International review of neurobiology最新文献

{"title":"Remote photobiomodulation: A systemic approach to neuroprotection.","authors":"Daniel M Johnstone, Luke C Gordon","doi":"10.1016/bs.irn.2026.01.018","DOIUrl":"https://doi.org/10.1016/bs.irn.2026.01.018","url":null,"abstract":"<p><p>Photobiomodulation (PBM) therapy is rapidly gaining traction in clinical settings, with an expanding body of clinical trials investigating its efficacy as a non-invasive, non-pharmacological intervention to enhance tissue resilience and mitigate disease pathology. Among the most promising developments is the application of PBM in treating neurological conditions, offering new hope to millions affected by these intractable diseases. The prevailing approach in this field is transcranial PBM, where light is administered directly to the head under the assumption that photons can penetrate the scalp and skull to stimulate neural cells relevant to the targeted condition. Encouragingly, this approach has yielded positive outcomes in many studies, reinforcing the assumption and shaping subsequent research. However, in the enthusiasm to pioneer these potentially transformative therapies, a critical aspect is often overlooked: PBM can also exert indirect, systemic effects. Delivering therapeutic doses of light to one part of the body can produce pronounced benefits in distal tissues - a phenomenon supported by numerous animal experiments and emerging human data. Drawing a parallel to remote ischemic conditioning - where brief, controlled ischemia in a limb can induce resilience in vital organs like the heart and brain - we introduced the term \"remote photobiomodulation\" to describe this modality. This Chapter explores the concept of remote photobiomodulation: its origins, proposed mechanisms, and its relationship to transcranial PBM. By examining current evidence and theoretical frameworks, we aim to demonstrate why this underappreciated approach warrants deeper investigation and how it could broaden the therapeutic landscape for neurological disorders.</p>","PeriodicalId":94058,"journal":{"name":"International review of neurobiology","volume":"189 ","pages":"35-70"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148803727","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}

{"title":"Energetic crisis, mitochondrial vulnerability and disruption of lactate shuttle in Alzheimer's disease.","authors":"Gowsika Baskar, Mahesh Kandasamy","doi":"10.1016/bs.irn.2026.05.012","DOIUrl":"https://doi.org/10.1016/bs.irn.2026.05.012","url":null,"abstract":"<p><p>Alzheimer's disease (AD) has traditionally been characterized by amyloid-beta (Aβ) plaques and neurofibrillary tangles. Emerging evidence reveals that metabolic dysfunction represents a key pathological feature central to disease progression. Mitochondrial dysfunction in AD leads to impaired electron transport chain activity and reduced level of adenosine triphosphate (ATP) synthesis, preceding neurodegeneration and structural abnormalities in cognitive centres of the brain. Early glucose hypometabolism and lactate deprivation or interference with their utilization represent a primary bioenergetic failure driving mitochondrial dysfunction and neuroinflammation prior to the clinical manifestation of AD. While the brain relies on lactate as a prominent energy substrate, astrocytic metabolic defects lead to impaired neuronal energy homeostasis, thereby promoting neurodegeneration. In turn, this metabolic uncoupling could also be associated with defects in regenerative mechanisms by impairing adult neurogenesis in the hippocampus due to energy deprivation, accounting for memory deficits. This chapter discusses the evidence for the energetic crisis in AD, focusing on the disruption of the astrocyte-neuron lactate shuttle (ANLS), hypometabolism of glucose, and mitochondrial vulnerability, as interconnected pathogenic mechanisms. We emphasise cerebral bioenergetic metabolic failure as a central driver of cognitive decline, arising from irreversible reactive gliosis and neuroblastosis mechanisms and highlight various therapeutic options, including restoration of ANLS to mitigate the pathogenesis and memory loss in AD.</p>","PeriodicalId":94058,"journal":{"name":"International review of neurobiology","volume":"188 ","pages":"67-89"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148702997","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}

{"title":"The Tau-mitochondria connection and its impact on cellular energy metabolism in Alzheimer's disease.","authors":"Abhay Kumar Singh, Supraja M R, Amal P S, Senthilkumar Krishnamoorthi, Ashok Iyaswamy, Siva Sundara Kumar Durairajan","doi":"10.1016/bs.irn.2026.06.002","DOIUrl":"https://doi.org/10.1016/bs.irn.2026.06.002","url":null,"abstract":"<p><p>Alzheimer's disease (AD) is a complex multifactorial neurodegenerative disease process resulting in progressive cognitive deterioration and synaptic dysfunction. The primary research approach in AD has traditionally focused on amyloid- pathology however an increasingly evidence suggests that tau protein is a key mediator of neuronal damage via a direct action on mitochondrial bioenergetics. In this chapter we look at the nature of the tau-mitochondrial interface, and propose a paradigm of tau-induced energy failure in AD. Physiologically tau provides stability to the microtubules and is involved in transport mechanisms within cells. In AD, tau is excessively post-translationally modified hyperphosphorylated and truncated tau species form toxic oligomers that incorrectly translocate to mitochondria, interacting pathologically with critical proteins such as voltage-dependent anion channel 1 (VDAC1) and adenine nucleotide translocase (ANT), impeding the mitochondrial ATP/ADP exchange and reducing oxidative phosphorylation efficiency. Tau also further damages mitochondria by excessive fission, inhibition of axonal transport and Inhibition of mitophagy by interrupting PINK1-Parkin signaling. In turn, the build-up of dysfunctional mitochondria leads to ROS production, mtDNA damage and calcium imbalance creating a vicious cycle toward oxidative stress and tau pathology. At the cellular level they cause an energy depletion of the synapse and at the systems level cause glucose hypometabolism and activation of neuroinflammation. The chapter additionally discusses novel therapeutic approaches that target both tau and mitochondrial abnormalities, namely antisense oligonucleotides (ASO), mitochondria targeted compounds and mitophagy modifiers, stressing that it would be more effective to utilize a cocktail of these inhibitors. As a whole, in the context of decreased bioenergetics, the tau-mitochondria axis is an important factor to consider in the successful treatment of AD.</p>","PeriodicalId":94058,"journal":{"name":"International review of neurobiology","volume":"188 ","pages":"299-361"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148703115","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}

{"title":"Peripheral manifestations of nigrostriatal neurodegeneration in Parkinson's disease.","authors":"Jerly Helan Mary Joseph, Mahesh Kandasamy","doi":"10.1016/bs.irn.2026.06.003","DOIUrl":"https://doi.org/10.1016/bs.irn.2026.06.003","url":null,"abstract":"<p><p>Parkinson's disease (PD), a neurodegenerative condition, is characterized by dysfunction of dopaminergic pathways leading to prominent movement and non-movement disorders, including cognitive decline and memory loss. The clinical symptoms of PD progressively worsen over time, and there is no precise confirmatory laboratory test for early diagnosis. Although abnormal neuroimaging signatures and changes in cerebrospinal fluid represent significant diagnostic value, their limited accessibility, high cost, and invasiveness restrict their clinical applications. As a potential alternative, blood-borne biomarkers represent a feasible and adaptable indicator, as blood sample collection is minimally invasive, cost-effective, suitable for large-scale populations, and permits repeated sampling for disease diagnosis and monitoring. Notably, altered cellular and biochemical composition of circulating blood can reflect pathogenic changes involved in many diseases, including PD. Abnormal levels of circulating α-synuclein, factors related to chronic inflammation, oxidative damage, impaired mitochondrial function, and neuronal injury in the blood are considered potential biomarkers of PD. This chapter provides an overview of blood biomarkers that aid in predicting the pathogenic state of PD. Various categories of biomarkers, including protein aggregates, inflammation-related factors, oxidative stress markers, metabolomic and lipidomic signatures, genetic and epigenetic status, and PD-related exosomes are discussed. These blood biomarkers could serve as a diagnostic tool for PD and may provide predictive measures of disease outcomes, as well as neurobiological correlates of brain changes, thereby offering valuable indications for treatment strategies.</p>","PeriodicalId":94058,"journal":{"name":"International review of neurobiology","volume":"191 ","pages":"487-507"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149043016","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}

{"title":"Mitochondrial rescue in Alzheimer's disease: Exploring marine-derived compounds for brain metabolism regulation.","authors":"Periyasamy Vijayalakshmi, Asha Monica Alex, Saravanan Muthupandian, Deepali Desai, Mani Jayaprakashvel, Sanjeev Kumar Singh, Chandrabose Selvaraj","doi":"10.1016/bs.irn.2026.02.003","DOIUrl":"10.1016/bs.irn.2026.02.003","url":null,"abstract":"<p><p>Alzheimer Disease (AD) is a progressive neurodegenerative condition because of its cognitive impairment, synaptic impairment and loss of neurons. Mitochondrial dysfunction has become one of the key factors of disease development and progression and one of the several pathological characteristics of AD. The mitochondrial cascade hypothesis suggests that amyloid-β and tau pathology depend on age-related mitochondrial impairment, which is an earlier and faster process and provokes neurodegeneration. Mitochondria play critical roles in metabolism of neuronal energy, maintenance of calcium and regulation of reactive oxygen species (ROS); their dysfunction leads to bioenergetic impairment, oxidative stress, and synaptic failure. Marine ecosystems constitute an unexampled source of bioactive therapeutic-related compounds of structural diversity. Marine-derived compounds (MDCs) such as polysaccharides, oligosaccharides, polyphenols, lipids, alkaloids and peptides have antioxidant, anti-inflammatory, and neuroprotective effects. Recent reports indicate that MDCs can salvage mitochondrial performance by increasing biogenesis, restoring dynamics (fusion fission balance), modulating metabolism and improving mitochondrial quality control. The compounds also control metabolism of the brain affecting the use of glucose, lipid metabolism, and synthesis of neurotransmitters. This chapter clearly discusses the insights of marine-derived compounds as a mitochondrial rescue in AD. We stress their chemical heterogeneity, biologic activity and mode of action including the regulation of signaling pathways, e.g. AMPK, PI3K/Akt, MAPK, and SIRT1. We also talk about their effects on synaptic plasticity, neuronal survival and cognitive function. Lastly, we have also find the research gaps, research challenges, and perspectives and highlight the necessity of translational research, better bioavailability, and sustainable harvesting plans. Marine-derived compounds as a group are one of the brightest prospects in AD therapeutics by providing innovative methods to restore the state of mitochondria and control the metabolism in the brain.</p>","PeriodicalId":94058,"journal":{"name":"International review of neurobiology","volume":"186 ","pages":"187-213"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148229852","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}

{"title":"Crosstalk in Alzheimer's-delirium nexus: Molecular mechanisms and therapeutic repurposing.","authors":"Saleem Iqbal, Bairong Shen","doi":"10.1016/bs.irn.2026.01.004","DOIUrl":"https://doi.org/10.1016/bs.irn.2026.01.004","url":null,"abstract":"<p><p>Alzheimer's disease (AD) and delirium, though distinct in clinical tempo, converge mechanistically at the intersection of neurovascular dysfunction, glial activation, and metabolic collapse. This chapter explores the integrative framework of neurovascular-glia crosstalk, emphasizing how endothelial injury, astrocytic reactivity, and microglial hyperactivation collectively undermine brain energy metabolism. We highlight evidence that blood-brain barrier^c (BBB) breakdown, mitochondrial insufficiency, and oxidative stress establish a \"metabolic vulnerability state\" predisposing the AD brain to delirium. Single-cell and transcriptomic analyses delineate shared molecular circuits involving MAPK, TP53, APOE, and δ-secretase (LGMN)-the latter regulated by disease-relevant miRNAs such as miR-124 and miR-146a. These networks couple neuroinflammation with impaired energy dynamics, bridging chronic neurodegeneration and acute encephalopathic stress. We further discuss how tyrosine-kinase signaling, serotonergic dysregulation, and glial-vascular miscommunication coalesce into a unified pathophysiological axis. Therapeutic repurposing strategies-ranging from tyrosine kinase inhibitors (nilotinib, imatinib) to metabolic modulators (metformin, pioglitazone)-offer promising cross-disease interventions. Finally, we underscore the transformative role of artificial intelligence (AI) and large language models (LLMs) in accelerating drug repurposing through integrative omics and pathway-based reasoning. Together, these advances redefine the AD-delirium nexus as a systems-level disorder of energy and communication, opening translational avenues for precision therapeutics that restore neurovascular balance and cognitive resilience.</p>","PeriodicalId":94058,"journal":{"name":"International review of neurobiology","volume":"187 ","pages":"133-157"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148440390","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}

{"title":"Glial molecular signatures as a liquid biopsy marker in Alzheimer's disease diagnosis.","authors":"Kunal Yadav, Sachin Suresh Tiwari","doi":"10.1016/bs.irn.2026.02.001","DOIUrl":"10.1016/bs.irn.2026.02.001","url":null,"abstract":"<p><p>Alzheimer's disease (AD) is a neurodegenerative condition that is characterized by the misfolding of Amyloid Precursor Protein, hyperphosphorylation of tau protein, and neuroinflammation. This leads to the formation of extracellular senile amyloid beta plaque and neurofibrillary tangles in neurons, leading to neuronal degeneration. AD is the biggest cause of dementia globally. Currently, no therapies are available for AD and early diagnosis of the disease is a challenge. The most common fluid biomarkers for AD are: p-tau181, p-tau231, p-tau217, Aβ42/Aβ40 ratio, Neurogranin (Ng), Alzheimer's-associated neuronal thread protein (AD7c-NTP). All these biomarkers are detected in Blood, CSF, Saliva, and Urine with the help of different assays, PET scan, and MRI Imaging. These biomarkers are of neuronal origin and indicate neuronal stress. Brain also contains glial cells along with the neurons, which interact with the neurons in health and disease conditions. These glial cells also release molecules in disease induced stress. These markers can be used for early and differential diagnosis of AD and other dementia conditions. Studies also show that these glia biomarkers are released decades before the actual neuron degeneration begins. In this review, we will discuss these glial cells biomarkers identified in liquid biopsy for AD detection and progression.</p>","PeriodicalId":94058,"journal":{"name":"International review of neurobiology","volume":"187 ","pages":"385-411"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148440396","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}

{"title":"Preface.","authors":"Anna Rostedt Punga, Carolina Barnett-Tapia","doi":"10.1016/S0074-7742(25)00122-9","DOIUrl":"https://doi.org/10.1016/S0074-7742(25)00122-9","url":null,"abstract":"","PeriodicalId":94058,"journal":{"name":"International review of neurobiology","volume":"183 ","pages":"xiii"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145310363","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}

{"title":"Maternal exposure to rubella infection elevates risk of congenital rubella syndrome (CRS).","authors":"Sasikumar Pitchaikani, Pothiaraj Govindan, Harshavardhan Shakila","doi":"10.1016/bs.irn.2025.04.008","DOIUrl":"10.1016/bs.irn.2025.04.008","url":null,"abstract":"<p><p>The rise in neurodevelopmental disorders linked to maternal viral infections, particularly during the first and second trimesters of pregnancy, is concerning. Rubella, a contagious viral disease, primarily affects children and young adults, presenting as a rash and mild fever. It can also cause symptoms such as a swollen spleen, blueberry muffin skin spots, small head circumference, meningoencephalitis, developmental delays, and jaundice. When contracted in the first trimester, rubella can lead to severe birth defects or fetal death, with the risk declining after 20 weeks. Congenital rubella syndrome (CRS) caused by rubella's teratogenic effects, remains a major public health challenge, with an estimated 100,000 CRS cases annually. Following the approval of the rubella vaccine in 1969, significant strides have been made to reduce CRS and rubella incidences. This chapter provides disease management, prevention strategies, treatment options, and immunological response, focusing on prognosis and insights from current research on rubella and CRS.</p>","PeriodicalId":94058,"journal":{"name":"International review of neurobiology","volume":"180 ","pages":"501-526"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144144435","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}

{"title":"Effects of psychedelics on human oscillatory brain activity.","authors":"Kate Godfrey, Lisa X Luan, Christopher Timmermann","doi":"10.1016/bs.irn.2025.04.012","DOIUrl":"10.1016/bs.irn.2025.04.012","url":null,"abstract":"<p><p>This chapter reviews the effects of classic psychedelics on human oscillatory brain activity, as measured by resting-state electroencephalography (EEG) and magnetoencephalography (MEG). Across moderate to high doses of LSD, psilocybin, ayahuasca, and DMT, a consistent reduction in alpha power (8-13 Hz) emerges, particularly in occipital regions. Below 30 Hz, desynchronization is typical, although DMT can preserve or even increase delta/theta activity, possibly reflecting its immersive, immersive visual phenomenology. Complementing these spectral findings, measures of signal diversity (e.g., Lempel-Ziv complexity) reliably increase during psychedelic states, indicating a more variable and unpredictable pattern of neural firing. Retrospective subjective ratings of the psychedelic experience often fail to align consistently with M/EEG changes, possibly because fleeting, key experiences are obscured by data averaging or recording short segments of a long experience. In contrast, real-time evaluations of subjective intensity and plasma levels robustly covary with changes in spectral power and complexity, highlighting the potential for objective, real-time EEG biomarkers of drug activity. Limited research on functional connectivity and cortical travelling waves suggest that directed, top-down control may decrease while bottom-up signaling increases, indicating a transient reversal of typical hierarchical organization, though replications are warrented. Future work should implement more unified methodological approaches, alongside high-resolution behavioral sampling, to further our understanding of how these altered brain dynamics give rise to the distinctive qualities of the psychedelic experience. Notably, EEG has yet to be evaluated in clinical studies, and future work should aim to explore the relationship between acute EEG changes and clinical responses to psychedelic therapy.</p>","PeriodicalId":94058,"journal":{"name":"International review of neurobiology","volume":"181 ","pages":"171-202"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144337316","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}