International Review Of Neurobiology[JOURNAL]
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200 papers
Glutamate-Glutamine metabolism and transport, implications in Parkinson's disease.
Raghu R, Chinnathambi S
Int Rev Neurobiol · 2026 · PMID 42276624 · Publisher ↗
Parkinson's disease (PD) is a common neurodegenerative condition caused by the selective loss of dopaminergic neurons in the substantia nigra (SN) and the formation of Lewy bodies due to α-Synuclein (α-Syn) aggregation i...
Parkinson's disease (PD) is a common neurodegenerative condition caused by the selective loss of dopaminergic neurons in the substantia nigra (SN) and the formation of Lewy bodies due to α-Synuclein (α-Syn) aggregation in the midbrain. Glutamate (Glu) is an excitatory neurotransmitter that plays an important role in the normal functioning of the basal ganglia circuit. It has been shown recently that Glu receptors are involved in the regulation of neurotransmitter release, neuron excitability and long-term plasticity and the altered mechanisms in Parkinson's disease. Glu is produced in the cytoplasm and is packed and stored in vesicles by vesicular glutamate transporters (VGLUTs). Following its release into the synaptic cleft, it exerts its physiological effects by binding to ligand-gated ion channels (ionotropic glutamate receptors (iGluRs)) and G-protein coupled receptors (metabotropic glutamate receptors (mGluRs)). Lack of glutamate reuptake or enzymatic decomposition results in Glu accumulation at the synapse, causing excitotoxicity. This is prevented by excitatory amino acid transporters (EAATs), which reabsorb the extracellular Glu. Furthermore, elevated extracellular glutamate levels prevent cystine uptake, which results in oxidative glutamate toxicity and glutathione depletion. Currently, there are no effective treatments for Parkinson's disease, as most of the drugs that exist have greater side effects, like dyskinesia. Hence, the identification of new potential drug targets is an important factor for improving the therapeutic strategies to combat the disease. Therefore, in this review, we aim to discuss about characteristics of these receptors and transporters and highlight the neuroprotective effects and pharmacological manifestations in Parkinson's disease.
Redox bioenergetics of neuronal senescence in Alzheimer's disease.
Atasever E, Turgut Ş, Andican G … +1 more , Çakatay U
Int Rev Neurobiol · 2026 · PMID 42276623 · Publisher ↗
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 stre...
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.
Neurovascular coupling and energy substrate delivery in Alzheimer's disease.
Malviya S, Saha D, Kamble A … +3 more , Singh DR, Sundaram SM, Devanathan V
Int Rev Neurobiol · 2026 · PMID 42276622 · Publisher ↗
The brain has exceptionally high metabolic demands and depends on a continuous supply of oxygen and glucose to maintain neuronal activity and cognitive function. Despite accounting for only about 2 % of body weight, it c...
The brain has exceptionally high metabolic demands and depends on a continuous supply of oxygen and glucose to maintain neuronal activity and cognitive function. Despite accounting for only about 2 % of body weight, it consumes more than 20 % of the body's energy. This demand is met through tightly regulated cerebral blood flow mediated by neurovascular coupling (NVC), a process that links neuronal activity with local vascular responses. The cellular components responsible for this regulation including neurons, astrocytes, endothelial cells, pericytes, and vascular smooth muscle cells form the neurovascular unit (NVU), which maintains blood brain barrier (BBB) integrity, metabolic homeostasis, and efficient substrate delivery. Increasing evidence suggests that disruption of neurovascular and metabolic regulation is an early and critical contributor to Alzheimer's disease (AD). Impairment of NVU function leads to reduced cerebral blood flow, endothelial dysfunction, pericyte loss, and breakdown of the BBB. These vascular changes compromise the delivery of oxygen and glucose, resulting in cerebral hypometabolism that often precedes classical pathological hallmarks such as amyloid-β plaques and tau neurofibrillary tangles. Alterations in glucose transport across the BBB, particularly reduced expression of the GLUT1 transporter, further exacerbate neuronal energy deficits. Disturbances in lactate metabolism and mitochondrial dysfunction also contribute to oxidative stress and progressive neurodegeneration. Understanding the interaction between neurovascular dysfunction, impaired brain metabolism, and AD pathology provides important insight into disease progression. Therapeutic strategies aimed at restoring vascular function, improving metabolic substrate delivery, and enhancing neuronal energy metabolism may offer promising avenues for early intervention in AD.
From metals to mitochondria: Linking trace elements to energy crisis in Alzheimer's disease.
Medeiros CMDS, da Conceição RSV, Mendes MKA … +2 more , de Jesus JR, Lopes Júnior CA
Int Rev Neurobiol · 2026 · PMID 42276621 · Publisher ↗
Alzheimer's disease (AD) is a chronic, progressive neurodegenerative disorder and the most common cause of dementia, with a high incidence in the global population, especially in the elderly. AD presents a complex pathog...
Alzheimer's disease (AD) is a chronic, progressive neurodegenerative disorder and the most common cause of dementia, with a high incidence in the global population, especially in the elderly. AD presents a complex pathogenesis including protein misfolding and aggregation, neuroinflammation, oxidative stress, mitochondrial dysfunction, and on. Currently, the imbalance of essential metals has been associated with AD pathology. Although trace elements such as iron (Fe), zinc (Zn), copper (Cu), and manganese (Mn) are vital for physiological processes in the brain, their dyshomeostasis, whether due to deficiency or excess, mainly impairs energy metabolism by increasing the production of free radicals (e.g., ROS), resulting in oxidative stress and, subsequent mitochondrial dysfunction. Excess metals impair the tricarboxylic acid (TCA) cycle and electron transport chain (ETC) in mitochondria. Thus, metal ions are closely linked to the mitochondrial energy-transducing capacity and redox homeostasis. The brain is highly susceptible and sensitive to metal-mediated metabolic crisis, leading to neuronal dysfunction, a key factor in the progression and severity of AD. Traditional treatments for AD pathology are based on acetylcholinesterase inhibitors and anti-amyloid approaches, but metal chelation has shown potential in reversing the clinical condition of the disease. Herein, we discuss the contribution of metal imbalance to the metabolic energy impairment of the brain in AD, highlighting its relationship with mitochondrial dysfunction. Some therapeutic approaches involving restoration of metal ion homeostasis are discussed.
Invisible threats of microplastics induced toxicity: Oxidative and inflammatory pathways in the CNS and retina.
Shenoy A, Eva TA, Palanivel V … +6 more , Salkar A, Gupta VB, Chitranshi N, Graham SL, Gupta V, Basavarajappa D
Int Rev Neurobiol · 2026 · PMID 42276620 · Publisher ↗
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 toxi...
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.
Starved synapses: Gut microbiome dysbiosis and its role in Alzheimer's glucose impairment.
Upadhyay R, Santhosh S, Malathi R … +3 more , Kumari PS, Vijayanand S, Sevanan M
Int Rev Neurobiol · 2026 · PMID 42276619 · Publisher ↗
Alzheimer's disease (AD) is increasingly recognised as a multifactorial disorder driven by metabolic, microbial, and neuroinflammatory imbalances. The study of the research results proposes that gut dysbiosis and impaire...
Alzheimer's disease (AD) is increasingly recognised as a multifactorial disorder driven by metabolic, microbial, and neuroinflammatory imbalances. The study of the research results proposes that gut dysbiosis and impaired brain glucose metabolism are closely interrelated through the gut-brain metabolism axis. Changes in the intestinal microbiome may disrupt insulin sensitivity, cause systemic inflammation, and disrupt the blood-brain barrier, worsening neuronal glucose deficits and facilitating amyloid-β (Aβ) aggregation and tau phosphorylation. Alongside, neurodegenerative cascades are further enhanced by neuronal metabolic reprogramming, characterised by decreased glucose uptake, dysfunctional glycolytic enzymes, and oxidative stress. Short-chain fatty acids (SCFAs) are mainly butyrate, which have a neuroprotective effect in regulating inflammation and gut integrity, and dysbiosis causes increased pro-inflammatory cytokines and endotoxin leakage. This two-way communication network provides new therapeutic opportunities, such as probiotics, prebiotics, nutritional control, and metabolic reprogramming interventions, to regain homeostasis and prevent the advancement of AD.
Circadian rhythm, metabolic stress, and Alzheimer's disease.
Saini V, Singh S, Kumar R … +2 more , Shahadab M, Jha HC
Int Rev Neurobiol · 2026 · PMID 42276618 · Publisher ↗
Alzheimer's disease (AD) is a multifactorial neurodegenerative disorder. Beyond hereditary factors related to an individual's genetics, acquired traits are becoming increasingly common, including lifestyle changes such a...
Alzheimer's disease (AD) is a multifactorial neurodegenerative disorder. Beyond hereditary factors related to an individual's genetics, acquired traits are becoming increasingly common, including lifestyle changes such as diet and pathogenic infections. This brings about the involvement of metabolic stress and gut-brain axis dysfunction in the progression of AD. Recent studies have revealed that circadian rhythms not only regulate brain energy metabolism but also orchestrate changes in gut microbiota, inducing neurological modulations. Gut-derived metabolites and microbial signals can modulate host circadian gene expression, thereby influencing neuroinflammation. Metabolic stresses, characterized by impaired glucose utilization, mitochondrial dysfunction, and oxidative stress, exacerbate this cycle through systemic inflammation and gut dysbiosis. Additionally, dietary patterns and timing, such as time-restricted feeding, have been known to benefit both the circadian clock and gut-brain axes, thereby reducing neuroinflammation and improving cognitive outcomes. Therefore, this chapter synthesizes the emerging evidence on the interconnected roles of circadian rhythm, gut microbiota, and metabolic stresses in AD pathogenesis. It highlights the mechanistic insights into how chronobiology and nutrition can be leveraged to restore gut-brain metabolic homeostasis, offering innovative strategies for early intervention of Alzheimer's disease.
Mitochondrial rescue in Alzheimer's disease: Exploring marine-derived compounds for brain metabolism regulation.
Vijayalakshmi P, Alex AM, Muthupandian S … +4 more , Desai D, Jayaprakashvel M, Singh SK, Selvaraj C
Int Rev Neurobiol · 2026 · PMID 42276617 · Publisher ↗
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 dev...
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.
TMEM230 and mitochondrial regulation in Alzheimer's disease.
Zucchi I, Cocola C, Pelucchi P … +5 more , Mazzaccaro D, Nano G, Palizban M, Porta G, Reinbold RA
Int Rev Neurobiol · 2026 · PMID 42276616 · Publisher ↗
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...
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.
Environmental toxins, PFAS exposure, and brain metabolism: A new angle in Alzheimer's disease pathophysiology.
Jain V, Bharti S
Int Rev Neurobiol · 2026 · PMID 42276615 · Publisher ↗
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 cha...
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.
Glutamate and glutamine metabolism in neurodegenerative diseases.
Karthikeyan K, Velmurugan G, Upadhyay R … +2 more , Sevanan M, Chinnathambi S
Int Rev Neurobiol · 2026 · PMID 42276614 · Publisher ↗
Glutamate is known as the most important excitatory neurotransmitter in brain. Glutamate and glutamine recycling is very essential to maintain the nitrogen metabolism. Despite of its major functions, its dysregulation is...
Glutamate is known as the most important excitatory neurotransmitter in brain. Glutamate and glutamine recycling is very essential to maintain the nitrogen metabolism. Despite of its major functions, its dysregulation is a basic pathology which is common to neurodegenerative diseases such as Parkinson's disease (PD), Alzheimer's disease (AD), and Amyotrophic lateral sclerosis (ALS). Amyloid-β and Tau in AD disrupt glutamate uptake and the glutamate-glutamine cycle, accelerating synaptic failure, whereas loss of astrocytic EAAT2 in ALS generates unrelenting excitotoxicity and motor neuron demise. Toxic α-synuclein aggregation in PD exacerbates dopamine-glutamate imbalance through destabilizing corticostriatal transmission. This review explores on the key mechanisms by which glutamate impairment leads to the pathogenies of neurogenerative disorders and also about current medications like amantadine, memantine, and riluzole which are glutamate antagonists, are shown to partially alleviative but cannot halt the advancement of the disease. One of the potential targets for disease-modifying treatments could be the receptor modulation, astrocytic function, and elimination of excess glutamate.
Preface.
Int Rev Neurobiol · 2025 · PMID 41242768 · Publisher ↗
Abstract loading — click title to view on PubMed.
Neural dynamics of hypnotic responding: From unique to multicomponent perspectives on hypnotic phenomena.
Brunel J, Rainville P, Landry M
Int Rev Neurobiol · 2025 · PMID 41242767 · Publisher ↗
Understanding the neural and cognitive mechanisms underlying hypnosis has been a central focus of investigation over recent decades. Dominant approaches have often aimed to identify a single, distinct neural signature ca...
Understanding the neural and cognitive mechanisms underlying hypnosis has been a central focus of investigation over recent decades. Dominant approaches have often aimed to identify a single, distinct neural signature capable of accounting for the emergence of hypnotic phenomena. However, despite robust behavioural evidence supporting the concept of hypnotic responding, findings from neuroimaging and electrophysiological studies have been highly heterogeneous, limiting the establishment of a consistent neurophysiological framework. This chapter provides an up-to-date overview of the neural dynamics associated with hypnotic responses and explores the primary sources of variability in brain-based markers of hypnosis. We propose a componential approach, suggesting that the hypnotic process comprises multiple distinct yet interacting mechanisms. Specifically, we describe how different aspects of hypnotic phenomena correspond to specific neural patterns: large-scale network connectivity changes induced by hypnotic induction, localized modulations driven by suggestion, and individual susceptibility amplifying these neural responses. We further argue that additional variability may stem from individual differences beyond susceptibility, contributing to the lack of convergence across studies. The chapter concludes by advocating for a multi-componential framework as a promising direction for future research that better captures the complexity of the cognitive and neural architecture underlying hypnotic responding.
Heterogeneity in high hypnotic suggestibility: Models, evidence, and synthesis.
Terhune DB
Int Rev Neurobiol · 2025 · PMID 41242766 · Publisher ↗
Most empirical studies and theoretical models in research on suggestion and hypnosis presuppose that highly suggestible individuals comprise a uniform population. This assumption contrasts with consistent evidence for he...
Most empirical studies and theoretical models in research on suggestion and hypnosis presuppose that highly suggestible individuals comprise a uniform population. This assumption contrasts with consistent evidence for heterogeneity in this group, yet these findings have not been systematically integrated or evaluated against competing models of heterogeneity. In this article, I first outline the characteristics of heterogeneity among highly suggestible individuals, highlight methodological considerations, and review the assumptions of different models of heterogeneity. Next, I consider evidence for heterogeneity spanning responsiveness to hypnotic inductions and suggestions, strategy use during response to suggestion, developmental trajectories, cognitive-perceptual profiles, and symptomatology. I identify key limitations in this research area, highlight convergent findings within and across these domains, assess the explanatory scope of different models, and propose priorities for future research on heterogeneity. Elucidating the characteristics and latent structure of heterogeneity among highly suggestible individuals is essential for advancing our understanding of the neurocognitive substrates of suggestion.
Interoceptive predictive coding, active inference and the generation of hypnotic suggestion responses.
Jamieson GA
Int Rev Neurobiol · 2025 · PMID 41242765 · Publisher ↗
Hypnosis research flourishes when competing theoretical models make testable predictions about significant psychological, physiological and clinical outcomes. Neurocomputational theories are currently unifying theory and...
Hypnosis research flourishes when competing theoretical models make testable predictions about significant psychological, physiological and clinical outcomes. Neurocomputational theories are currently unifying theory and research in these diverse domains and are poised to enter the field of hypnosis. Here we explore three current attempts to employ Bayesian predictive coding models to understand the mechanisms used to generate responses to hypnotic suggestions. Predictive coding is shown to be a framework able to generate multiple theorical explanations with testable predictions and distinct consequences for the growth of knowledge and clinical practice. Current theories of dissociated control, absorption and response expectancy can be modelled within this unifying framework. The unique Bayesian mechanism of Active Inference plays a central role in each of the accounts compared and testable neurophysiological predictions are drawn from each model. This provides a foundation for future research programs and successful grant funding to drive the next wave in the understanding of hypnotic suggestion, hypnotic responses and closely related social and clinical phenomena.
Symptom modelling using hypnosis.
Currell EA, Deeley Q
Int Rev Neurobiol · 2025 · PMID 41242764 · Publisher ↗
Research on psychiatric disorders faces the challenge that symptoms of psychopathology are by their nature elusive. Functional symptoms, hallucinations, delusions, and passivity phenomena involve private changes in exper...
Research on psychiatric disorders faces the challenge that symptoms of psychopathology are by their nature elusive. Functional symptoms, hallucinations, delusions, and passivity phenomena involve private changes in experience which are often unpredictable in nature, co-morbid, confounded, and heterogeneous. Hypnosis and experimental suggestion provide a potential means of overcoming these limitations. By eliciting precise, transient alterations in experience under controlled conditions, symptom models created by suggestion in hypnosis allow researchers to probe mechanisms that are otherwise difficult to study, such as disruptions in self-monitoring, agency, and belief evaluation. This chapter reviews the historical and contemporary development of hypnotic symptom modelling, evaluates the methodological debates concerning suggestibility, demand characteristics, and phenomenological characterisation, and considers applications ranging from hallucinations and delusional misidentification to functional neurological symptoms. We conclude that while suggested symptoms do not replicate clinical disorders in full, they provide useful experimental analogues that can bridge laboratory and clinic, refine cognitive theories, and highlight potential therapeutic strategies. Moreover, by linking mechanistic insights from modelling to therapeutic practice, clinical hypnosis and suggestion can potentially alleviate distress in clinical contexts.
The effects of task-relevant suggestions on motivated cognitive control.
Zahedi A, Sommer W
Int Rev Neurobiol · 2025 · PMID 41242763 · Publisher ↗
To deal with the only constant in life, change, we use a set of top-down processes called cognitive control. Cognitive control enables us to develop new stimulus-response associations appropriate for the task at hand ins...
To deal with the only constant in life, change, we use a set of top-down processes called cognitive control. Cognitive control enables us to develop new stimulus-response associations appropriate for the task at hand instead of being rigidly bound to our existing repertoire of responses. Given the central role cognitive control has in our lives, it is not a surprise that different methods have been tested for improving it; however, few have shown generalizable, long-term effects. One approach, which has shown great promise in enhancing performance in different tasks requiring cognitive control (e.g., Stroop, Simon, Flanker, Go-NoGo, and tone-monitoring tasks), is using task-relevant direct-verbal suggestions, including posthypnotic and nonhypnotic suggestions. The observed effects of suggestions are both reliable, as they have been replicated by different labs over three decades, and generalizable, as they have proven effective in enhancing different aspects of cognitive control, such as inhibition and working memory updating. In the current review, we discuss recent developments in the understanding of cognitive control and its hierarchies and elucidate the effects of suggestions on cognitive control and their underlying mechanisms. Finally, we argue that besides the applicability of task-relevant suggestions in training regimens for enhancing cognitive control, their effects have theoretical implications for conceptual questions regarding both motivated hierarchical cognitive control and hypnotic phenomena.
Preface.
Int Rev Neurobiol · 2025 · PMID 41161949 · Publisher ↗
Abstract loading — click title to view on PubMed.
Experimental pain modulation via hypnosis: Neurophysiological perspectives.
De Pascalis V, De Benedittis G
Int Rev Neurobiol · 2025 · PMID 41161948 · Publisher ↗
This chapter reviews key electrophysiological and neuroimaging findings on the neural mechanisms underlying hypnosis and its modulation of experimentally induced pain, with an emphasis on the roles of hypnotizability and...
This chapter reviews key electrophysiological and neuroimaging findings on the neural mechanisms underlying hypnosis and its modulation of experimentally induced pain, with an emphasis on the roles of hypnotizability and the content of suggestions. Highly hypnotizable (HH) individuals consistently report reduced pain and emotional distress under hypnotic hypoalgesia, although effects on somatosensory-evoked potentials (SERPs) vary due to methodological differences in induction techniques and experimental paradigms. EEG time-frequency analyses and oscillatory studies offer more consistent results, particularly in HH individuals, highlighting gamma-band oscillations as markers that distinguish hypnosis from distraction. Neuroimaging studies demonstrate that hypnotic hypoalgesia engages distributed brain networks, with activity changes in the anterior and medial cingulate cortices (ACC and MCC), thalamus, primary sensory cortex, dorsolateral prefrontal cortex, and insula correlating with the modulation of pain's sensory and affective dimensions. Functional connectivity analyses reveal enhanced interactions between the ACC, periaqueductal gray (PAG), and insula during preparatory suggestion phases relative to a control condition. Additionally, hypnosis influences autonomic nervous system function by reducing sympathetic arousal and enhancing parasympathetic tone. Overall, hypnosis emerges as a multifaceted process shaped by individual susceptibility, the induction method, and the structure of suggestions, engaging diverse neural pathways that support its potential as a personalized tool for pain management.
Non-invasive brain stimulation (NIBS) in the modulation of hypnotic experience and hypnotizability.
Perri RL, Di Filippo G
Int Rev Neurobiol · 2025 · PMID 41161947 · Publisher ↗
Non-Invasive Brain Stimulation (NIBS) techniques, including Transcranial Magnetic Stimulation (TMS) and Transcranial Direct Current Stimulation (tDCS), have emerged as valuable tools in neuroscience, clinical interventio...
Non-Invasive Brain Stimulation (NIBS) techniques, including Transcranial Magnetic Stimulation (TMS) and Transcranial Direct Current Stimulation (tDCS), have emerged as valuable tools in neuroscience, clinical interventions, and hypnosis research. NIBS enables the modulation of neural activity to explore brain-behaviour relationships through causal approaches. TMS, relying on magnetic fields to induce cortical stimulation, has demonstrated its utility in enhancing hypnotic suggestibility, albeit with limitations such as imprecise targeting of stimulated neuronal populations and variability in individual responses. These limitations, including imprecise targeting and inter-individual variability in responses, are also common to tDCS, which applies weak electrical currents to influence cortical excitability, offer more practical adaptability, making it a promising alternative for applications in hypnosis. In hypnosis research, NIBS studies have primarily targeted the dorsolateral prefrontal cortex (DLPFC), a region implicated in executive processes and hypnotic phenomena. Findings from TMS and tDCS studies suggest a modulatory role of the DLPFC in hypnotizability, with inhibitory stimulation enhancing hypnotic depth and responsiveness for some individuals. However, methodological challenges highlight the need for further exploration. Additionally, both TMS and tDCS suffer from further issues such as the challenge of ensuring effective blinding, the presence of placebo effects (which may interfere with the genuineness of observed effects), and high inter-subject variation even within the same study population. Despite these challenges, NIBS suggests clinical potential in augmenting hypnotic responsiveness, which could enhance pain management, emotional regulation, and broaden the applicability of hypnotherapy to resistant individuals. Further, these advancements promise to deepen our understanding of the neurophysiological basis of hypnosis, opening avenues for personalized and targeted neuromodulation strategies.
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