International review of neurobiology最新文献_第6页

Genetic and epigenetic complexity of Parkinson's disease: From dopamine pathways to estrogen interplay. 帕金森病的遗传和表观遗传复杂性：从多巴胺途径到雌激素的相互作用。

International review of neurobiology Pub Date : 2026-01-01 Epub Date: 2026-06-16 DOI: 10.1016/bs.irn.2026.05.021

Krishnan Deena, Lakshman Nathish, Er Antony Fenwick, Muthuswamy Karthi, Ramasamy Sivasamy

{"title":"Genetic and epigenetic complexity of Parkinson's disease: From dopamine pathways to estrogen interplay.","authors":"Krishnan Deena, Lakshman Nathish, Er Antony Fenwick, Muthuswamy Karthi, Ramasamy Sivasamy","doi":"10.1016/bs.irn.2026.05.021","DOIUrl":"10.1016/bs.irn.2026.05.021","url":null,"abstract":"Parkinson's disease (PD) is a progressive neurodegenerative disorder characterized by selective loss of nigrostriatal dopaminergic neurons and extensive circuit disruption, clinically presenting with motor deficits and many non-motor symptoms. Pathologically, PD is linked to the aggregation of α-synuclein, mitochondrial and lysosomal stress, and chronic neuroinflammation. This chapter integrates the genetic and epigenetic framework of Parkinson's disease, encompassing rare monogenic factors such as SNCA, LRRK2, GBA1, PINK1, and PRKN that converge on proteostasis disruption, compromised mitophagy, and lysosomal dysfunction, alongside polygenic susceptibility that may be exacerbated by environmental influences. Epigenetic dysregulation further influences susceptibility and disease progression: altered DNA methylation and hydroxymethylation at PD-relevant loci such as PARK7 and NR4A2, maladaptive histone regulation (including increased HDAC2/3 activity), and non-coding RNA networks (miR-7, HOTAIR, circSNCA) that modulate α-synuclein expression, inflammatory pathways, mitochondrial dynamics, and clearance mechanisms. Sex dimorphism is emphasized as a biologically significant modifier, with males exhibiting a higher incidence and accelerated progression in numerous cohorts, whereas estrogen-associated signaling may provide neuroprotection through increased dopamine biosynthesis, enhanced antioxidant capacity, and inhibition of microglial activation-effects that may diminish post-menopause. This chapter integrates recent advancements by linking mechanistic insights to translational potential, focusing on epigenetic biomarkers and disease-modifying techniques designed to restore lysosomal function, rectify dopamine processing, and strategically exploit hormone pathways.","PeriodicalId":94058,"journal":{"name":"International review of neurobiology","volume":"187 ","pages":"159-192"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148440426","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

Exploring the effect of red and near-infrared light on neurodegenerative disease: A focus on amyotrophic lateral sclerosis, Charcot's devastating disease of the motor system. 探讨红光和近红外光对神经退行性疾病的影响：以肌萎缩性侧索硬化症（Charcot's毁灭性运动系统疾病）为重点。

International review of neurobiology Pub Date : 2026-01-01 Epub Date: 2026-02-09 DOI: 10.1016/bs.irn.2026.01.013

Audrey Valverde, Hélène Blasco, Philippe Corcia, Olivier Herault, Pierre Magistretti, Laurent Herault, Corrado Cali, Luca Bartesaghi, Jonathan Stone, John Mitrofanis

{"title":"Exploring the effect of red and near-infrared light on neurodegenerative disease: A focus on amyotrophic lateral sclerosis, Charcot's devastating disease of the motor system.","authors":"Audrey Valverde, Hélène Blasco, Philippe Corcia, Olivier Herault, Pierre Magistretti, Laurent Herault, Corrado Cali, Luca Bartesaghi, Jonathan Stone, John Mitrofanis","doi":"10.1016/bs.irn.2026.01.013","DOIUrl":"https://doi.org/10.1016/bs.irn.2026.01.013","url":null,"abstract":"All neurodegenerative diseases, from Alzheimer's disease to amyotrophic lateral sclerosis (ALS), are characterised by a relentless and progressive degeneration of neurones. The degenerating neurones suffer from mitochondrial dysfunction, glutamate excitotoxicity, metabolic disorder and atypical protein aggregations; there is also widespread neuroinflammation and damage to the neurovascular unit across the nervous system. Unfortunately, there is no current treatment option that addresses all, if not many, of these striking abnormalities, one that stops or even slows the progression of the disease (ie neuroprotective). In this chapter, we explore the potential effectiveness of red and near infrared light (R-NIr) on ALS, one of the most devastating of all the neurodegenerative diseases. This condition impacts the motor system, from the cerebral cortex and brainstem to the spinal cord, as well as many skeletal muscles. Individuals suffer greatly and the survival period after onset of the first signs is often very short, averaging just over 2 years, as against 4-8 years in dementia. We outline two main reasons why R-NIr may have positive outcomes in ALS; (1) R-NIr has been shown to be neuroprotective in many other neurodegenerative diseases, improving cell function and survival, and; (2) unlike many other treatments attempted previously, R-NIr addresses many, if not all features of pathology associated with ALS. In summary, we suggest that R-NIr, with its multi-modal effect, could be a valuable treatment option for patients with ALS, particularly if the treatment is started early, before the development of excessive cellular damage.","PeriodicalId":94058,"journal":{"name":"International review of neurobiology","volume":"189 ","pages":"205-236"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148803568","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

Cognitive enhancement through transcranial infrared laser stimulation: Insights from our research. 经颅红外激光刺激增强认知能力：来自我们研究的见解。

International review of neurobiology Pub Date : 2026-01-01 Epub Date: 2026-02-16 DOI: 10.1016/bs.irn.2026.01.015

Francisco Gonzalez-Lima

{"title":"Cognitive enhancement through transcranial infrared laser stimulation: Insights from our research.","authors":"Francisco Gonzalez-Lima","doi":"10.1016/bs.irn.2026.01.015","DOIUrl":"https://doi.org/10.1016/bs.irn.2026.01.015","url":null,"abstract":"Photobiomodulation (PBM), particularly transcranial infrared laser stimulation (TILS), has emerged as a promising non-invasive method to enhance cognitive functions in healthy individuals and those with neuropsychiatric or neurodevelopmental disorders. Conventional pharmacotherapy often fails to improve cognition effectively and can produce adverse effects. In contrast, TILS of the prefrontal cortex modulates brain energy metabolism through mechanisms like mitochondrial upregulation, improved cerebral oxygenation, and enhanced neuroplasticity. This chapter synthesizes findings and insights from human studies led by our group to evaluate TILS mechanisms and efficacy in cognitive enhancement. Examples of our research include studies on healthy young and older adults, and patients with neurocognitive disorder, bipolar disorder, depression, ADHD and autism. The evidence highlights TILS as a safe and physiologically grounded approach with wide-ranging applications. To maximize its potential, future research should explore optimal dosing, individual differences in response, long-term outcomes, and the use of neuroimaging biomarkers for personalized treatment strategies.","PeriodicalId":94058,"journal":{"name":"International review of neurobiology","volume":"189 ","pages":"141-163"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148803630","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

Photobiomodulation for traumatic brain injury. 外伤性脑损伤的光生物调节。

International review of neurobiology Pub Date : 2026-01-01 Epub Date: 2026-02-19 DOI: 10.1016/bs.irn.2026.01.016

Michael R Hamblin

{"title":"Photobiomodulation for traumatic brain injury.","authors":"Michael R Hamblin","doi":"10.1016/bs.irn.2026.01.016","DOIUrl":"https://doi.org/10.1016/bs.irn.2026.01.016","url":null,"abstract":"There is a notable lack of therapeutic alternatives for what is fast becoming a global epidemic of traumatic brain injury (TBI). Photobiomodulation (PBM) employs red or near-infrared (NIR) light (600-1300 nm) from lasers or LEDs to stimulate healing, protect tissue from dying, increase mitochondrial function, improve blood flow and tissue oxygenation. PBM can also act to reduce swelling, increase antioxidants, decrease inflammation, protect against apoptosis, and modulate microglial activation state. All these mechanisms of action strongly suggest that PBM delivered to the head should be beneficial in cases of both acute and chronic TBI. Many studies in small animal models of acute TBI have found positive effects on neurological function, learning and memory, and reduced inflammation and cell death in the brain. There is evidence that PBM can help the brain to repair itself by stimulating neurogenesis, upregulating BDNF synthesis, and encouraging synaptogenesis. Clinical studies have been conducted in patients suffering from acute TBI and the chronic effects of TBI. There have been reports of improvements in executive function, working memory, and improved sleep. Functional magnetic resonance imaging has shown modulation of the activation in intrinsic brain networks likely to be damaged in TBI (default mode network and salience network).","PeriodicalId":94058,"journal":{"name":"International review of neurobiology","volume":"189 ","pages":"105-139"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148803724","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

Roadmap for functional neurological disorders: Shared circuitry and future directions. 功能性神经疾病的路线图：共享电路和未来方向。

International review of neurobiology Pub Date : 2026-01-01 Epub Date: 2026-08-26 DOI: 10.1016/bs.irn.2026.08.014

D Dilara Ertenu, Apurva Papolu, Julio Quezada, Sneha Jadhav, Shannon Dean, Jay A Salpekar

引用次数: 0

GFAP and the genetic code of astrocyte activation in Alzheimer's disease. GFAP与阿尔茨海默病星形细胞激活的遗传密码。

International review of neurobiology Pub Date : 2026-01-01 Epub Date: 2026-02-07 DOI: 10.1016/bs.irn.2026.01.007

Riddhi Upadhyay, Thanga Balaji Srinivasan, R Umapriya, Vani Chandrapragasam, Murugan Sevanan

{"title":"GFAP and the genetic code of astrocyte activation in Alzheimer's disease.","authors":"Riddhi Upadhyay, Thanga Balaji Srinivasan, R Umapriya, Vani Chandrapragasam, Murugan Sevanan","doi":"10.1016/bs.irn.2026.01.007","DOIUrl":"https://doi.org/10.1016/bs.irn.2026.01.007","url":null,"abstract":"Astrocytes play a crucial role in controlling homeostasis of the central nervous system (CNS), synapse, metabolism and neuroimmune communications. The growing body of evidence indicates that astrocyte dysfunction plays the leading role in the pathogenesis of Alzheimer's disease (AD). Reactive astrogliosis, characterised by cell hypertrophy, transcriptional reprogramming, and elevated glial fibrillary acidic protein (GFAP) expression, arises early in response to amyloid-β accumulation, neuroinflammation, and blood-brain barrier (BBB) disruption. Transcriptional, epigenetic and inflammatory signalling, including JAK/STAT3, NF-KB, MAPK and non-coding RNAs, control the expression of GFAP, which is a structural intermediate filament protein. High GFAP shows activation of astrocytes and a part of disrupted neuronal support, glutamate imbalance, oxidative distress and defective glymphatic clearance. Consequently, GFAP is an efficient biomarker in CSF, plasma, and saliva, which is associated with amyloid pathology, cognitive impairment, and AD. The knowledge of the astrocyte responses to GFAP can be used to extract significant information about AD mechanisms and find opportunities to identify diagnosis, prognosis and therapy.","PeriodicalId":94058,"journal":{"name":"International review of neurobiology","volume":"191 ","pages":"113-144"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149042890","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

Redox bioenergetics of neuronal senescence in Alzheimer's disease. 阿尔茨海默病中神经元衰老的氧化还原生物能量学。

International review of neurobiology Pub Date : 2026-01-01 Epub Date: 2026-05-22 DOI: 10.1016/bs.irn.2026.05.002

Erdem Atasever, Şeydanur Turgut, Gülnur Andican, Ufuk Çakatay

{"title":"Redox bioenergetics of neuronal senescence in Alzheimer's disease.","authors":"Erdem Atasever, Şeydanur Turgut, Gülnur Andican, Ufuk Çakatay","doi":"10.1016/bs.irn.2026.05.002","DOIUrl":"10.1016/bs.irn.2026.05.002","url":null,"abstract":"Neuronal aging is a key but often overlooked part of Alzheimer's disease. It links age-related loss of cellular energy to long-lasting problems in neuronal function. Even though neurons don't usually divide, ongoing stressors like oxidative damage, mitochondrial dysfunction, and problems with protein handling can make them appear old. This is seen as lasting DNA damage, calcium imbalance, and the release of substances that cause inflammation. These changes are closely tied to loss of balance in cell energy and redox function. Mitochondria, which make most neurons' energy, are both a main source and a target for reactive oxygen species (ROS). Long-term redox imbalance damages energy production, lowers NAD+, and disrupts SIRT1 regulation. Eventually, this leads to energy failure and loss of synaptic function. In AD, excessive ROS production and redox imbalances interact with amyloid-β toxicity, tau hyperphosphorylation, and metal ion disturbances. This convergence increases mitochondrial damage and fragmentation. When mitophagy is impaired, dysfunctional mitochondria are not removed, leading to ROS accumulation that further damages cellular structures and reinforces oxidative stress. This forms a self-perpetuating cycle that accelerates neuronal aging and neurodegeneration. Notably, research shows that energy failure and redox imbalance often precede the formation of amyloid plaques and tangles, suggesting that these mechanisms may initiate disease onset. This chapter reviews core mechanisms underlying redox signaling and neuronal senescence. It details how altered mitochondrial function disrupts neuronal energy homeostasis and triggers a cascade of molecular events that underlie Alzheimer's disease. The proposed framework connects redox failure, cellular senescence, and neurodegeneration as interdependent drivers of disease progression.","PeriodicalId":94058,"journal":{"name":"International review of neurobiology","volume":"186 ","pages":"49-74"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148229813","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

Activation of Nrf2 neuroprotective pathways for treatment of Parkinson's disease: A state of art review. 激活Nrf2神经保护通路治疗帕金森病：最新进展

International review of neurobiology Pub Date : 2026-01-01 Epub Date: 2026-02-03 DOI: 10.1016/bs.irn.2026.01.006

Anastasia Bougea

{"title":"Activation of Nrf2 neuroprotective pathways for treatment of Parkinson's disease: A state of art review.","authors":"Anastasia Bougea","doi":"10.1016/bs.irn.2026.01.006","DOIUrl":"https://doi.org/10.1016/bs.irn.2026.01.006","url":null,"abstract":"The regulation of Nuclear Factor-Erythroid 2 Like 2 (NRF2) signaling has been shown to be a promising strategy to modulate the progression of the neurodegeneration associated to Parkinson's Disease (PD). Aim of this review is to update the knowledge of Nrf2 as neuroprotective agent of PD. Activation of Nrf2, a transcription factor that regulates the expression of antioxidant and cytoprotective genes, has emerged as a promising therapeutic strategy for PD. Nrf2 is a master regulator of the cellular antioxidant response and is responsible for activating the expression of genes that encode antioxidant enzymes such as superoxidedismutase, catalase, and glutathione peroxidase. Pharmacological agents such as sulforaphane, curcumin, and resveratrol have been shown to activate Nrf2 and upregulate the expression of antioxidant genes in preclinical PD models. Clinical trials are currently underway to evaluate the efficacy of these pharmacological agents in patients with PD. While the neuroprotective role of Nrf2 in PD holds great promise for the development of novel therapies, there are several challenges and limitations that need to be addressed in order to harness the full potential of this pathway in the clinic. Overcoming these obstacles will require interdisciplinary collaborations, innovative research approaches, and a greater understanding of the complex pathophysiology of PD. By addressing these challenges, we can move closer to developing effective neuroprotective therapies that can slow or stop the progression of PD and improve the quality of life for patients with this devastating disease.","PeriodicalId":94058,"journal":{"name":"International review of neurobiology","volume":"187 ","pages":"331-348"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148440345","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

Metallospecies and their biological functions in Alzheimer's disease. 金属物种及其在阿尔茨海默病中的生物学功能。

International review of neurobiology Pub Date : 2026-01-01 Epub Date: 2026-03-12 DOI: 10.1016/bs.irn.2026.02.005

Marcos V de S Pereira, Jemmyson R de Jesus

引用次数: 0

Non-invasive brain stimulation to prevent aging-related diseases: What does photobiomodulation offer compared with other methods. 无创脑刺激预防衰老相关疾病：与其他方法相比，光生物调节提供了什么？

International review of neurobiology Pub Date : 2026-01-01 Epub Date: 2026-03-20 DOI: 10.1016/bs.irn.2026.03.001

Marjorie Dole

{"title":"Non-invasive brain stimulation to prevent aging-related diseases: What does photobiomodulation offer compared with other methods.","authors":"Marjorie Dole","doi":"10.1016/bs.irn.2026.03.001","DOIUrl":"https://doi.org/10.1016/bs.irn.2026.03.001","url":null,"abstract":"The issue of the maintenance of cognitive and brain health across ageing is a striking concern in our ageing societies. Non-invasive brain stimulation methods have been proposed as tools to fight against various neurological pathologies and to this aim, could also be used against age-related brain changes. In this chapter, we examine the potential of transcranial photobiomodulation (tPBM), in comparison with other neurostimulation methods, to improve brain function and protect neurons. In particular, it is hypothesised that the double action of tPBM - both on neuronal function and at a more systemic level, particularly on neuroinflammation, is a particular strength of tPBM relatively to the other techniques. The main challenge faced by the tPBM research community include the question of quantifying more precisely the energy quantity reaching the targeted regions; to this aim, computational modelling of light propagation can help defining more precisely the dosing parameters. Another challenge is related to the standardisation of the stimulation protocols, and is shared by all the neurostimulation methods examined in this review.","PeriodicalId":94058,"journal":{"name":"International review of neurobiology","volume":"189 ","pages":"1-33"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148803599","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