{"title":"Cognitive function in central disorders of hypersomnolence.","authors":"Amir Sharafkhaneh, Ahmed S BaHammam","doi":"10.1016/bs.pbr.2026.08.003","DOIUrl":"10.1016/bs.pbr.2026.08.003","url":null,"abstract":"<p><p>Central disorders of hypersomnolence (CDH), a group that includes narcolepsy type 1 (NT1), narcolepsy type 2 (NT2), idiopathic hypersomnia (IH), and Kleine-Levin syndrome (KLS), are defined by excessive daytime sleepiness (EDS) and prolonged or fragmented sleep, but their impact extends well beyond wakefulness. Cognitive dysfunction is a core, disabling feature of the CDH spectrum, affecting attention, processing speed, memory, and executive function to varying degrees across subtypes. This chapter reviews current evidence on the nature, magnitude, neurobiological mechanisms, comorbidity interactions, treatment responsiveness, and clinical consequences of cognitive impairment in CDH, and aims to give the clinical neuroscientist and sleep specialist a practical framework.</p>","PeriodicalId":20598,"journal":{"name":"Progress in brain research","volume":"301 ","pages":"37-59"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148991039","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Heba Hares, Sukhroop Kaur, Ebtisam Abounajmi, Bashar Qatanany, Amir Sharafkhaneh, K S Jagannatha Rao, Mohammad Nami
{"title":"Sleep, attention, and executive function in health and disease.","authors":"Heba Hares, Sukhroop Kaur, Ebtisam Abounajmi, Bashar Qatanany, Amir Sharafkhaneh, K S Jagannatha Rao, Mohammad Nami","doi":"10.1016/bs.pbr.2026.07.004","DOIUrl":"10.1016/bs.pbr.2026.07.004","url":null,"abstract":"<p><p>This chapter examines the intricate relationship between sleep and higher-order cognitive functions, particularly attention and executive control. Sleep is presented as a critical modulator of cognitive performance, influencing neural systems that underpin attentional regulation, working memory, and decision-making. The chapter highlights the vulnerability of attention to sleep deprivation, with impairments in sustained attention and processing efficiency linked to disruptions in dopaminergic and noradrenergic systems. The chapter also examines how sleep parameters and sleep architecture affect ADHD pathophysiology and symptomatology. Executive functions, including cognitive flexibility and inhibitory control, are shown to depend heavily on the integrity of prefrontal cortical networks, which are particularly sensitive to sleep disturbances. Neurobiological mechanisms underlying these relationships are explored, including thalamocortical circuitry, cholinergic modulation, and neuroendocrine influences such as cortisol dysregulation. Structural and functional neuroimaging studies reveal that insufficient sleep is associated with reduced prefrontal activity and altered connectivity, contributing to observable cognitive deficits. The chapter also discusses clinical implications, emphasizing the role of sleep interventions such as cognitive behavioral therapy in enhancing sleep quality, cognitive outcomes, and ADHD management. The bidirectional relationship between sleep and cognition is underscored, positioning sleep as a modifiable factor in optimizing cognitive resilience and mitigating neuropsychiatric risk.</p>","PeriodicalId":20598,"journal":{"name":"Progress in brain research","volume":"299 ","pages":"217-247"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148670659","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Jayanth K S Rao, Lakshmi Sowmya Emani, Sejali Padhi, Amir Sharafkhaneh, Mohammad Nami, Jagannatha Rao Kosagisharaf
{"title":"Sleep, anxiety, and depression: The bidirectional brain-behavior axis.","authors":"Jayanth K S Rao, Lakshmi Sowmya Emani, Sejali Padhi, Amir Sharafkhaneh, Mohammad Nami, Jagannatha Rao Kosagisharaf","doi":"10.1016/bs.pbr.2026.07.007","DOIUrl":"10.1016/bs.pbr.2026.07.007","url":null,"abstract":"<p><p>Sleep, anxiety, and depression are interconnected processes that greatly influence mental health throughout life. Recent studies indicate that sleep issues are not just symptoms of mental illness but can also cause emotional and cognitive problems. Anxiety and depression can disrupt sleep patterns, and ongoing sleep difficulties can raise the likelihood of mood disorders. This reciprocal relationship involves neural pathways, neurochemicals, hormones, immune responses, and social factors. This chapter explores how sleep, anxiety, and depression interact from various scientific and clinical viewpoints. Topics include circadian rhythms, stress hormones, immune signalling, genetic and environmental effects, cognitive impairments, developmental factors, and new treatment options. Understanding these links is crucial for creating comprehensive approaches to simultaneously address sleep and mental health issues.</p>","PeriodicalId":20598,"journal":{"name":"Progress in brain research","volume":"300 ","pages":"35-64"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148913174","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Jayanth K S Rao, Lakshmi Sowmya Emani, Sejali Padhi, Amir Sharafkhaneh, Mohammad Nami, Jagannatha Rao Kosagisharaf
{"title":"Sleep, circadian rhythms, chronobiology, and neural synchrony: Integrative mechanisms in brain function, health, and disease.","authors":"Jayanth K S Rao, Lakshmi Sowmya Emani, Sejali Padhi, Amir Sharafkhaneh, Mohammad Nami, Jagannatha Rao Kosagisharaf","doi":"10.1016/bs.pbr.2026.07.011","DOIUrl":"10.1016/bs.pbr.2026.07.011","url":null,"abstract":"<p><p>Sleep and circadian rhythms are crucial for regulating metabolism, cognitive function, and nightly brain repair. Chronobiology studies these biological timing systems by focusing on mechanisms such as neural synchrony, which underlies coordinated brain wave patterns that support transitions between sleep stages, memory encoding, and cognitive performance. Recent work in genetics, brain imaging, and computational modeling has uncovered specific pathways connecting circadian clocks to sleep regulation and neural network synchronization. For example, clock genes drive rhythmic cellular activity, and thalamocortical circuits create oscillatory patterns required for brain repair and memory consolidation. Disruptions in the integration of these mechanisms harm health by impairing neural communication and timing, leading to neurodegeneration, mental health issues, and metabolic or cognitive decline. This review explores how these systems develop and interact at the molecular and network levels, highlighting the suprachiasmatic nucleus as the central pacemaker, clock gene feedback loops as timekeepers, and thalamocortical circuits as mediators of neural synchrony. It also details how chronotherapy, light treatments targeting the circadian system, and AI-based sleep pattern analysis act on these mechanisms to benefit brain health. By clarifying how chronobiology and neuroscience intersect at the level of specific biological mechanisms, this review provides a comprehensive foundation for understanding and future research.</p>","PeriodicalId":20598,"journal":{"name":"Progress in brain research","volume":"300 ","pages":"1-34"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148913204","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Restless legs syndrome and periodic limb movement disorders.","authors":"Ali-Mohammad Kamali, Mohammad Nami","doi":"10.1016/bs.pbr.2026.07.014","DOIUrl":"10.1016/bs.pbr.2026.07.014","url":null,"abstract":"<p><p>Clinical confusion around restless legs syndrome (RLS), periodic limb movements during sleep (PLMS), and periodic limb movement disorder (PLMD) usually begins with a familiar sequence: the patient sleeps badly, the sleep study shows leg movements, and the report starts to sound like the diagnosis. The labels need more separation than that. RLS is diagnosed clinically from the history: an urge to move, often with uncomfortable sensations, brought out by rest, eased by movement, and worse in the evening or at night. PLMS are scored motor events. PLMD is reserved for the smaller group in whom those events plausibly account for sleep disturbance or daytime impairment after RLS, sleep-disordered breathing, narcolepsy, REM sleep behavior disorder, drug effects, and other neurological or medical causes have been considered. Biology is not a tidy dopamine story. Iron handling in the brain remains one of the more reproducible findings, although ferritin and transferrin saturation are only rough clinical proxies for central iron. Dopaminergic, adenosinergic, glutamatergic, spinal, autonomic, and genetic findings each explain part of the syndrome. Large genetic datasets, quantitative imaging, home movement recording, automated PLMS scoring, and autonomic measures have widened the field. Their immediate value is uneven: some help with mechanisms, some with measurement, and only a few currently change treatment decisions. Management still begins at the bedside. A typical RLS history, an incidental PLMS index, and possible PLMD lead to different choices. Iron indices should be checked early, medication and respiratory triggers need to be addressed, and dopamine agonist escalation should be avoided when augmentation is suspected. Current treatment is more cautious than older dopamine-centered practice: iron repletion when indicated, alpha-2-delta ligands for many chronic persistent cases, specialist use of opioids for severe refractory disease, and a selective role for device-based therapy. The chapter follows that clinical order rather than treating leg movement as a single target.</p>","PeriodicalId":20598,"journal":{"name":"Progress in brain research","volume":"301 ","pages":"63-91"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148991149","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Mohamed Rozaik, Aasea Alhashmi, Mira Aljallad, Bashar Qatanany, K S Jagannatha Rao, Mohammad Nami
{"title":"Neuroanatomy of dreaming and REM phenomenology.","authors":"Mohamed Rozaik, Aasea Alhashmi, Mira Aljallad, Bashar Qatanany, K S Jagannatha Rao, Mohammad Nami","doi":"10.1016/bs.pbr.2026.07.005","DOIUrl":"10.1016/bs.pbr.2026.07.005","url":null,"abstract":"<p><p>This chapter includes an extensive examination of the neuroanatomical and neurophysiological basis of dreaming and is primarily concerned with the phenomenology of rapid eye movement (REM) sleep. Relying on integrated findings from neuroimaging, electrophysiology, and neurochemical studies, the chapter describes that dreaming results from the interaction of brain regions such as the brainstem, thalamus, limbic system, and prefrontal cortex. The chapter underscores the central contribution of pontine cholinergic mechanisms to the generation of REM, combined with thalamocortical integration, to define perceptual and narrative features of dreams. Limbic activation in the amygdala and hippocampus is responsible for the emotional intensity and memory-related features of dream content, and relative prefrontal deactivation helps minimize logical constraint and promotes associative reasoning. Oscillatory dynamics, particularly theta and gamma activity, are considered important underpinnings of dream vividness and perceptual integration. With its focus on clinical conditions, including post-traumatic stress disorder (PTSD), depression, and REM sleep behavior disorder, the chapter provides a translational perspective beyond simple mechanistic models associated with the brain. The modulation of acetylcholine, serotonin, and norepinephrine is proposed to be one of the most important mechanisms of regulation with therapeutic potential. The chapter also addresses new domains such as dream neuropharmacology, neuromodulation, ethical implications, and cross-cultural perspectives of dream interpretation. More generally, it places dreaming as a neurobiologically driven, functionally relevant phenomenon with significance for emotional regulation, memory consolidation, and clinical intervention in sleep medicine.</p>","PeriodicalId":20598,"journal":{"name":"Progress in brain research","volume":"299 ","pages":"97-136"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148670648","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Neuromodulation in sleep disorders.","authors":"Bashar Qatanany, Nazia Uzma, Aaliya Nizam, Sukhroop Kaur, Ali-Mohammad Kamali, Mohammad Nami","doi":"10.1016/bs.pbr.2026.07.012","DOIUrl":"10.1016/bs.pbr.2026.07.012","url":null,"abstract":"<p><p>Sleep disorders are a growing global health issue with profound consequences on cardiovascular health, metabolic functioning, cognitive output and overall quality of life. Although there have been numerous clinical advances in brain-based treatments for sleep disorders, there are still a number of sleep disorders that are not well understood and need new treatment options to address the underlying neural mechanisms of sleep-wake regulation. Recent advances in neuroscience have highlighted neuromodulation as a promising treatment option for the complex neural mechanisms of sleep-wake dysfunction. This chapter provides an overview on the neurobiological basics of neuromodulation in sleep medicine, including neurobiological circuits, circadian processes of sleep, wakefulness and their disorders in brain and potential targeting biomarkers for brain stimulation. Present non-invasive neuromodulation strategies include transcranial magnetic stimulation (TMS), transcranial direct current stimulation (tDCS), transcranial alternating current stimulation (tACS), vagus nerve stimulation, etc.; new and invasive neuromodulation strategies such as deep brain stimulation (DBS) for insomnia, obstructive sleep apnea (OSA) and periodic leg movement disorder (PLMD). In this paper, we review the current level of evidence and provide an overview on the road ahead to bring brain stimulation to the daily practice of sleep medicine.</p>","PeriodicalId":20598,"journal":{"name":"Progress in brain research","volume":"300 ","pages":"221-265"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148913016","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Adejoke Elizabeth Memudu, Baliqis Adejoke Olukade, Kenechukwu Emmanuel Nwanama, Gideon S Alex
{"title":"Models developed to explain the effects of stress on brain and behavior.","authors":"Adejoke Elizabeth Memudu, Baliqis Adejoke Olukade, Kenechukwu Emmanuel Nwanama, Gideon S Alex","doi":"10.1016/bs.pbr.2025.01.018","DOIUrl":"10.1016/bs.pbr.2025.01.018","url":null,"abstract":"<p><p>There is an integral relationship between stress, brain function and behavior. Over the year's extensive research has led to the development of various models to explain the intricate intersection between brain and stress. This chapter delves into some of the theoretical frameworks that explains the neurobiological and behavioral responses to stress using key models of stress such as the allostatic load model, which is the most common model that describes how chronic stress affect brain structure and function resulting in long-term changes in regions such as the hippocampus, amygdala, and prefrontal cortex which phenotypically express as cognitive impairments, emotional dysfunction seen in various forms of neurological disorder. The neuro-endocrine model, follows the glucocorticoid cascade hypothesis, that associates prolonged stress exposure to hippocampal damage and cognitive decline via alteration in the hypothalamic-pituitary-adrenal (HPA) axis and the overproduction of stress hormones like cortisol which can induce hippocampal atrophy, impair learning and memory, and promote depressive-like behaviors. The neurobiological stress model addresses the role of the hypothalamic-pituitary-adrenal (HPA) axis and stress-related neurotransmitters in shaping behavioral responses, emphasizing alterations in neuroplasticity and synaptic function. These models demonstrate how chronic stress can alter neural plasticity, neurotransmitter systems, and synaptic connectivity, affecting behavior and cognitive function. Hence by integrating molecular, neurobiological, and behavioral perspectives, these models offer a comprehensive understanding of how stress alters brain activity and behavior. The chapter further showcase how these models direct the development of medical interventions, shedding light on potential therapies that target the underlying molecular mechanisms of stress-induced brain changes.</p>","PeriodicalId":20598,"journal":{"name":"Progress in brain research","volume":"291 ","pages":"339-361"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144035461","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Measuring residual visual function after cerebral damage - a potential path for optimising rehabilitation approaches.","authors":"Denis Schluppeck, Paul V McGraw","doi":"10.1016/bs.pbr.2025.04.003","DOIUrl":"10.1016/bs.pbr.2025.04.003","url":null,"abstract":"<p><p>The integrity of the visual field can be assessed using clinical techniques such as perimetry that rely on subjective report, or can be quantified objectively using functional magnetic resonance imaging (fMRI). In the case of central lesions (e.g. following strokes), fMRI visual field maps can reveal spared regions of cortex that may be missed if patient assessment relies on perimetry and anatomy of lesions alone. Even when perimetry results look stereotypical and can be categorised into hemianopia or quadrantanopia, the areas of spared cortex can be highly variable. FMRI field maps could serve as an important guide for selecting and optimising training and rehabilitation programmes for patients with damage to central visual pathway structures. Alongside a standardised battery of visual function tests, anatomical scans, and tractography data on connections between brain areas, this would provide a much richer clinical picture. Importantly, this approach may also offer useful information for a personalised approach to visual developmental disorders such as cerebral visual impairment (CVI). Here, we survey some recent results from the neuroimaging literature on measuring residual visual function, anatomy, and structural connectivity in stroke survivors, discuss recent results from rehabilitation approaches, and put forward a potential approach for characterising visual function using brain imaging in individuals with CVI.</p>","PeriodicalId":20598,"journal":{"name":"Progress in brain research","volume":"292 ","pages":"71-87"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144132813","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}