International review of neurobiology最新文献_第2页

Imaging the glymphatic system in Huntington's disease: The benefits of a multimodal approach and clinical implications. 亨廷顿舞蹈病的淋巴系统成像：多模式方法的益处和临床意义。

International review of neurobiology Pub Date : 2026-01-01 Epub Date: 2026-09-04 DOI: 10.1016/bs.irn.2026.08.017

Alexander Calvano, Daniel J van Wamelen

引用次数: 0

Stress and medial prefrontal cortex: Sex-dependent effects in rodent models. 应激和内侧前额皮质：啮齿动物模型的性别依赖效应。

International review of neurobiology Pub Date : 2026-01-01 Epub Date: 2026-09-14 DOI: 10.1016/bs.irn.2026.08.013

Hailey Storsved, Cara L Wellman

{"title":"Stress and medial prefrontal cortex: Sex-dependent effects in rodent models.","authors":"Hailey Storsved, Cara L Wellman","doi":"10.1016/bs.irn.2026.08.013","DOIUrl":"https://doi.org/10.1016/bs.irn.2026.08.013","url":null,"abstract":"Chronic stress significantly alters rodent medial prefrontal cortical (mPFC) structure and function, contributing to cognitive and affective dysfunction associated with stress-related psychiatric disorders. Although the effects of stress on the male mPFC have been extensively characterized, growing evidence demonstrates that females exhibit distinct behavioral, structural, and molecular responses to chronic stress. This review synthesizes current findings regarding sex differences in stress-induced plasticity within the adult mPFC, discussing the behavioral outcomes, activation, and neural plasticity of the region in response to stress exposure. Across stress paradigms, males generally exhibit earlier dendritic retraction, spine loss, and impairments in cognitive flexibility, whereas females often demonstrate delayed mPFC effects despite persistent affective behavioral deficits. Emerging evidence suggests that females may recruit compensatory inhibitory mechanisms, particularly through parvalbumin neuron activation, that transiently buffer pyramidal cells from stress-induced remodeling. In contrast, stress in males may influence mPFC structure and function via somatostatin interneuron signaling, glucocorticoid receptor-mediated pathways, and microglial-dependent synaptic remodeling. However, sex differences are strongly influenced by stress modality, duration, and intensity, which contributes to variability across studies. Despite this variability, patterns in the literature suggest that males and females recruit distinct mPFC mechanisms in response to stress. Improved understanding of sex-specific stress adaptations may inform the development of targeted interventions for stress-related psychiatric disorders.","PeriodicalId":94058,"journal":{"name":"International review of neurobiology","volume":"190 ","pages":"31-54"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149019213","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Parkinson's disease-Crucial advances and on-going challenges. 帕金森病——关键的进展和持续的挑战。

International review of neurobiology Pub Date : 2026-01-01 Epub Date: 2026-09-10 DOI: 10.1016/bs.irn.2026.08.019

Grażyna Söderbom

{"title":"Parkinson's disease-Crucial advances and on-going challenges.","authors":"Grażyna Söderbom","doi":"10.1016/bs.irn.2026.08.019","DOIUrl":"https://doi.org/10.1016/bs.irn.2026.08.019","url":null,"abstract":"Dramatic advances have been seen over the past 5 years in neurodegenerative disease medicine. In Parkinson's disease (PD), significant advances have been made in molecular biomarkers and imaging tools. These have led to improved diagnostic accuracy for clinical trial recruitment and stratification, as well as contributing fundamentally to biomarker-based disease frameworks that define PD by its biology. In combination, these advances may enable the tracking of disease progression and improved evaluation of disease-modifying therapies in the research setting. Biofluid-based biomarkers currently available in research settings have the potential to reach real-world settings as commercially viable diagnostic tests. These will provide physicians with the necessary tools required to diagnose PD early and accurately without relying solely on the presence of clinical symptoms. Moreover, with each trial that reports, greater insights are gained into those individuals likely to benefit from different therapeutic options for PD, particularly with monoclonal antibody immunotherapy strategies targeting α-synuclein, where disease-modifying signals have been reported in some trials. This review focuses on some of the groundbreaking advances and the immediate challenges faced by researchers, clinicians, and individuals with PD, as they collaborate to address the great-and ever-growing-clinical need in PD.","PeriodicalId":94058,"journal":{"name":"International review of neurobiology","volume":"190 ","pages":"75-112"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149019160","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

TMEM230 and mitochondrial regulation in Alzheimer's disease. TMEM230和线粒体调控在阿尔茨海默病中的作用。

International review of neurobiology Pub Date : 2026-01-01 Epub Date: 2026-04-15 DOI: 10.1016/bs.irn.2026.02.002

Ileana Zucchi, Cinzia Cocola, Paride Pelucchi, Daniela Mazzaccaro, Giovanni Nano, Mira Palizban, Giovanni Porta, Rolland A Reinbold

{"title":"TMEM230 and mitochondrial regulation in Alzheimer's disease.","authors":"Ileana Zucchi, Cinzia Cocola, Paride Pelucchi, Daniela Mazzaccaro, Giovanni Nano, Mira Palizban, Giovanni Porta, Rolland A Reinbold","doi":"10.1016/bs.irn.2026.02.002","DOIUrl":"10.1016/bs.irn.2026.02.002","url":null,"abstract":"Aging is associated with an attrition of cell subcellular components of the endomembrane system due to long-term exposure to environmental stresses or physical/chemical insults. Tissue morphology physiology and function are strongly dependent on the linked dynamic activities of the endomembrane of organelles of the endomembrane system (ES). This is especially true for nervous tissue and the brain where ES components must interact over long (neurite) distances for proper synapse functions. As the endoplasmic reticulum (ER) is the primary organelle responsible for generating plasma membrane and subcellular membrane components, dysregulation of the ER has a significant role in nervous tissue physiology and diseases in which membrane function is critical, such as in age associated Alzheimer's Disease (AD). Understanding why the ER fails to respond effectively to stress may provide a promising platform for developing antiaging treatments. In this review we characterizegene pathways induced by the transmembrane (TMEM) protein, TMEM230 in the ER in Alzheimer's disease (AD). TMEM230 upregulates oxidative phosphorylation and mitochondria pathways associated cell metabolism. High levels of expression of TMEM230 associated with AD, due chronic inflammation drives hyperoxidation leading to aberrant structural changes in the tethering of the mitochondria and ER membrane and consequently, intra-organelle calcium balance. Sustained elevated levels of expression of TMEM230 leads to catastrophic oxidative stress and irreversible mitochondria damage as seen in some AD patients. Our studies support that Parkinson's Disease and Huntington's Disease may be similarly driven by chronic high levels TMEM230 which results in decoupling of ER-mitochondrial regulation.","PeriodicalId":94058,"journal":{"name":"International review of neurobiology","volume":"186 ","pages":"145-185"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148229779","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Environmental toxins, PFAS exposure, and brain metabolism: A new angle in Alzheimer's disease pathophysiology. 环境毒素、PFAS暴露与脑代谢：阿尔茨海默病病理生理学的新视角

International review of neurobiology Pub Date : 2026-01-01 Epub Date: 2026-02-12 DOI: 10.1016/bs.irn.2026.01.011

Vedika Jain, Sharda Bharti

{"title":"Environmental toxins, PFAS exposure, and brain metabolism: A new angle in Alzheimer's disease pathophysiology.","authors":"Vedika Jain, Sharda Bharti","doi":"10.1016/bs.irn.2026.01.011","DOIUrl":"10.1016/bs.irn.2026.01.011","url":null,"abstract":"Alzheimer's disease (AD) is a progressive neurodegenerative disease with a complicated cause and effect, usually associated with amyloid-β plaques, tau pathology, and neuroinflammation. Recent research indicates that changes in brain energy metabolism play a crucial role in the progression of AD. Additionally, persistent environmental toxins, particularly per- and polyfluoroalkyl substances (PFAS), have attracted considerable attention due to their widespread occurrence, ability to accumulate in living organisms, and neurotoxic effects. This chapter explores the connection between PFAS exposure and metabolic dysfunction in the brain as a potential new factor in the etiology of Alzheimer's disease. This study explored the potential impacts of PFAS on insulin signaling, lipid homeostasis, glucose metabolism, mitochondrial dynamics, and brain energy supply. The epidemiological associations between PFAS exposure and cognitive impairment are also examined, along with the mechanisms underlying oxidative stress, neuroinflammation, and dysregulation of metabolic systems. Finally, prevention, management, therapeutic approaches, and the research gap in PFAS-induced neurotoxicity are explored. Findings from this study emphasize the need to incorporate environmental toxicology into the Alzheimer's disease metabolic model for the sake of future treatment and preventive efforts.","PeriodicalId":94058,"journal":{"name":"International review of neurobiology","volume":"186 ","pages":"107-144"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148229810","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Invisible threats of microplastics induced toxicity: Oxidative and inflammatory pathways in the CNS and retina. 微塑料诱导毒性的无形威胁：中枢神经系统和视网膜的氧化和炎症途径。

International review of neurobiology Pub Date : 2026-01-01 Epub Date: 2026-01-28 DOI: 10.1016/bs.irn.2026.01.003

Avinash Shenoy, Taslima Akter Eva, Viswanthram Palanivel, Akanksha Salkar, Veer B Gupta, Nitin Chitranshi, Stuart L Graham, Vivek Gupta, Devaraj Basavarajappa

{"title":"Invisible threats of microplastics induced toxicity: Oxidative and inflammatory pathways in the CNS and retina.","authors":"Avinash Shenoy, Taslima Akter Eva, Viswanthram Palanivel, Akanksha Salkar, Veer B Gupta, Nitin Chitranshi, Stuart L Graham, Vivek Gupta, Devaraj Basavarajappa","doi":"10.1016/bs.irn.2026.01.003","DOIUrl":"10.1016/bs.irn.2026.01.003","url":null,"abstract":"The global spread of microplastics has become a serious public health concern. Once thought to be inert, microplastics are now recognized as biologically active agents capable of accumulating in the body and causing toxic effects across organ systems. This review summarizes current evidence on their oxidative and inflammatory effects in the central nervous system (CNS) and the eye. Studies show that microplastics can cross biological barriers such as the blood-brain barrier (BBB) and blood-retinal barrier (BRB), where they are taken up by cells, impair mitochondria, and trigger inflammation. Microplastics have been found in cerebrospinal fluid, brain tissue, and ocular structures, raising concern about their link to neurodegenerative and retinal diseases, including Alzheimer's, Parkinson's, macular degeneration, and other disorders. Mechanistic data indicate activation of NF-κB and TGF-β1 pathways, promotion of protein aggregation, and disruption of neural signaling. In the eye, microplastics have been linked to oxidative stress, corneal thinning, and photoreceptor damage. However, human studies are limited due to challenges in detecting tiny particles and lack of microplastic-free controls. Research is further hindered by inconsistent definitions, particle diversity, and non-physiological exposure models. We highlight the need for standardized methods, multi-omics tools, and long-term studies to better understand exposure impacts. Given the rise in neurological and ocular diseases, clarifying the role of microplastics is essential for effective public health strategies.","PeriodicalId":94058,"journal":{"name":"International review of neurobiology","volume":"186 ","pages":"25-47"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148229867","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Metabolic drivers of Alzheimer's disease pathogenesis: Impairments in glucose utilization, lipid homeostasis, and alternative substrate metabolism. 阿尔茨海默病发病机制的代谢驱动因素：葡萄糖利用、脂质稳态和替代底物代谢的损伤。

International review of neurobiology Pub Date : 2026-01-01 Epub Date: 2026-06-02 DOI: 10.1016/bs.irn.2026.05.019

Shiva Chaudhary, Shreya Verma, Vidisha Kumari, Meghana Tare

{"title":"Metabolic drivers of Alzheimer's disease pathogenesis: Impairments in glucose utilization, lipid homeostasis, and alternative substrate metabolism.","authors":"Shiva Chaudhary, Shreya Verma, Vidisha Kumari, Meghana Tare","doi":"10.1016/bs.irn.2026.05.019","DOIUrl":"10.1016/bs.irn.2026.05.019","url":null,"abstract":"Alzheimer's disease (AD) is one of the widespread neurodegenerative disorders, marked by the accumulation of amyloid-β plaques, neurofibrillary tangles of hyperphosphorylated Tau protein, and the gradual loss of neurons. While genetic and environmental factors have been associated with its onset, metabolic dysfunction has also been identified as one of the initial and most significant contributors its pathogenesis. The mitochondria are at the centre of this problem; their compromised function affects some crucial aspects of the neuronal health. Neurons have high energy demands so they are quite sensitive to the changes in the supply of the fuel. During AD pathogenesis, the loss of glucose transporters and the downregulation of key glycolytic enzymes deprives neurons of essential energy reserve. This metabolic dysregulation is further exacerbated by dysregulated lipid metabolism, pathological lipid droplet accumulation and ApoE4-driven failures in lipid trafficking which collectively leads to the oxidative stress, neuroinflammation, and Aβ aggregation. This situation is further aggravated by amino acid imbalances specifically within the glutamate-glutamine cycle. To counter this, ketone bodies have emerged as an alternative fuel source, capable of partially bypassing the impaired glucose oxidation while also demonstrating neuroprotective properties. Moreover, systemic metabolic disorders including type 2 diabetes mellitus, insulin resistance, obesity, and metabolic syndrome significantly amplify these deficits, functioning as major risk factors for AD onset and progression. Even the gut-brain axis plays a role in adding to the complexity. Taken together, these metabolic health changes not only reshape our understanding of AD but also open potential prospects for early detection through metabolic biomarkers and for novel therapeutic strategies targeting mitochondrial bioenergetics, glucose restoration, and ketogenic interventions.","PeriodicalId":94058,"journal":{"name":"International review of neurobiology","volume":"187 ","pages":"349-383"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148440444","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Metabolic therapeutic targets in Alzheimer's disease. 阿尔茨海默病代谢治疗靶点。

International review of neurobiology Pub Date : 2026-01-01 Epub Date: 2026-05-27 DOI: 10.1016/bs.irn.2026.05.010

Ignatius Raymond Peter L, Debojyoti Chatterjee, A Froilanmark Chrishone, Dileep Francis

{"title":"Metabolic therapeutic targets in Alzheimer's disease.","authors":"Ignatius Raymond Peter L, Debojyoti Chatterjee, A Froilanmark Chrishone, Dileep Francis","doi":"10.1016/bs.irn.2026.05.010","DOIUrl":"https://doi.org/10.1016/bs.irn.2026.05.010","url":null,"abstract":"Alzheimer's disease (AD) is increasingly recognized as a disorder marked not only by amyloid-β and tau pathology, but also by profound disturbances in brain energy metabolism that arise early in disease progression. Accumulating evidence indicates that impairments in glucose utilization, insulin signaling, and mitochondrial function precede neurodegeneration and contribute directly to synaptic failure and cognitive decline. This chapter presents a comprehensive overview of Alzheimer's disease through the lens of metabolic dysfunction, highlighting disrupted neuronal bioenergetics as a central and unifying feature of pathogenesis. We examine key metabolic pathways implicated in AD, including cerebral glucose hypometabolism, brain insulin resistance, impaired glycolysis, mitochondrial oxidative phosphorylation deficits, oxidative stress, and altered mitochondrial dynamics. The chapter further discusses therapeutic strategies aimed at restoring metabolic homeostasis, such as insulin sensitization, enhancement of glucose transport, activation of mitochondrial biogenesis, modulation of the electron transport chain, and the use of mitochondria-targeted antioxidants. In parallel, alternative energy approaches-including ketone metabolism, fatty acid oxidation, and pentose phosphate pathway activation-are explored as promising avenues to bypass glucose-dependent energy deficits and reinforce neuronal resilience. Emerging directions in metabolic therapeutics are also highlighted, including combination treatment strategies, NAD+-sirtuin and AMPK signaling, and the expanding role of the gut microbiome-brain metabolism axis. By integrating insights from experimental models, neuroimaging studies, and clinical trials, this chapter underscores the potential of metabolic interventions to enable early, disease-modifying strategies for Alzheimer's disease.","PeriodicalId":94058,"journal":{"name":"International review of neurobiology","volume":"188 ","pages":"1-32"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148703031","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Light on nonmotor symptoms in Parkinson's disease patients: The impact on quality of life. 帕金森病患者的非运动症状：对生活质量的影响

International review of neurobiology Pub Date : 2026-01-01 Epub Date: 2026-03-24 DOI: 10.1016/bs.irn.2026.01.017

Catherine Hamilton, Frank Nicklason

{"title":"Light on nonmotor symptoms in Parkinson's disease patients: The impact on quality of life.","authors":"Catherine Hamilton, Frank Nicklason","doi":"10.1016/bs.irn.2026.01.017","DOIUrl":"https://doi.org/10.1016/bs.irn.2026.01.017","url":null,"abstract":"Non-motor symptoms of Parkinson's disease contribute substantially to a reduction in health-related quality of life for patients and carers. Whilst some non-motor symptoms are dopamine-responsive, current treatment options for many are limited and often unsatisfactory. We report on early observations of non-motor symptoms in seven Parkinson's disease patients treated with daily transcranial red and near infrared photobiomodulation, over periods ranging from six to thirty-four months. Six of seven patients used home-made devices, including bucket light hats with unpulsed 630 nm-850 nm LED strips, and/or a commercial helmet delivering 40Hz-pulsed sequential 670 nm and 810 nm light. One patient used a home-made 660nm intra-nasal device. Progress was assessed by the subjects themselves, their spouse and attending clinicians. A range of non-motor symptoms appeared to improve during photobiomodulation treatment, especially fatigue, sleep, apathy, mood, anxiety, concentration/attention, anhedonia and olfaction. There were also improvements in motor signs and in the \"sense of self\". Photobiomodulation was well-tolerated, with no adverse effects and high patient compliance. In summary, daily photobiomodulation helped elicited and maintain improvements in otherwise difficult to treat symptoms.","PeriodicalId":94058,"journal":{"name":"International review of neurobiology","volume":"189 ","pages":"165-204"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148803602","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Blood biomarkers of oxidative stress and mitochondrial dysfunction in Parkinson's disease and Alzheimer's disease. 帕金森病和阿尔茨海默病中氧化应激和线粒体功能障碍的血液生物标志物。

International review of neurobiology Pub Date : 2026-01-01 Epub Date: 2026-07-28 DOI: 10.1016/bs.irn.2026.07.003

Deepak Kumar, Snehasish Shee, Ashok Kumar Datusalia, Shyam Sunder Sharma

{"title":"Blood biomarkers of oxidative stress and mitochondrial dysfunction in Parkinson's disease and Alzheimer's disease.","authors":"Deepak Kumar, Snehasish Shee, Ashok Kumar Datusalia, Shyam Sunder Sharma","doi":"10.1016/bs.irn.2026.07.003","DOIUrl":"https://doi.org/10.1016/bs.irn.2026.07.003","url":null,"abstract":"Parkinson's disease (PD) and Alzheimer's disease (AD) are the most prevalent neurodegenerative disorders and represent a major global health burden. Despite distinct clinical features, both diseases share key pathogenic mechanisms, particularly oxidative stress and mitochondrial dysfunction, which contribute to neuronal injury and progression. Current diagnostic approaches based on clinical evaluation, neuroimaging, and cerebrospinal fluid (CSF) biomarkers are invasive, costly, and often detect disease only after significant neuronal loss, underscoring the need for minimally invasive, pathway-relevant assays. This chapter reviews blood- and CSF-based biomarker assays reflecting oxidative stress and mitochondrial dysfunction in PD and AD, including lipid peroxidation products, antioxidant capacity, oxidative DNA damage markers, mitochondrial bioenergetic indices, and quality-control proteins. Emerging assay platforms targeting circulating cell-free mitochondrial DNA, mitochondrial-derived vesicles, extracellular vesicle cargo, and regulatory non-coding RNAs are also discussed. The mechanistic relevance of these biomarkers is examined in relation to impaired mitochondrial quality control, disrupted redox homeostasis, defective oxidative phosphorylation, and interactions with disease-defining proteins such as α-synuclein, amyloid-β, and phosphorylated tau. Collectively, these assay-based biomarkers hold promise for early detection, disease monitoring, and therapeutic stratification, although challenges related to standardization, sensitivity, and longitudinal validation remain.","PeriodicalId":94058,"journal":{"name":"International review of neurobiology","volume":"191 ","pages":"27-59"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149042821","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0