claudia Cortés-Pérez, Sarah Milne, Renée N Douville","doi":"10.1186/s40035-026-00538-4","DOIUrl":"10.1186/s40035-026-00538-4","url":null,"abstract":"<p><p>Tauopathies are characterized by aberrant tau structure and function, which is associated with neurodegenerative dementias, such as Alzheimer's disease, Pick's disease, and frontotemporal dementia, as well as the motor neuron disease amyotrophic lateral sclerosis. Consistent association of these neurodegenerative conditions with viruses suggests an interplay between viral activity and the development of tauopathy. In this review, we explore how tau dysregulation may facilitate viral activity, and conversely, how viruses may drive tauopathy. We further discuss how stress granules (SGs) are a likely hub for the interactions between tau and viral components, leading to tau deregulation. Within the network of SG proteins analyzed, 15 proteins were identified to be both tau interactors and implicated in viral processes, having dual functionality. These SG proteins are further discussed in terms of their relationship with tauopathy, viral replication, and neurodegeneration. Concrete examples of synergistic and competing effects between tau and viruses are highlighted, revealing both pathological and protective mechanisms. This dichotomy underscores a complexity that is both disease- and virus-specific, within the context of SG biology and tau pathology. While the viral involvement in tauopathies could be considered detrimental, it may provide insights into antiviral therapeutics to target the accumulation and misfolding of tau in these neurodegenerative diseases.</p>","PeriodicalId":23269,"journal":{"name":"Translational Neurodegeneration","volume":"15 1","pages":"4"},"PeriodicalIF":19.1,"publicationDate":"2026-02-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12896018/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146166883","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Microbiota and Alzheimer's disease: mechanistic insights from a multi-organ perspective.","authors":"Jiewen Liao, Hanmeng Mou, Shilin Luo, Lu Shen, Bin Jiao","doi":"10.1186/s40035-026-00541-9","DOIUrl":"10.1186/s40035-026-00541-9","url":null,"abstract":"<p><p>Alzheimer's disease (AD) is a progressive neurodegenerative disorder driven by multifactorial mechanisms. Increasing evidence suggests that dysbiosis, a term denoting an imbalance in the composition of the microbiota, may play a pivotal role in the pathogenesis of AD across multiple bodily sites, including the gut, oral cavity, nasal passages, lungs, and skin. Microbial imbalances may promote neuroinflammation, immune dysfunction, and metabolic disturbances through complex host-microbiota networks. This review synthesizes current advances in the understanding of microbiota-driven modulation of AD, introduces the \"Multi-Axis Co-Regulation\" concept, and evaluates microbial biomarkers for early diagnosis. Finally, the translational potential of microbiota-targeting interventions, including probiotics, dietary modulation, fecal microbiota transplantation, and oral microbiome-based therapies, are discussed, which represent novel strategies for precision prevention and treatment of AD.</p>","PeriodicalId":23269,"journal":{"name":"Translational Neurodegeneration","volume":"15 1","pages":"3"},"PeriodicalIF":19.1,"publicationDate":"2026-02-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12892757/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146166949","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mapping cellular vulnerability in Parkinson's disease using retro-AAVs and preformed α-synuclein fibrils.","authors":"Fanni F Geibl, Ahmed A S Musa, Leo Dietrich, Helena Wolter, David L Wokosin, Sharof Khudayberdiev, Marco B Rust, Rong Chen, Valina L Dawson, Ted M Dawson, Wolfgang H Oertel, D James Surmeier, Martin T Henrich","doi":"10.1186/s40035-026-00535-7","DOIUrl":"10.1186/s40035-026-00535-7","url":null,"abstract":"<p><strong>Background: </strong>Parkinson disease (PD) is characterized by progressive neuronal loss within defined brain regions, accompanied by α-synuclein (αSyn)-rich inclusions, termed Lewy pathology (LP). However, it is unclear which cellular factors render certain neuronal populations vulnerable, while others stay devoid of LP throughout the course of disease.</p><p><strong>Methods: </strong>This study aimed to identify and compare the cellular architecture of vulnerable and non-vulnerable neurons exposed to αSyn pathology by using a projection-based retro-AAV approach in combination with an in vivo α-synucleinopathy mouse model. To do so, a set of viral genetic, immunohistochemical, and optical tools was used in combination with the preformed αSyn fibril (PFF) model.</p><p><strong>Results: </strong>αSyn pathology propagated robustly into the input connectome of the pedunculopontine nucleus (PPN). However, we observed a marked mismatch between the anatomically expected and the actual distribution of pathology. While anatomically connected neurons in the bed nucleus of the stria terminalis (BST) and the central amygdala (CEA) accumulated substantial αSyn pathology, equally strong connected neurons of the substantia nigra pars reticulata (SNr), and the dentate nucleus (DN) were devoid of pathology. Second, cellular vulnerability and resilience were consistent and reproducible features. When PFFs were injected into alternative major output projection sites of BST, CEA, SNr, and DN, we observed similar patterns of αSyn accumulation. Third, projection-specific axonal mapping revealed that the αSyn-accumulating BST and CEA neurons possessed larger axonal arbors than the more resilient neurons in SNr and DN. Correspondingly, neurons in BST and CEA exhibited higher basal mitochondrial oxidation levels, indicating an increased bioenergetic burden. Finally, the site of initial seeding significantly influenced the extent of developing brain-wide pathology, suggesting that certain brain regions may function as \"super-seeders\", promoting widespread propagation of pathology, while others contribute relatively little to the global LP burden.</p><p><strong>Conclusions: </strong>αSyn pathology propagates along anatomical pathways, but cell-autonomous factors determine if a neuron exposed to misfolded αSyn will develop Lewy-like pathology or not.</p>","PeriodicalId":23269,"journal":{"name":"Translational Neurodegeneration","volume":"15 1","pages":"2"},"PeriodicalIF":19.1,"publicationDate":"2026-01-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12859986/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146094300","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Proximity labeling in neuroscience: decoding molecular landscapes for precision neurology.","authors":"Xia Gao, Jianjun Lu, Peipei Chen, Xinna Wang, Longlong Zheng, Yuyin Shao, Huali Shen, Qian Yang","doi":"10.1186/s40035-026-00534-8","DOIUrl":"10.1186/s40035-026-00534-8","url":null,"abstract":"<p><p>The intricate cellular architecture and dynamic molecular interplay in the nervous system have long challenged mechanistic studies of neurological diseases. Conventional approaches often miss the transient, low-affinity, or spatially confined interactions that underlie neural homeostasis and pathogenesis. Proximity labeling (PL) technologies overcome this limitation by enabling in situ capture of these elusive molecular events within living systems. Through spatially restricted biotinylation, PL methods, including engineered biotin ligases (e.g., TurboID), peroxidases (e.g., APEX2), and emerging photocatalytic platforms, allow high-resolution mapping of proteomes and interactomes within defined subcellular compartments, cell types, and cell-cell interfaces. In this review, we systematically outline the principles of PL and its transformative applications in constructing molecular atlases of the nervous system. We highlight how these tools are revolutionizing our understanding of brain function by elucidating pathophysiological mechanisms in Alzheimer's disease, Parkinson's disease and other neurological disorders. Furthermore, we discuss how PL accelerates the translation of basic research into clinical practice by facilitating the discovery of mechanistic biomarkers and druggable targets. Finally, we address current challenges and future directions, including integration with multi-omics and single-cell methodologies, and conclude that PL can advance precision neurology by bridging molecular neurobiology with therapeutic innovation.</p>","PeriodicalId":23269,"journal":{"name":"Translational Neurodegeneration","volume":"15 1","pages":"1"},"PeriodicalIF":19.1,"publicationDate":"2026-01-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12853706/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146094304","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pretargeted brain PET imaging reveals amyloid-β pathology using a TCO-modified antibody and a fluorine-18-labeled tetrazine.","authors":"Sara Lopes van den Broek, Jonas Eriksson, Qiaojun Yang, Nadja M Bucher, Eva Schlein, Lorenzo J I Balestri, Luke R Odell, Dag Sehlin, Stina Syvänen","doi":"10.1186/s40035-025-00532-2","DOIUrl":"10.1186/s40035-025-00532-2","url":null,"abstract":"<p><strong>Background: </strong>Antibody-based positron emission tomography (PET) imaging holds great promise for visualizing disease-related proteins in the brain. However, its clinical utility is limited by poor antibody penetration across the blood-brain barrier (BBB) and the requirement for long-lived radionuclides due to slow antibody pharmacokinetics. Pretargeted imaging strategies, in which antibody administration and radioligand injection are separated in time, enable the use of short-lived, high-resolution PET-compatible radionuclides such as fluorine-18.</p><p><strong>Methods: </strong>A bispecific antibody, Bapi-Fab8D3, which targets both amyloid beta (Aβ) and the transferrin receptor (TfR) for TfR-mediated transport across the BBB, was conjugated with trans-cyclooctene (TCO) to enable in vivo click chemistry. Following antibody administration to Alzheimer's disease (AD) model mice and sufficient time for accumulation at intrabrain Aβ deposits, a fluorine-18-labeled tetrazine was injected to react in vivo with the TCO handles on the antibody. PET imaging, autoradiography, ex vivo quantification, and histological analyses were performed to evaluate the specificity and distribution of the imaging signal.</p><p><strong>Results: </strong>Bapi-Fab8D3 retained its binding affinity for both Aβ and TfR after TCO-conjugation. In brain sections, reactive TCOs were detected up to three days after antibody injection, indicating successful transcytosis across the BBB and stable target engagement. Pretargeted PET imaging after fluorine-18-labeled tetrazine injection revealed significantly higher signals in AD mice that received TCO-Bapi-Fab8D3 compared to wild-type controls or AD mice that received the unmodified antibody. The uptake pattern corresponded to Aβ plaque distribution, and quantitative analysis showed increased signal in AD-relevant brain regions including the hippocampus and thalamus.</p><p><strong>Conclusions: </strong>This study demonstrates successful pretargeted PET imaging of brain Aβ pathology using a systemically administered bispecific antibody capable of BBB penetration and a fluorine-18-labeled tetrazine. These findings establish a generalizable strategy for high-contrast in vivo imaging of brain protein targets using pretargeted PET, with the potential to expand molecular imaging to protein targets in the brain that are currently inaccessible.</p>","PeriodicalId":23269,"journal":{"name":"Translational Neurodegeneration","volume":"14 1","pages":"72"},"PeriodicalIF":15.2,"publicationDate":"2025-12-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12742193/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145834759","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Microfluidic platform for understanding Parkinson's disease and α-synuclein conformation.","authors":"Tregub Pavel, Zembatov Georgy, Namiot Eugenia, Kolotyeva Natalia, Yurchenko Stanislav, Illarioshkin Sergey, Salmina Alla","doi":"10.1186/s40035-025-00526-0","DOIUrl":"10.1186/s40035-025-00526-0","url":null,"abstract":"<p><p>Microfluidic systems are an innovative engineering solution that is increasingly being used in a wide range of scientific fields. These systems use fluids in microchannels (1 to 300 microns) to analyze extremely small volumes of sample and reagent, allowing precise delivery and mixing while maintaining accurate results. Parkinson's disease (PD) poses significant diagnostic challenges, with early detection being critical to improved treatment outcomes. A key pathological feature of PD is the presence of Lewy bodies composed of α-synuclein (αSyn) fibrils. Recent research has shown that αSyn oligomers can be toxic and contribute to neuronal loss. Therefore, microfluidics offers a promising approach for the diagnosis of different stages of αSyn pathology. This review comprehensively analyzes the application of microfluidics in single-cell analysis and protein aggregation studies. We discuss the concept of lab-on-a-chip analysis and examine different substrates for αSyn detection, citing relevant studies and expected protein concentrations and their correlations with disease progression and severity.</p>","PeriodicalId":23269,"journal":{"name":"Translational Neurodegeneration","volume":"14 1","pages":"71"},"PeriodicalIF":15.2,"publicationDate":"2025-12-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12729760/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145820708","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cortical layer multi-parameter analysis of neurovascular impairments in AD/ADRD rodent model with in vivo optical imaging.","authors":"Hyomin Jeong, Jiaxiang Ren, Wensheng Cheng, Nora D Volkow, Haibin Ling, Donghui Zhu, Congwu Du, Yingtian Pan","doi":"10.1186/s40035-025-00530-4","DOIUrl":"10.1186/s40035-025-00530-4","url":null,"abstract":"<p><strong>Background: </strong>Neurovascular biomarkers have the potential to enhance early diagnosis of Alzheimer's disease (AD) and AD-related dementias (ADRD), as cerebrovascular alterations often precede neurodegeneration. However, their clinical application remains challenging due to insufficient specificity, heterogeneity, and technical limitations.</p><p><strong>Methods: </strong>Here, we report that vessel- and cortical layer-specific parameters exhibit promising diagnostic sensitivity for neurovascular impairments in an AD/ADRD mouse model, apolipoprotein E (APOE) 4 knock-in (KI), compared to APOE3-KI at 12 months of age. Using two in vivo imaging modalities, 3D capillary-resolution optical Doppler tomography and laser speckle contrast imaging, we measured 36 morphological and functional vascular parameters and evaluated their diagnostic performance using a machine-learning Support Vector Machine classifier.</p><p><strong>Results: </strong>APOE4 mice showed significant alterations including reduced venular and arterial cerebral blood flow velocities and diameters, increased vascular tortuosity, layer-dependent decreases in vascular density, and impaired cerebrovascular reactivity. Venule- and microcirculation-related parameters and dynamic vasoactivity to brain stimuli demonstrated high diagnostic accuracy (~ 90%).</p><p><strong>Conclusion: </strong>Together, these findings provide in vivo evidence for early, cortical layer-specific neurovascular dysfunction caused by APOE4 that increases the susceptibility to dementia and highlight the potential of combining neurovascular biomarkers from optical imaging with AI-based classifier for identification of increased AD/ADRD risk.</p>","PeriodicalId":23269,"journal":{"name":"Translational Neurodegeneration","volume":"14 1","pages":"70"},"PeriodicalIF":19.1,"publicationDate":"2025-12-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12720472/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145805376","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}