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The subcortical visual pathway to the amygdala has long been considered a rapid and crude stream for processing emotionally salient information that is reliant on low spatial frequency (LSF) information. Recently, research has called this LSF dependency into question. To resolve this debate, we take advantage of an anatomical hemiretinal asymmetry, whereby the nasal hemiretina sends a higher proportion of information through the subcortical pathway than the temporal hemiretina. We recorded brain activity using electroencephalography (EEG) in human participants (N = 40) while they completed a monocular viewing paradigm. Pairs of faces (one fearful and one neutral, or both neutral) were projected simultaneously to the nasal and temporal hemiretina in three contrast-equated blocks; faces filtered to display only (i) LSF, (ii) high spatial frequency (HSF), or (iii) unfiltered information (broadband spatial frequency; BSF). BSF fearful faces were found to produce a greater naso-temporal asymmetry, with greater N170 amplitudes evoked by BSF faces in the nasal field, compared to HSF faces. Conversely, the naso-temporal asymmetry for LSF fearful faces did not differ between BSF and HSF. Collectively, these findings provide crucial evidence that the subcortical pathway carries combined spatial frequency visual signals, with a potential bias against HSF content. [ABSTRACT FROM AUTHOR]

Thalamus plays a pivotal role in the pathophysiology of neuropsychiatric conditions due to its strategic position and intricate connectivity with the cerebral cortex, limbic system, and other subcortical structures. In the present study, the potential involvement of the thalamus and subregions of the thalamus are explored in bipolar disorder (BD). In particular, functional and structural magnetic resonance imaging was performed on 73 adult patients with BD‐I and 78 healthy controls (HCs). Seed‐based thalamus and thalamic subregional functional connectivity (FC) were compared between the BD‐I patients and HCs. Compared to HCs, patients with BD‐I showed higher FC between the left thalamus and right lingual gyrus and altered FC between the dorsal thalamus and the default mode network and prefrontal regions, which may be correlated with mania symptomatology. In patients with BD‐I, the anterior subregions of the thalamus had higher FC than the posterior subregions. No significant difference in gray matter volume or local functional activity was found in the thalamus and thalamic subregions between BD‐I and HC. These findings provide evidence of disorganized thalamocortical FC in BD‐I, suggesting that the thalamus and its subregions may play important and specific roles in the neural circuitry of BD. [ABSTRACT FROM AUTHOR]

Brain iron increases in several neurodegenerative diseases are associated with disease progression. However, the causes of increased brain iron remain unclear. This study investigates relationships between subcortical iron, systemic iron and inflammatory status. Brain magnetic resonance imaging (MRI) scans and blood plasma samples were collected from cognitively healthy females (n = 176, mean age = 61.4 ± 4.5 years, age range = 28–72 years) and males (n = 152, mean age = 62.0 ± 5.1 years, age range = 32–74 years). Regional brain iron was quantified using quantitative susceptibility mapping. To assess systemic iron, haematocrit, ferritin and soluble transferrin receptor were measured, and total body iron index was calculated. To assess systemic inflammation, C‐reactive protein (CRP), neutrophil:lymphocyte ratio (NLR), macrophage colony‐stimulating factor 1 (MCSF), interleukin 6 (IL6) and interleukin 1β (IL1β) were measured. We demonstrated that iron levels in the right hippocampus were higher in males compared with females, while iron in the right caudate was higher in females compared with males. There were no significant associations observed between subcortical iron levels and blood markers of iron and inflammatory status indicating that such blood measures are not markers of brain iron. These results suggest that brain iron may be regulated independently of blood iron and so directly targeting global iron change in the treatment of neurodegenerative disease may have differential impacts on blood and brain iron. [ABSTRACT FROM AUTHOR]

Introduction. Epilepsy is a disease characterized by abnormal paroxysmal bioelectrical activity in the brain cortex and subcortical structures. Seizures per se change brain metabolism in epileptic focus and in distal parts of the brain. However, interictal phenomena can also affect functional connectivity (FC) and brain metabolism in other parts of the brain. Aim of study. We hypothesised that epilepsy affects functional connectivity not only among cortical, but also between subcortical, structures of the brain in a resting state condition. Clinical rationale for study. Investigating functional connectivity in patients with epilepsy could provide insights into the underlying pathophysiological mechanisms. Better understanding may lead to more effective treatment strategies. Material and methods. Functional connectivity was analysed in 35 patients with epilepsy and in 28 healthy volunteers. The group of patients was divided into generalised and focal epilepsy (temporal and extratemporal subgroups). Each patient and healthy volunteer underwent an fMRI resting-state session. During the study, EEG signals were simultaneously recorded with fMRI to facilitate the subsequent detection of potential interictal epileptiform discharges (IEDs). Their potential impact on BOLD signals was mitigated through linear regression. The data was processed and correlation coefficients (FC values) between the BOLD signal from selected structures of the central nervous system were determined and compared between study groups. The results were presented as significant differences in correlation coefficients between brain/subcortical structures in the epilepsy and control groups. Results. Lower FC values for the epilepsy group compared to the control group were shown for connections related to the MPFC, hippocampus, thalamus, amygdala, and the parahippocampal gyrus. Conclusions. Epilepsy alters the functional connectivity of resting state subcortical networks. Patterns of pathological changes of FC differ between epilepsy subtypes, with predominant lower FC between the hippocampus, parahippocampal gyrus, amygdala and thalamus in patients with epilepsy. Clinical implications. This study suggests that epilepsy affects subcortical structures. Identifying distinct patterns of altered FC in epilepsy subtypes may help to tailor treatment strategies. Changes in FC detected by fMRI may precede clinical symptoms, aiding in the early diagnosis of cognitive and emotional disorders in focal epilepsy. [ABSTRACT FROM AUTHOR]

ObjectivesAbnormal tau, a hallmark Alzheimer's disease (AD) pathology, may appear in the locus coeruleus (LC) decades before AD symptom onset. Reports of subjective cognitive decline are also often present prior to formal diagnosis. Yet, the relationship between LC structural integrity and subjective cognitive decline has remained unexplored. Here, we aimed to explore these potential associations.MethodsWe examined 381 community-dwelling men (mean age = 67.58; SD = 2.62) in the Vietnam Era Twin Study of Aging who underwent LC-sensitive magnetic resonance imaging and completed the Everyday Cognition scale to measure subjective cognitive decline along with their selected informants. Mixed models examined the associations between rostral-middle and caudal LC integrity and subjective cognitive decline after adjusting for depressive symptoms, physical morbidities, and family. Models also adjusted for current objective cognitive performance and objective cognitive decline to explore attenuation.ResultsFor participant ratings, lower rostral-middle LC contrast to noise ratio (LCCNR) was associated with significantly greater subjective decline in memory, executive function, and visuospatial abilities. For informant ratings, lower rostral-middle LCCNR was associated with significantly greater subjective decline in memory only. Associations remained after adjusting for current objective cognition and objective cognitive decline in respective domains.ConclusionsLower rostral-middle LC integrity is associated with greater subjective cognitive decline. Although not explained by objective cognitive performance, such a relationship may explain increased AD risk in people with subjective cognitive decline as the LC is an important neural substrate important for higher order cognitive processing, attention, and arousal and one of the first sites of AD pathology.

White matter hyperintensities (WMHs) are associated with age-related cognitive impairment and increased risk of Alzheimer's disease. However, the manner by which WMHs contribute to cognitive impairment is unclear. Using a combination of predictive modeling and network neuroscience, we investigated the relationship between structural white matter connectivity and age, fluid cognition, and WMHs in 68 healthy adults (18–78 years). Consistent with previous work, WMHs were increased in older adults and exhibited a strong negative association with fluid cognition. Extending previous work, using predictive modeling, we demonstrated that age, WMHs, and fluid cognition were jointly associated with widespread alterations in structural connectivity. Subcortical-cortical connections between the thalamus/basal ganglia and frontal and parietal regions of the default mode and frontoparietal networks were most prominent. At the network level, both age and WMHs were negatively associated with network density and communicability, and positively associated with modularity. Spatially, WMHs were most prominent in arterial zones served by the middle cerebral artery and associated lenticulostriate branches that supply subcortical regions. Finally, WMHs overlapped with all major white matter tracts, most prominently in tracts that facilitate subcortical-cortical communication and are implicated in fluid cognition, including the anterior thalamic-radiations and forceps minor. Finally, results of mediation analyses suggest that whole-brain WMH load influences age-related decline in fluid cognition. Thus, across multiple levels of analysis, we showed that WMHs were increased in older adults and associated with altered structural white matter connectivity and network topology involving subcortical-cortical pathways critical for fluid cognition. [ABSTRACT FROM AUTHOR]

According to the predictive processing framework, perception emerges fromthe reciprocal exchange of predictions and prediction errors (PEs) between hierarchically organized neural circuits. The nonlemniscal division of the inferior colliculus (IC) is the earliest source of auditory PE signals, but their neuronal generators, properties, and functional relevance have remained mostly undefined. We recorded single-unitmismatch responses to auditory oddball stimulation at different intensities, together with activity evoked by two sequences of alternating tones to control frequency-specific effects. Our results reveal a differential treatment of the unpredictable "many-standards" control and the predictable "cascade" control by lemniscal and nonlemniscal IC neurons that is not present in the auditory thalamus or cortex. Furthermore, we found that frequency response areas of nonlemniscal IC neurons reflect their role in subcortical predictive processing, distinguishing three hierarchical levels: (1) nonlemniscal neurons with sharply tuned receptive fields exhibitmild repetition suppression without signaling PEs, thereby constituting the input level of the local predictive processing circuitry. (2) Neurons with broadly tuned receptive fields formthemain, "spectral" PE signaling system, which provides dynamic gain compensation to near-threshold unexpected sounds. This early enhancement of saliency reliant on spectral features was not observed in the auditory thalamus or cortex. (3) Untuned neurons form an accessory, "nonspectral" PE signaling system, which reports all surprising auditory deviances in a robust and consistentmanner, resembling nonlemniscal neurons in the auditory cortex. These nonlemniscal IC neurons show unstructured and unstable receptive fields that could result from inhibitory input controlled by corticofugal projections conveying top-down predictions. [ABSTRACT FROM AUTHOR]

Objective To investigate the clinical, imaging and histopathological features of intracerebral parenchymal or subcortical meningioma without meningeal attachment. Methods The clinical, imaging, and histopathological characteristics of 4 patients with subcortical meningioma without meningeal attachment who underwent surgical treatment at Hainan Provincial People's Hospital from December 2019 to December 2022 were analyzed retrospectively. The principles of surgical management, surgical efficacy, and long-term follow-up results were summarized in conjunction with literature. Results The most common site for all patients was the frontal and parietal lobes, with 3 cases having cystic and solid lesions. Epilepsy was a common symptom before and after surgery. Three dimensional magnetic resonance imaging(MRI)showed that all tumors were located in the brain, and preoperative MRI, as well as intraoperative and postoperative pathology, confirm the absence of dural attachment. 4 patients underwent total resection, two were WHO grade Ⅰ, two were WHO grade Ⅱ, one had postoperative recurrence of atypical meningioma, one had no postoperative radiotherapy, and three received postoperative radiotherapy. After an average follow-up of 1. 5 years, 3 cases survived. Conclusions Intracortical or subcortical meningiomas without meningeal attachment are easily misdiagnosed before surgery. Peritumoral edema in some subcortical or subcortical meningiomas occurs in areas where the lesion adheres to surrounding brain tissue, not surrounding the entire tumor surface. MRI spectroscopy and other features may be helpful in distinguishing. WHO grade Ⅱ atypical meningiomas have a high rate of proliferation, invasion of brain parenchyma, and a high probability of recurrence. Surgical treatment is the first choice, and complete tumor resection is the most important factor in preventing tumor recurrence. For atypical or malignant meningiomas, radiotherapy is recommended immediately after initial operation. [ABSTRACT FROM AUTHOR]

Abstract Thalamus plays a pivotal role in the pathophysiology of neuropsychiatric conditions due to its strategic position and intricate connectivity with the cerebral cortex, limbic system, and other subcortical structures. In the present study, the potential involvement of the thalamus and subregions of the thalamus are explored in bipolar disorder (BD). In particular, functional and structural magnetic resonance imaging was performed on 73 adult patients with BD‐I and 78 healthy controls (HCs). Seed‐based thalamus and thalamic subregional functional connectivity (FC) were compared between the BD‐I patients and HCs. Compared to HCs, patients with BD‐I showed higher FC between the left thalamus and right lingual gyrus and altered FC between the dorsal thalamus and the default mode network and prefrontal regions, which may be correlated with mania symptomatology. In patients with BD‐I, the anterior subregions of the thalamus had higher FC than the posterior subregions. No significant difference in gray matter volume or local functional activity was found in the thalamus and thalamic subregions between BD‐I and HC. These findings provide evidence of disorganized thalamocortical FC in BD‐I, suggesting that the thalamus and its subregions may play important and specific roles in the neural circuitry of BD.

Left-right asymmetry is an important organizing feature of the healthy brain that may be altered in schizophrenia, but most studies have used relatively small samples and heterogeneous approaches, resulting in equivocal findings. We carried out the largest case-control study of structural brain asymmetries in schizophrenia, with MRI data from 5,080 affected individuals and 6,015 controls across 46 datasets, using a single image analysis protocol. Asymmetry indexes were calculated for global and regional cortical thickness, surface area, and subcortical volume measures. Differences of asymmetry were calculated between affected individuals and controls per dataset, and effect sizes were meta-analyzed across datasets. Small average case-control differences were observed for thickness asymmetries of the rostral anterior cingulate and the middle temporal gyrus, both driven by thinner left-hemispheric cortices in schizophrenia. Analyses of these asymmetries with respect to the use of antipsychotic medication and other clinical variables did not show any significant associations. Assessment of age- and sex-specific effects revealed a stronger average leftward asymmetry of pallidum volume between older cases and controls. Case-control differences in a multivariate context were assessed in a subset of the data (N = 2,029), which revealed that 7% of the variance across all structural asymmetries was explained by case-control status. Subtle case-control differences of brain macrostructural asymmetry may reflect differences at the molecular, cytoarchitectonic, or circuit levels that have functional relevance for the disorder. Reduced left middle temporal cortical thickness is consistent with altered left-hemisphere language network organization in schizophrenia.

Progressive apraxia of speech (PAOS) is a neurodegenerative motor-speech disorder that most commonly arises from a four-repeat tauopathy. Recent studies have established that progressive apraxia of speech is not a homogenous disease but rather there are distinct subtypes: the phonetic subtype is characterized by distorted sound substitutions, the prosodic subtype by slow and segmented speech and the mixed subtype by a combination of both but lack of predominance of either. There is some evidence that cross-sectional patterns of neurodegeneration differ across subtypes, although it is unknown whether longitudinal patterns of neurodegeneration differ. We examined longitudinal patterns of atrophy on MRI, hypometabolism on 18F-fluorodeoxyglucose-PET and tau uptake on flortaucipir-PET in a large cohort of subjects with PAOS that had been followed for many years. Ninety-one subjects with PAOS (51 phonetic, 40 prosodic) were recruited by the Neurodegenerative Research Group. Of these, 54 (27 phonetic, 27 prosodic) returned for annual follow-up, with up to seven longitudinal visits (total visits analysed = 217). Volumes, metabolism and flortaucipir uptake were measured for subcortical and cortical regions, for all scans. Bayesian hierarchical models were used to model longitudinal change across imaging modalities with PAOS subtypes being compared at baseline, 4 years from baseline, and in terms of rates of change. The phonetic group showed smaller volumes and worse metabolism in Broca's area and the striatum at baseline and after 4 years, and faster rates of change in these regions, compared with the prosodic group. There was also evidence of faster spread of hypometabolism and flortaucipir uptake into the temporal and parietal lobes in the phonetic group. In contrast, the prosodic group showed smaller cerebellar dentate, midbrain, substantia nigra and thalamus volumes at baseline and after 4 years, as well as faster rates of atrophy, than the phonetic group. Greater hypometabolism and flortaucipir uptake were also observed in the cerebellar dentate and substantia nigra in the prosodic group. Mixed findings were observed in the supplementary motor area and precentral cortex, with no clear differences observed across phonetic and prosodic groups. These findings support different patterns of disease spread in PAOS subtypes, with corticostriatal patterns in the phonetic subtype and brainstem and thalamic patterns in the prosodic subtype, providing insight into the pathophysiology and heterogeneity of PAOS. [ABSTRACT FROM AUTHOR]

Neurological and neurodevelopmental conditions are a major public health concern for which new therapies are urgently needed. The development of effective therapies relies on the precise mapping of the neural substrates causally involved in behaviour generation. Direct electrical stimulation (DES) performed during cognitive and neurological monitoring in awake surgery is currently considered the gold standard for the causal mapping of brain functions. However, DES is limited by the focal nature of the stimulation sites, hampering a real holistic exploration of human brain functions at the network level. We used 4137 DES points derived from 612 glioma patients in combination with human connectome data—resting-state functional MRI, n = 1000 and diffusion weighted imaging, n = 284—to provide a multimodal description of the causal macroscale functional networks subtending 12 distinct behavioural domains. To probe the validity of our procedure, we (i) compared the network topographies of healthy and clinical populations; (ii) tested the predictive capacity of DES-derived networks; (iii) quantified the coupling between structural and functional connectivity; and (iv) built a multivariate model able to quantify single subject deviations from a normative population. Lastly, we probed the translational potential of DES-derived functional networks by testing their specificity and sensitivity in identifying critical neuromodulation targets and neural substrates associated with postoperative language deficits. The combination of DES and human connectome data resulted in an average 29.4-fold increase in whole brain coverage compared to DES alone. DES-derived functional networks are predictive of future stimulation points (97.8% accuracy) and strongly supported by the anatomical connectivity of subcortical stimulations. We did not observe any significant topographical differences between the patients and the healthy population at both group and single subject level. Showcasing concrete clinical applications, we found that DES-derived functional networks overlap with effective neuromodulation targets across several functional domains, show a high degree of specificity when tested with the intracranial stimulation points of a different stimulation technique and can be used effectively to characterize postoperative behavioural deficits. The integration of DES with the human connectome fundamentally advances the quality of the functional mapping provided by DES or functional imaging alone. DES-derived functional networks can reliably predict future stimulation points, have a strong correspondence with the underlying white matter and can be used for patient specific functional mapping. Possible applications range from psychiatry and neurology to neuropsychology, neurosurgery and neurorehabilitation. [ABSTRACT FROM AUTHOR]

Grey matter heterotopia (GMH) are neurodevelopmental disorders associated with abnormal cortical function and epilepsy. Subcortical band heterotopia (SBH) and periventricular nodular heterotopia (PVNH) are two well-recognized GMH subtypes in which neurons are misplaced, either forming nodules lining the ventricles in PVNH, or forming bands in the white matter in SBH. Although both PVNH and SBH are commonly associated with epilepsy, it is unclear whether these two GMH subtypes differ in terms of pathological consequences or, on the contrary, share common altered mechanisms. Here, we studied two robust preclinical models of SBH and PVNH, and performed a systematic comparative assessment of the physiological and morphological diversity of heterotopia neurons, as well as the dynamics of epileptiform activity and input connectivity. We uncovered a complex set of altered properties, including both common and distinct physiological and morphological features across heterotopia subtypes, and associated with specific dynamics of epileptiform activity. Taken together, these results suggest that pro-epileptic circuits in GMH are, at least in part, composed of neurons with distinct, subtype-specific, physiological and morphological properties depending on the heterotopia subtype. Our work supports the notion that GMH represent a complex set of disorders, associating both shared and diverging pathological consequences, and contributing to forming epileptogenic networks with specific properties. A deeper understanding of these properties may help to refine current GMH classification schemes by identifying morpho-electric signatures of GMH subtypes, to potentially inform new treatment strategies. [ABSTRACT FROM AUTHOR]

Adolescent subcortical structural brain development might underlie psychopathological symptoms, which often emerge in adolescence. At the same time, sex differences exist in psychopathology, which might be mirrored in underlying sex differences in structural development. However, previous studies showed inconsistencies in subcortical trajectories and potential sex differences. Therefore, we aimed to investigate the subcortical structural trajectories and their sex differences across adolescence using for the first time a single cohort design, the same quality control procedure, software, and a general additive mixed modeling approach. We investigated two large European sites from ages 14 to 24 with 503 participants and 1408 total scans from France and Germany as part of the IMAGEN project including four waves of data acquisition. We found significantly larger volumes in males versus females in both sites and across all seven subcortical regions. Sex differences in age‐related trajectories were observed across all regions in both sites. Our findings provide further evidence of sex differences in longitudinal adolescent brain development of subcortical regions and thus might eventually support the relationship of underlying brain development and different adolescent psychopathology in boys and girls. [ABSTRACT FROM AUTHOR]

The sense of body ownership (i.e. the feeling that our body or its parts belong to us) plays a key role in bodily self-consciousness and is believed to stem from multisensory integration. Experimental paradigms such as the rubber hand illusion have been developed to allow the controlled manipulation of body ownership in laboratory settings, providing effective tools for investigating malleability in the sense of body ownership and the boundaries that distinguish self from other. Neuroimaging studies of body ownership converge on the involvement of several cortical regions, including the premotor cortex and posterior parietal cortex. However, relatively less attention has been paid to subcortical structures that may also contribute to body ownership perception, such as the cerebellum and putamen. Here, on the basis of neuroimaging and neuropsychological observations, we provide an overview of relevant subcortical regions and consider their potential role in generating and maintaining a sense of ownership over the body. We also suggest novel avenues for future research targeting the role of subcortical regions in making sense of the body as our own. [ABSTRACT FROM AUTHOR]

Executive functions are high-level cognitive processes involving abilities such as working memory/updating, set-shifting and inhibition. These complex cognitive functions are enabled by interactions among widely distributed cognitive networks, supported by white matter tracts. Executive impairment is frequent in neurological conditions affecting white matter; however, whether specific tracts are crucial for normal executive functions is unclear. We review causal and correlation evidence from studies that used direct electrical stimulation during awake surgery for gliomas, voxel-based and tract-based lesion-symptom mapping, and diffusion tensor imaging to explore associations between the integrity of white matter tracts and executive functions in healthy and impaired adults. The corpus callosum was consistently associated with all executive processes, notably its anterior segments. Both causal and correlation evidence showed prominent support of the superior longitudinal fasciculus to executive functions, notably to working memory. More specifically, strong evidence suggested that the second branch of the superior longitudinal fasciculus is crucial for all executive functions, especially for flexibility. Global results showed left lateralization for verbal tasks and right lateralization for executive tasks with visual demands. The frontal aslant tract potentially supports executive functions, however, additional evidence is needed to clarify whether its involvement in executive tasks goes beyond the control of language. Converging evidence indicates that a right-lateralized network of tracts connecting cortical and subcortical grey matter regions supports the performance of tasks assessing response inhibition, some suggesting a role for the right anterior thalamic radiation. Finally, correlation evidence suggests a role for the cingulum bundle in executive functions, especially in tasks assessing inhibition. We discuss these findings in light of current knowledge about the functional role of these tracts, descriptions of the brain networks supporting executive functions and clinical implications for individuals with brain tumours. [ABSTRACT FROM AUTHOR]

Subcortical brain regions play essential roles in the pathology of social anxiety disorder (SAD). While adolescence is the peak period of SAD, the relationships between altered development of the subcortical regions during this period and SAD are still unclear. This study investigated the age-dependent alterations in structural co-variance among subcortical regions and between subcortical and cortical regions, aiming to reflect aberrant coordination during development in the adolescent with SAD. High-resolution T1-weighted images were obtained from 76 adolescents with SAD and 67 healthy controls (HC), ranging from 11 to 17.9 years. Symptom severity was evaluated with the Social Anxiety Scale for Children (SASC) and the Depression Self Rating Scale for Children (DSRS-C). Structural co-variance and sliding age-window analyses were used to detect age-dependent group differences in inter-regional coordination patterns among subcortical regions and between subcortical and cortical regions. The volume of the striatum significantly correlated with SAD symptom severity. The SAD group exhibited significantly enhanced structural co-variance among key regions of the striatum (putamen and caudate). While the co-variance decreased with age in healthy adolescents, the co-variance in SAD adolescents stayed high, leading to more apparent group differences in middle adolescence. Moreover, the striatum's mean structural co-variance with cortical regions decreased with age in HC but increased with age in SAD. Adolescents with SAD suffer aberrant developmental coordination among the key regions of the striatum and between the striatum and cortical regions. The degree of incoordination is age-dependent, which may represent a neurodevelopmental trait of SAD. [ABSTRACT FROM AUTHOR]

Introduction: The relation between traumatic brain injury (TBI), its acute and chronic symptoms, and the potential for remote neurodegenerative disease is a priority for military research. Structural and functional connectivity (FC) of the basal ganglia, involved in motor tasks such as walking, are altered in some samples of Service Members and Veterans with TBI, but any behavioral implications are unclear and could further depend on the context in which the TBI occurred. Methods: In this study, FC from caudate and pallidum seeds was measured in Service Members and Veterans with a history of mild TBI that occurred during combat deployment, Service Members and Veterans whose mild TBI occurred outside of deployment, and Service Members and Veterans who had no lifetime history of TBI. Results: FC patterns differed for the two contextual types of mild TBI. Service Members and Veterans with deployment-related mild TBI demonstrated increased FC between the right caudate and lateral occipital regions relative to both the nondeployment mild TBI and TBI-negative groups. When evaluating the association between FC from the caudate and gait, the non-deployment mild TBI group showed a significant positive relationship between walking time and FC with the frontal pole, implicated in navigational planning, whereas the deployment-related mild TBI group trended towards a greater negative association between walking time and FC within the occipital lobes, associated with visuo-spatial processing during navigation. Discussion: These findings have implications for elucidating subtle motor disruption in Service Members and Veterans with deployment-related mild TBI. Possible implications for future walking performance are discussed. [ABSTRACT FROM AUTHOR]

Anatomists have long expressed interest in neurons of the white matter, which is by definition supposed to be free of neurons. Hypotheses regarding their biochemical signature and physiological function are mainly derived from animal models. Here, we investigated 15 whole‐brain human postmortem specimens, including cognitively normal cases and those with pathologic Alzheimer's disease (AD). Quantitative and qualitative methods were used to investigate differences in neuronal size and density, and the relationship between neuronal processes and vasculature. Double staining was used to evaluate colocalization of neurochemicals. Two topographically distinct populations of neurons emerged: one appearing to arise from developmental subplate neurons and the other embedded within deep, subcortical white matter. Both populations appeared to be neurochemically heterogeneous, showing positive reactivity to acetylcholinesterase (AChE) [but not choline acetyltransferase (ChAT)], neuronal nuclei (NeuN), nicotinamide adenine dinucleotide phosphate‐diaphorase (NADPH‐d), microtubule‐associated protein 2 (MAP–2), somatostatin (SOM), nonphosphorylated neurofilament protein (SMI‐32), and calcium‐binding proteins calbindin‐D28K (CB), calretinin (CRT), and parvalbumin (PV). PV was more richly expressed in superficial as opposed to deep white matter neurons (WMNs); subplate neurons were also significantly larger than their deeper counterparts. NADPH‐d, a surrogate for nitric oxide synthase, allowed for the striking morphological visualization of subcortical WMNs. NADPH‐d‐positive subcortical neurons tended to embrace the outer walls of microvessels, suggesting a functional role in vasodilation. The presence of AChE positivity in these neurons, but not ChAT, suggests that they are cholinoceptive but noncholinergic. WMNs were also significantly smaller in AD compared to control cases. These observations provide a landscape for future systematic investigations. [ABSTRACT FROM AUTHOR]

Multiple cortical (planum temporale, supramarginal gyrus, fusiform gyrus) and subcortical (caudate, putamen, and thalamus) regions have shown different functional lateralization patterns for skilled vs. dyslexic readers. The extent to which skilled and dyslexic adult readers show differential structural lateralization remains to be seen. Method: Participants included 72 adults (N = 41 skilled; N = 31 dyslexic) who underwent a high-resolution MRI brain scan. The grey matter volume of the cortical and subcortical structures was extracted. Results: While there were clear behavioral differences between the groups, there were no differences in any of the isolated structures (i.e., either total size or asymmetry index) and limited evidence for any brain–behavior relationships. We did find a significant cortical–cortical relationship (p = 0.006) and a subcortical–subcortical relationship (p = 0.008), but not cross-over relationships. Overall, this work provides unique information on neural structures as they relate to reading in skilled and dyslexic readers. [ABSTRACT FROM AUTHOR]

During late childhood behavioral changes, such as increased risk-taking and emotional reactivity, have been associated with the maturation of cortico-cortico and cortico-subcortical circuits. Understanding microstructural changes in both white matter and subcortical regions may aid our understanding of how individual differences in these behaviors emerge. Restriction spectrum imaging (RSI) is a framework for modelling diffusion-weighted imaging that decomposes the diffusion signal from a voxel into hindered, restricted, and free compartments. This yields greater specificity than conventional methods of characterizing diffusion. Using RSI, we quantified voxelwise restricted diffusion across the brain and measured age associations in a large sample (n = 8086) from the Adolescent Brain and Cognitive Development (ABCD) study aged 9-14 years. Older participants showed a higher restricted signal fraction across the brain, with the largest associations in subcortical regions, particularly the basal ganglia and ventral diencephalon. Importantly, age associations varied with respect to the cytoarchitecture within white matter fiber tracts and subcortical structures, for example age associations differed across thalamic nuclei. This suggests that age-related changes may map onto specific cell populations or circuits and highlights the utility of voxelwise compared to ROI-wise analyses. Future analyses will aim to understand the relevance of this microstructural developmental for behavioral outcomes.

Network representation has been an incredibly useful concept for understanding the behavior of complex systems in social sciences, biology, neuroscience, and beyond. Network science is mathematically founded on graph theory, where nodal importance is gauged using measures of centrality. Notably, recent work suggests that the topological centrality of a node should not be over-interpreted as its dynamical or causal importance in the network. Hence, identifying the influential nodes in dynamic causal models (DCM) remains an open question. This paper introduces causal centrality for DCM, a dynamics-sensitive and causally-founded centrality measure based on the notion of intervention in graphical models. Operationally, this measure simplifies to an identifiable expression using Bayesian model reduction. As a proof of concept, the average DCM of the extended default mode network (eDMN) was computed in 74 healthy subjects. Next, causal centralities of different regions were computed for this causal graph, and compared against several graph-theoretical centralities. The results showed that the subcortical structures of the eDMN were more causally central than the cortical regions, even though the graph-theoretical centralities unanimously favored the latter. Importantly, model comparison revealed that only the pattern of causal centrality was causally relevant. These results are consistent with the crucial role of the subcortical structures in the neuromodulatory systems of the brain, and highlight their contribution to the organization of large-scale networks. Potential applications of causal centrality—to study causal models of other neurotypical and pathological functional networks—are discussed, and some future lines of research are outlined. [ABSTRACT FROM AUTHOR]

When humans reach to visual targets, extremely rapid (;90 ms) target-directed responses can be observed in task-relevant proximal muscles. Such express visuomotor responses are inflexibly locked in time and space to the target and have been proposed to reflect rapid visuomotor transformations conveyed subcortically via the tecto-reticulo-spinal pathway. Previously, we showed that express visuomotor responses are sensitive to explicit cue-driven information about the target, suggesting that the express pathway can be modulated by cortical signals affording contextual prestimulus expectations. Here, we show that the express visuomotor system incorporates information about the physical hand-to-target distance and contextual rules during visuospatial tasks requiring different movement amplitudes. In one experiment, we recorded the activity from two shoulder muscles as 14 participants (6 females) reached toward targets that appeared at different distances from the reaching hand. Increasing the reaching distance facilitated the generation of frequent and large express visuomotor responses. This suggests that both the direction and amplitude of veridical hand-to-target reaches are encoded along the putative subcortical express pathway. In a second experiment, we modulated the movement amplitude by asking 12 participants (4 females) to deliberately undershoot, overshoot, or stop (control) at the target. The overshoot and undershoot tasks impaired the generation of large and frequent express visuomotor responses, consistent with the inability of the express pathway to generate responses directed toward nonveridical targets as in the anti-reach task. Our findings appear to reflect strategic, cortically driven modulation of the express visuomotor circuit to facilitate rapid and effective response initiation during target-directed actions. [ABSTRACT FROM AUTHOR]

Introduction: Frailty is a geriatric syndrome frequently associated with executive dysfunction and white matter hyperintensities (WMH). But the relation between executive dysfunction and brain changes is poorly understood in frail subjects. Our hypothesis is that frontal-WMH mediates the association between frailty and executive dysfunction. Methods: A convenience sample of 113 subjects older than 65 years without dementia was studied with neuropsychological test, a structured clinical interview, physical examination and brain MRI. They were classified as robust or pre-frail and frail using the frailty phenotype score (0-5). The frontal WMH (F-WMH) were manually graduated (0-6) using the "Age-Related White Matter Changes score" from FLAIR sequences at a 3 Tesla brain MRI. A mediation analysis was done for testing whether F-WMH could act as a link factor between frailty phenotype score and executive dysfunction. Results: The group's mean age was 74 ± 6 years, subjects with higher frailty score had more depressive symptoms and worse performance in executive function tests. A regression analysis that explained 52% of the variability in executive functions, revealed a significant direct effect of frailty score (Standardized ßcoeff [95% CI] -0.201, [-0.319, -0.049], and F-WMH (-0.152[-0.269, -0.009]) on executive functions, while the F-WMH showed a small partial mediation effect between frailty and executive functions (-0.0395, [-0.09, -0.004]). Discussion: Frontal matter hyperintensities had a small mediation effect on the association between frailty and executive dysfunction, suggesting that other neuropathological and neurofunctional changes might also be associated with executive dysfunction in frail subjects. [ABSTRACT FROM AUTHOR]

Background: Childhood trauma influences the clinical features of schizophrenia. In this study, we examined how childhood trauma and perceived stress are associated with clinical manifestations and subcortical gray matter volumes (GMVs) in patients with schizophrenia. Methods: We recruited 127 patients with schizophrenia and 83 healthy controls for assessment of early childhood trauma, perceived stress, and clinical symptoms. With structural brain imaging, we identified the GMVs of subcortical structures and examined the relationships between childhood trauma, perceived stress, clinical symptoms, and subcortical GMVs. Results: Compared to controls, patients with schizophrenia showed higher levels of childhood trauma and perceived stress. Patients with schizophrenia showed significantly smaller amygdala and hippocampus GMVs as well as total cortical GMVs than age-matched controls. Childhood trauma score was significantly correlated with the severity of clinical symptoms, depression, perceived stress, and amygdala GMVs. Perceived stress was significantly correlated with clinical symptoms, depression, and hippocampus and amygdala GMVs. Further, the association between childhood trauma (emotional neglect) and stress coping ability was mediated by right amygdala GMV in patients with schizophrenia. Conclusions: Patients with schizophrenia had more exposure to early-life trauma and poorer stress coping. Both childhood trauma and perceived stress were associated with smaller amygdala volumes. The relationship between early-life trauma and perceived stress was mediated by right amygdala GMV in patients with schizophrenia. These findings together suggest the long-term effects of childhood trauma on perceived stress and the subcortical volumetric correlates of the effects in schizophrenia. [ABSTRACT FROM AUTHOR]

In recent years, with the development of technology, three-dimensional software has entered our lives. Volumetric measurements made with Magnetic Resonance Imaging (MRI) are essential in the morphometry of the brain and subcortical structures. In this study, we aim to share the volume and asymmetry of the hippocampus, its sub-branches, and other subcortical structures and their interaction with age/sex using volBrain, a web-based automated software. 1.5 T T1-weighted volumetric MRI, of 90 healthy individuals (51 females, 39 males) of both genders were included in our study. Pallidum, hippocampus, Cornu Ammonis1 (CA1), Cornu Ammonis2-3 (CA2-CA3), and Cornu Ammonis4-Dentate Gyrus (CA4-DG) measurements in females and males had a statistically higher mean in the right region (p < 0.05). In addition, females' hippocampus, CA1, CA2-CA3, and CA4-DG averages decreased more rapidly in the right region than in the left region. Subiculum measurement had a higher mean in the left region in both males and females (p < 0.05). The mean subiculum of males decreased more rapidly in the right region than in the left region. When the total values of the subcortical region in males and females were compared according to age categories, amygdala, pallidum, putamen, hippocampus, CA2-CA3, and subiculum values did not differ to gender in individuals aged 50 and over (p > 0.05). In individuals under 50 years old, the mean of females was statistically lower than the mean of males (p < 0.05). The Stratum radiatum (SR), Stratum lacunosum (SL), and Stratum molecuare (SM) asymmetry values of males in the examined subcortical regions had a higher mean than females (p = 0.039). In other regions, there was no statistically asymmetrical difference (p > 0.05). Studies evaluating the volumetric analysis and asymmetry of hippocampus subbranches and other subcortical structures in adults are very limited. As a result, the morphometry of the hippocampus subbranches and other subcortical structures was examined in detail. It was determined that the structures differed according to age, gender and body side. [ABSTRACT FROM AUTHOR]

Brain function originates from hierarchical spatial-temporal neural dynamics distributed across cortical and subcortical networks. However, techniques available to assess large-scale brain network activity with single-neuron resolution in behaving animals remain limited. Here, we present Mesotrode that integrates chronic wide-field mesoscale cortical imaging and compact multi-site cortical/subcortical cellular electrophysiology in head-fixed mice that undergo self-initiated running or orofacial movements. Specifically, we harnessed the flexibility of chronic multi-site tetrode recordings to monitor single-neuron activity in multiple subcortical structures while simultaneously imaging the mesoscale activity of the entire dorsal cortex. A mesoscale spike-triggered averaging procedure allowed the identification of cortical activity motifs preferentially associated with single-neuron spiking. Using this approach, we were able to characterize chronic single-neuron-related functional connectivity maps for up to 60 days post-implantation. Neurons recorded from distinct subcortical structures display diverse but segregated cortical maps, suggesting that neurons of different origins participate in distinct cortico-subcortical pathways. We extended the capability of Mesotrode by implanting the micro-electrode at the facial motor nerve and found that facial nerve spiking is functionally associated with the PTA, RSP, and M2 network, and optogenetic inhibition of the PTA area significantly reduced the facial movement of the mice. These findings demonstrate that Mesotrode can be used to sample different combinations of cortico-subcortical networks over prolonged periods, generating multimodal and multi-scale network activity from a single implant, offering new insights into the neural mechanisms underlying specific behaviors.

Subcortical nuclei and other deep brain structures play essential roles in regulating the central and peripheral nervous systems. However, many of these nuclei and their subregions are challenging to identify and delineate in conventional MRI due to their small size, hidden location, and often subtle contrasts compared to neighboring regions. To address these limitations, we scanned the whole brain of the marmoset monkeys in ex vivo using a clinically feasible diffusion MRI method, called the mean apparent propagator (MAP)-MRI, along with T2W and MTR (T1-like contrast) images acquired at 7 Tesla. Additionally, we registered these multimodal MRI volumes to the high-resolution images of matched whole-brain histology sections with seven different stains obtained from the same brain specimens. At high spatial resolution, the microstructural parameters and fiber orientation distribution functions derived with MAP-MRI can distinguish the subregions of many subcortical and deep brain structures, including fiber tracts of different sizes and orientations. The good correlation with multiple but distinct histological stains from the same brain serves as a thorough validation of the structures identified with MAP-MRI and other MRI parameters. Moreover, the anatomical details of deep brain structures found in the volumes of MAP-MRI parameters are not visible in conventional T1W or T2W images. The high-resolution mapping using novel MRI contrasts, combined and correlated with histology, can elucidate structures that were previously invisible radiologically. Thus, this multimodal approach offers a roadmap toward identifying salient brain areas in vivo in future neuroradiological studies. It also provides a useful anatomical standard reference for the region definition of subcortical targets and the generation of a 3D digital template atlas for the marmoset brain research (Saleem et al., 2023). Additionally, we conducted a cross-species comparison between marmoset and macaque monkeys using results from our previous studies (Saleem et al., 2021). We found that the two species had distinct patterns of iron distribution in subregions of the basal ganglia, red nucleus, and deep cerebellar nuclei, confirmed with T2W MRI and histology.

Pitch is a perceptual rather than physical phenomenon, important for spoken language use, musical communication, and other aspects of everyday life. Auditory stimuli can be designed to probe the relationship between perception and physiological responses to pitch-evoking stimuli. One technique for measuring physiological responses to pitch-evoking stimuli is the frequency following response (FFR). The FFR is an electroencephalographic (EEG) response to periodic auditory stimuli. The FFR contains nonlinearities not present in the stimuli, including correlates of the amplitude envelope of the stimulus; however, these nonlinearities remain undercharacterized. The FFR is a composite response reflecting multiple neural and peripheral generators, and their contributions to the scalp-recorded FFR vary in ill-understood ways depending on the electrode montage, stimulus, and imaging technique. The FFR is typically assumed to be generated in the auditory brainstem; there is also evidence both for and against a cortical contribution to the FFR. Here a methodology is used to examine the FFR correlates of pitch and the generators of the FFR to stimuli with different pitches. Stimuli were designed to tease apart biological correlates of pitch and amplitude envelope. FFRs were recorded with 256-electrode EEG nets, in contrast to a typical FFR setup which only contains a single active electrode. Structural MRI scans were obtained for each participant to co-register with the electrode locations and constrain a source localization algorithm. The results of this localization shed light on the generating mechanisms of the FFR, including providing evidence for both cortical and subcortical auditory sources.

While iron over‐accumulation has been reported in late stage Alzheimer's disease (AD), whether this occurs early in the asymptomatic stage of AD remains unknown. We aimed to assess brain iron levels in asymptomatic AD using quantitative MR relaxometry of effective transverse relaxation rate (R2*) and longitudinal relaxation rate (R1), and recruited 118 participants comprised of three groups including healthy young participants, and cognitively normal older individuals without or with positive AD biomarkers based on cerebrospinal fluid (CSF) proteomics analysis. Compared with the healthy young group, increased R2* was found in widespread cortical and subcortical regions in the older groups. Further, significantly higher levels of R2* were found in the cognitively normal older subjects with positive CSF AD biomarker (i.e., asymptomatic AD) compared with those with negative AD biomarker in subcortical regions including the left and right caudate, left and right putamen, and left and right globus pallidus (p <.05 for all regions), suggesting increased iron content in these regions. Subcortical R2* of some regions was found to significantly correlate with CSF AD biomarkers and neuropsychological assessments of visuospatial functions. In conclusion, R2* could be a valuable biomarker for studying early pathophysiological changes in AD. [ABSTRACT FROM AUTHOR]

Cerebral microinfarcts are associated with cognitive impairment and dementia. Small vessel diseases such as cerebral arteriolosclerosis and cerebral amyloid angiography (CAA) have been found to be associated with microinfarcts. Less is known about the associations of these vasculopathies with the presence, numbers, and location of microinfarcts. These associations were examined in the clinical and autopsy data of 842 participants in the Adult Changes in Thought (ACT) study. Both vasculopathies were categorized by severity (none, mild, moderate, and severe) and region (cortical and subcortical). Odds ratios (OR) and 95% CIs for microinfarcts associated with arteriolosclerosis and CAA adjusted for possible modifying covariates such as age at death, sex, blood pressure, APOE genotype, Braak, and CERAD were estimated. 417 (49.5%) had microinfarcts (cortical, 301; subcortical, 249), 708 (84.1%) had cerebral arteriolosclerosis, 320 (38%) had CAA, and 284 (34%) had both. Ors (95% CI) for any microinfarct were 2.16 (1.46–3.18) and 4.63 (2.90–7.40) for those with moderate (n = 183) and severe (n = 124) arteriolosclerosis, respectively. Respective Ors (95% CI) for the number of microinfarcts were 2.25 (1.54–3.30) and 4.91 (3.18–7.60). Similar associations were observed for cortical and subcortical microinfarcts. Ors (95% Cis) for the number of microinfarcts associated with mild (n = 75), moderate (n = 73), and severe (n = 15) amyloid angiopathy were 0.95 (0.66–1.35), 1.04 (0.71–1.52), and 2.05 (0.94–4.45), respectively. Respective Ors (95% Cis) for cortical microinfarcts were 1.05 (0.71–1.56), 1.50 (0.99–2.27), and 1.69 (0.73–3.91). Respective Ors (95% Cis) for subcortical microinfarcts were 0.84 (0.55–1.28), 0.72 (0.46–1.14), and 0.92 (0.37–2.28). These findings suggest a significant association of cerebral arteriolosclerosis with the presence, number, and location (cortical and subcortical) of microinfarcts, and a weak and non-significant association of CAA with each microinfarct, highlighting the need for future research to better understand the role of small vessel diseases in the pathogenesis of cerebral microinfarcts. [ABSTRACT FROM AUTHOR]

The positive relationship between socioeconomic status (SES) and cognitive performance is mediated, in part, by differences in brain structure in typically developing youth. Associations between brain regions that relate to SES overlap with brain regions known to be sensitive to prenatal alcohol exposure (PAE). Animal models demonstrate that PAE attenuates neural and cognitive benefits of early life enrichment. However, whether or not environmental factors related to SES are associated with brain development in youth affected by PAE remains unknown in humans.MethodsT1-weighted magnetic resonance imaging (MRI) scans were obtained in participants with PAE and compared to age- and sex- matched Controls (n = 197, 48% with PAE, 44% girls, 6.5-17.7 years old). General linear modeling was utilized to examine associations between SES and subcortical brain volumes for youth with PAE compared to Controls.ResultsGroup by SES interactions were observed within the hippocampus (HPC), nucleus accumbens (NAc) and ventral diencephalon (vDC) (corrected p values

Background: Previous reports have suggested that patients with cerebral amyloid angiopathy (CAA) may harbor smaller white matter, basal ganglia, and cerebellar volumes compared to age-matched healthy controls (HC) or patients with Alzheimer's disease (AD). We investigated whether CAA is associated with subcortical atrophy. Methods: The study was based on the multi-site Functional Assessment of Vascular Reactivity cohort and included 78 probable CAA (diagnosed according to the Boston criteria v2.0), 33 AD, and 70 HC. Cerebral and cerebellar volumes were extracted from brain 3D T1-weighted MRI using FreeSurfer (v6.0). Subcortical volumes, including total white matter, thalamus, basal ganglia, and cerebellum were reported as proportion (%) of estimated total intracranial volume. White matter integrity was quantified by the peak width of skeletonized mean diffusivity. Results: Participants in the CAA group were older (74.0 ± 7.0, female 44%) than the AD (69.7 ± 7.5, female 42%) and HC (68.8 ± 7.8, female 69%) groups. CAA participants had the highest white matter hyperintensity volume and worse white matter integrity of the three groups. After adjusting for age, sex, and study site, CAA participants had smaller putamen volumes (mean differences, -0.024% of intracranial volume; 95% confidence intervals, -0.041% to -0.006%; p = 0.005) than the HCs but not AD participants (-0.003%; -0.024 to 0.018%; p = 0.94). Other subcortical volumes including subcortical white matter, thalamus, caudate, globus pallidus, cerebellar cortex or cerebellar white matter were comparable between all three groups. Conclusion: In contrast to prior studies, we did not find substantial atrophy of subcortical volumes in CAA compared to AD or HCs, except for the putamen. Differences between studies may reflect heterogeneity in CAA presenting syndromes or severity. [ABSTRACT FROM AUTHOR]

Human evolution has been marked by a striking increase in total brain volume relative to body size. While a prominent and characteristic feature of this volumetric shift has been the disproportionate expansion of association cortex across our evolutionary lineage, descent with modification is apparent throughout all neural systems in both human and nonhuman primates. However, despite evidence for the ubiquitous and complex influence of evolutionary forces on brain biology, within the psychological sciences the vast majority of the literature on human brain evolution is entirely corticocentric. This selective focus has contributed to a flawed theoretical framework in which the evolution of association cortex is viewed as an isolated process, removed from the rest of the brain. Here, we review our current understanding of how evolutionary pressures have acted across anatomically and functionally coupled networks, highlighting the diverse set of rules and principles that govern human brain development. In doing so we challenge the systemic mischaracterization of human cognition and behavior as a competition that pits phylogenetically recent cortical territories against evolutionarily ancient subcortical and cerebellar systems. Rather, we propose a comprehensive view of human brain evolution with critical importance for the use of animal models, theory development, and network-focused approaches in the study of behavior across health and disease. [ABSTRACT FROM AUTHOR]

The basal forebrain provides cholinergic inputs to primary visual cortex (V1) that play a key modulatory role on visual function. While basal forebrain afferents terminate in the infragranular layers of V1, acetylcholine is delivered to more superficial layers through volume transmission. Nevertheless, direct synaptic contact in deep layers 5 and 6 may provide a more immediate effect on V1 modulation. Using helper viruses with cell type specific promoters to target retrograde infection of pseudotyped and genetically modified rabies virus evidence was found for direct synaptic input onto V1 inhibitory neurons. These inputs were similar in number to geniculocortical inputs and, therefore, considered robust. In contrast, while clear evidence for dorsal lateral geniculate nucleus input to V1 excitatory neurons was found, there was no evidence of direct synaptic input from the basal forebrain. These results suggest a direct and more immediate influence of the basal forebrain on local V1 inhibition.

Abstract Aphasia is a common post-stroke disorder characterized by impairments in speaking, listening, reading, and writing. Although cognitive impairments have been well studied in cortical aphasia, deficits associated with subcortical aphasia remain to be elucidated. The current study aimed to assess executive functions (EF) and working memory (WM) in patients with subcortical aphasia, and investigate the relationship between language abilities and cognition deficits. Participants of this research included patients with thalamus lesions (n = 9; mean age = 53.89 years) and healthy individuals (n = 9; mean age = 54.33 years). Assessment materials were the Mini-Mental State Examination (MMSE), Persian Western Aphasia Battery (P-WAB-1), digit span subtest of Adult Wechsler Test (WAIS-R), and Wisconsin Card Sorting Test (WCST). Obtained results revealed significant differences in all components of EF, as well as in WM forward and backward digit spans between patients and healthy individuals. However, investigating the relationship between MMSE and AQ scores and components of EF and WM revealed no significant difference. In conclusion, the findings of the present research indicated defects in cognitive functions, including WM and EF, in patients with subcortical stroke. Accordingly, it is crucial to provide optimal rehabilitation therapies for the improvement of language and cognitive problems upon subcortical aphasia. [ABSTRACT FROM AUTHOR]

Consciousness is a fascinating field of neuroscience research where questions often outnumber the answers. We advocate an open and optimistic approach where converging mechanisms in neuroscience may eventually provide a satisfactory understanding of consciousness. We first review several characteristics of conscious neural activity, including the involvement of dedicated systems for content and levels of consciousness, the distinction and overlap of mechanisms contributing to conscious states and conscious awareness of transient events, nonlinear transitions and involvement of large-scale networks, and finally the temporal nexus where conscious awareness of discrete events occurs when mechanisms of attention and memory meet. These considerations and recent new experimental findings lead us to propose an inclusive hypothesis involving four phases initiated shortly after an external sensory stimulus: (1) Detect—primary and higher cortical and subcortical circuits detect the stimulus and select it for conscious perception. (2) Pulse—a transient and massive neuromodulatory surge in subcortical-cortical arousal and salience networks amplifies signals enabling conscious perception to proceed. (3) Switch—networks that may interfere with conscious processing are switched off. (4) Wave—sequential processing through hierarchical lower to higher cortical regions produces a fully formed percept, encoded in frontoparietal working memory and medial temporal episodic memory systems for subsequent report of experience. The framework hypothesized here is intended to be nonexclusive and encourages the addition of other mechanisms with further progress. Ultimately, just as many mechanisms in biology together distinguish living from nonliving things, many mechanisms in neuroscience synergistically may separate conscious from nonconscious neural activity. [ABSTRACT FROM AUTHOR]

Distributed cortical regions show differential responses to visual objects belonging to different domains varying by animacy (e.g., animals vs tools), yet it remains unclear whether this is an organization principle also applying to the subcortical structures. Combining multiple fMRI activation experiments (two main experiments and six validation datasets; 12 females and 9 males in the main Experiment 1; 10 females and 10 males in the main Experiment 2), resting-state functional connectivity, and task-based dynamic causal modeling analysis in human subjects, we found that visual processing of images of animals and tools elicited different patterns of response in the pulvinar, with robust left lateralization for tools, and distinct, bilateral (with rightward tendency) clusters for animals. Such domain-preferring activity distribution in the pulvinar was associated with the magnitude with which the voxels were intrinsically connected with the corresponding domain-preferring regions in the cortex. The pulvinar-to-right-amygdala path showed a one-way shortcut supporting the perception of animals, and the modulation connection from pulvinar to parietal showed an advantage to the perception of tools. These results incorporate the subcortical regions into the object processing network and highlight that domain organization appears to be an overarching principle across various processing stages in the brain. [ABSTRACT FROM AUTHOR]

Introduction: Volumetric and morphological changes in subcortical brain structures are present in persons with dementia, but it is unknown if these changes occur prior to diagnosis. Methods: Between 2005 and 2016, 5522 Rotterdam Study participants (mean age: 64.4) underwent cerebral magnetic resonance imaging (MRI) and were followed for development of dementia until 2018. Volume and shape measures were obtained for seven subcortical structures. Results: During 12 years of follow‐up, 272 dementia cases occurred. Mean volumes of thalamus (hazard ratio [HR] per standard deviation [SD] decrease 1.94, 95% confidence interval [CI]: 1.55–2.43), amygdala (HR 1.66, 95% CI: 1.44–1.92), and hippocampus (HR 1.64, 95% CI: 1.43–1.88) were strongly associated with dementia risk. Associations for accumbens, pallidum, and caudate volumes were less pronounced. Shape analyses identified regional surface changes in the amygdala, limbic thalamus, and caudate. Discussion: Structure of the amygdala, thalamus, hippocampus, and caudate is associated with risk of dementia in a large population‐based cohort of older adults. [ABSTRACT FROM AUTHOR]

Three subtypes of distinct pathological proteins accumulate throughout multiple brain regions and shape the heterogeneous clinical presentation of frontotemporal lobar degeneration (FTLD). Besides the main pathological subtypes, co-occurring pathologies are common in FTLD brain donors. The objective of this study was to investigate how the location and burden of (co-)pathology correlate to early psychiatric and behavioural symptoms of FTLD. Eighty-seven brain donors from The Netherlands Brain Bank cohort (2008–2017) diagnosed with FTLD were included: 46 FTLD-TAR DNA-binding protein 43 (FTLD-TDP), 34 FTLD-tau, and seven FTLD-fused-in-sarcoma (FTLD-FUS). Post-mortem brain tissue was dissected into 20 standard regions and stained for phosphorylated TDP-43, phosphorylated tau, FUS, amyloid-β, and α-synuclein. The burden of each pathological protein in each brain region was assessed with a semi-quantitative score. Clinical records were reviewed for early psychiatric and behavioural symptoms. Whole-brain clinico-pathological partial correlations were calculated (local false discovery rate threshold = 0.01). Elaborating on the results, we validated one finding using a quantitative assessment of TDP-43 pathology in the granular layer of the hippocampus in FTLD-TDP brain donors with (n = 15) and without (n = 15) hallucinations. In subcortical regions, the presence of psychiatric symptoms showed positive correlations with increased hippocampal pathology burden: hallucinations with TDP-43 in the granular layer (R = 0.33), mania with TDP-43 in CA1 (R = 0.35), depression with TDP-43 in CA3 and with parahippocampal tau (R = 0.30 and R = 0.23), and delusions with CA3 tau (R = 0.26) and subicular amyloid-β (R = 0.25). Behavioural disinhibition showed positive correlations with tau burden in the thalamus (R = 0.29) and with both TDP-43 and amyloid-β burden in the subthalamus (R = 0.23 and R = 0.24). In the brainstem, the presence of α-synuclein co-pathology in the substantia nigra correlated with disinhibition (R = 0.24), tau pathology in the substantia nigra correlated with depression (R = 0.25) and in the locus coeruleus with both depression and perseverative/compulsive behaviour (R = 0.26 and R = 0.32). The quantitative assessment of TDP-43 in the granular layer validated the higher burden of TDP-43 pathology in brain donors with hallucinations compared to those without hallucinations (P = 0.007). Our results show that psychiatric symptoms of FTLD are linked to subcortical pathology burden in the hippocampus, and hallucinations are linked to a higher burden of TDP-43 in the granular layer. Co-occurring non-FTLD pathologies in subcortical regions could contribute to configuring the clinical phenotype of FTLD. [ABSTRACT FROM AUTHOR]

Several adults and larvae of Pytho abieticola were discovered in 2021 and 2022 at three different localities in two regions of Switzerland, the Jura mountains and the Swiss National Park in the Eastern Alps. This very rare saproxylic beetle has not been detected in Switzerland so far. Considered a relict of primeval forests, it is in strong decline or has already disappeared from large areas of Central Europe. The isolated Swiss populations are the westernmost in its distributional range. Information on the ecology and distribution of P. abieticola in Switzerland and Europe is provided and criteria to distinguish P. abieticola from the congeneric and syntopic P. depressus are defined. [ABSTRACT FROM AUTHOR]