Posterior Cingulate Research Articles (Page 1)

Dementia with Lewy bodies (DLB) and Parkinson disease (PD), especially when associated with REM sleep behavior disorder (RBD), represent partially overlapping phenotypes of overt α-synucleinopathies. We aimed to investigate overlapping and discrepant features between DLB with RBD (DLBRBD), PD with RBD (PDRBD), and PD without RBD (PD) patients. This was a cross-sectional study where consecutive patients with de novo PD, de novo PDRBD, and de novo DLBRBD underwent a full neuropsychological battery to study cognitive impairment, brain [18F]FDG PET as a marker of brain glucose metabolism, and [123I]FP-CIT SPECT as a marker of nigrostriatal dopaminergic functioning. Diagnosis was performed following current criteria, confirmed by evidence of dopaminergic deficit on [123I]FP-CIT SPECT and by at least 2 years of clinical follow-up. We recruited 31 de novo PD (mean age 71.8 ± 6.2; 38.7% females), 32 de novo PDRBD (mean age 72.6 ± 6, 28% females), and 30 de novo DLBRBD (mean age 78 ± 5.4; 40% females). Compared with de novo PD and de novo PDRBD, de novo DLBRBD patients were older, and had a lower education and significantly poorer cognitive performance (p < 0.001), especially involving attention, executive, and visuospatial functions. De novo DLBRBD patients showed significant reduced glucose metabolism involving the bilateral precuneus, bilateral cuneus, right angular gyrus, right posterior cingulate cortex, and right fusiform gyrus. Dopaminergic function was significantly worst in de novo PD, with a significantly lower [123I]FP-CIT binding in the least affected hemisphere (LAH) putamen (p = 0.042), LAH caudate (p = 0.027), and most affected hemisphere (MAH) putamen (p = 0.046) compared with de novo PDRBD patients, which was significantly lower also compared with de novo DLBRBD patients (p = 0.03). De novo DLBRBD had a lower binding compared with de novo PDRBD patients (p = 0.021) in the LAH caudate. The putamen/caudate ratio in the MAH was significantly lower in de novo PD compared with de novo PDRBD patients (p < 0.001) and in de novo PDRBD compared with de novo DLBRBD patients (p = 0.002). This study emphasizes how DLB with RBD and PD without RBD represent opposite ends of the neuronal α-synucleinopathy spectrum. The study highlights both overlapping and divergent clinical and neuroimaging features, with PD with RBD patients displaying an intermediate profile.

Humans are skilled at recognizing everyday objects from pictures, even if we have never encountered the depicted object in real life. But if we have encountered an object, how does that real-world experience affect the representation of its photographic image in the human brain? We developed a paradigm that involved brief real-world manual exploration of everyday objects prior to the measurement of brain activity with fMRI while viewing pictures of those objects (40 human participants, 28 female). We found that while object-responsive regions in lateral occipital and ventral temporal cortex contained robust visual representations of specific objects, those representations were not modulated by this brief real-world exploration. However, there was an effect of visual experience in object-responsive regions in the form of repetition suppression of the BOLD response over repeated presentations of the object images. Real-world experience with an object produced foci of increased activation in medial parietal and posterior cingulate cortex, regions that have previously been associated with the encoding and retrieval of remembered items in explicit memory paradigms. Our discovery that these regions are engaged during spontaneous recognition of real-world objects from their 2D image demonstrates that modulation of activity in medial regions by familiarity is neither stimulus nor task-specific. Overall, our results support separable coding in the human brain of the visual appearance of an object from the associations gained via real-world experience. The richness of object representations beyond their photographic image has important implications for understanding object recognition in the human brain and in computational models.Significance statement Humans and computers can both identify objects from pictures with ease (e.g. "a mug"). Yet unlike computers, humans spend much of their day physically interacting with familiar three-dimensional objects. Thus, our knowledge of objects is multifaceted and extends beyond their visual characteristics. Using brain imaging, we found that medial parietal cortical regions are preferentially engaged when people view photographs depicting objects they had previously manually explored. In contrast, visual brain areas contained robust representations of individual objects that were invariant across different photographs of the same object, but were not modulated by brief real-world experience. Together, our results suggest that an object's visual appearance is coded separately in the human brain from any associations developed via real-world experience.

Minimal hepatic encephalopathy (MHE) is the initial stage of hepatic encephalopathy (HE), MHE patients have associated with widespread neuro-psychological impairment. Liver transplantation (LT) can restore metabolic abnormalities but the mechanisms are unclear. This study aimed to longitudinally evaluate brain function alteration in MHE patients one month after LT and their correlation with cognitive changes by using resting-state functional magnetic resonance imaging (rs-fMRI). Rs-fMRI data was collected from 32 healthy controls and 27 MHE before and 1 month after LT. Between-group comparisons of demographic data and neuropsychological scores were analyzed using SPSS 25.0. Functional imaging data were analyzed using RESTplus and SPM12 software based on MATLAB 2017b. Gender, age, and years of education were used as covariates to obtain low-frequency fluctuationd (ALFF) and dynamic low-frequency fluctuation (dALFF) dindices. Correlation analyses were performed to explore the relationship between the change of ALFF and dALFF with the change of clinical indexes pre- and post-LT. Compared to controls, ALFF values increased in the Left Cerebelum 8, right orbital part of the inferior frontal gyrus (ORBinf), right superior occipital gyrus (SOG) and decreased in right PreCG and left middle frontal gyrus (MFG) in patients post-LT; dALFF values increased in the right temporal pole and middle temporal gyrus (TPOmid), right ORBinf, left caudate nucleus (CAU), right SOG and decreased in left PreCG, left PCUN, left ANG, left SMA and left MFG in patients post-LT. Compared to pre-LT, ALFF values of post-LT patients increased in the right calcarine fissure and surrounding cortex (CAL), right MOG and decreased in right cerebelum 8, left PCUN; dALFF values of post-LT patients decreased in right thalamus (THA), left posterior cingulate gyrus (PCG) and left MFG. The changes of ALFF in the left PCUN, right CAL and right MOG were correlated with change of digit symbol test (DST) scores ( P &amp;lt; 0.05). In summary, this study not only showcases the potential of ALFF/dALFF algorithms for assessing alterations in spontaneous neural activity in MHE, but also provides new insights into the altered brain functions in MHE patients 1 month after LT, which may facilitate the elucidation of elucidation of mechanisms underlying cognitive restoration post-LT in MHE patients.

BackgroundIt has become evident that various different neuropathologies including Alzheimer's disease neuropathologic change, limbic-predominant age-related TDP-43 encephalopathy neuropathological change (LATE-NC), and argyrophilic grain disease (AGD) coexist in patients with Lewy body disease (LBD). However, the effect of these comorbidities on brain atrophy remains understudied.ObjectiveThis study aimed to explore the morphological impacts of comorbidities using voxel-based morphometry (VBM).MethodsThirty-four individuals with a neuropathological diagnosis of LBD were included. Antemortem whole-brain 3D-T1-weighted images were preprocessed using Computational Anatomy Toolbox 12. Associations between gray matter (GM) atrophy and specific comorbid neuropathology, as well as interactions among them, were analyzed using VBM.ResultsNeurofibrillary tangle (NFT) pathology exhibited inverse correlations with GM volumes of the right temporal, bilateral frontal lobes, and left posterior cingulate gyrus. Neuritic plaque (NP) pathology-related GM atrophy was localized to the left posterior cingulate gyrus and parts of the parietal lobes. LATE-NC exhibited inverse correlations mainly in the left temporal lobe and left-dominant limbic lobes including the hippocampi. AGD pathology-related GM atrophy was predominant in the left-dominant limbic lobes and left temporal pole. Small vessel disease (SVD) scores were inversely correlated with GM volumes in the left frontal lobe and bilateral cerebellar hemispheres. Interactions between NFT and LATE-NC were limited to limbic and temporal lobes, while interactions between NFT and NP, SVD and NFT or LATE-NC showed more posterior-dominant distributions.ConclusionsVBM analyses revealed distinct atrophy patterns reflective of isolated neuropathologies. Furthermore, the study suggests that interactions between neuropathologies may influence brain atrophy patterns.

Major depression (MD) is a condition characterised by persistent sadness and apathy, sometimes accompanied by changes in sleep, appetite, and energy levels. It is highly heterogeneous, and depressive subtypes exhibit differing symptom profiles and patterns of brain activity. Background/Objectives: Currently, there are no physiological diagnostic means to detect depression or depressive subtypes. An emerging biomarker may be the electroencephalogram (EEG) band, gamma, due to the role of this frequency in reward processing and cognition. The aim of this work was to complete an exploratory study to investigate the interaction between gamma band power, depression, and four depressive subtypes. Methods: A correlative study between resting-state gamma band power and individual scores on the Zung Self-rating Depression Scale (SDS) was completed using exact standardised low-resolution electromagnetic tomography (eLORETA) using EEG data from a community sample of 100 participants, including not depressed and depressed participants, and four depressive subtypes (anhedonia-, cognitive- and somatic-depression and depressed mood). Results: There was no significant positive correlation between gamma band power and overall depression score. However, there was a significant positive correlation between anhedonia and gamma band power, predominantly in the left anterior cingulate cortex, which may be consistent with dysfunctional reward processing, a characteristic of anhedonia. Additional areas of significance included the posterior cingulate cortex and left middle and superior frontal cortex. Conclusions: These results provide preliminary support for neurophysiological indicators of depressive subtypes and may help inform diagnosis and treatment guidance for depression and depressive subtypes in the future.

Resting-state functional connectivity of the default mode network subsystems as a potential biomarker for delusions in patients with first-episode drug-naïve schizophrenia.

Cerebral white matter changes and their correlation with cognitive dysfunction and clinical indicators in patients with early coal workers' pneumoconiosis based on MR-diffusion spectrum imaging.

Ketosis Elevates Antioxidants and Markers of Energy Metabolism: A Proton Magnetic Resonance Spectroscopy Study.

Neural correlates of inhibitory control during a simple food go/no-go task in adolescents varying in familial obesity risk.

Neuroimaging evidence of structural and network disruptions in adolescents with conversion disorder with seizures.

Enhanced volume and resting-state functional connectivity of amygdala subregions in patients with insomnia disorder.

TMS-induced modulation of brain networks and its associations to rTMS treatment for depression: a concurrent fMRI-EEG-TMS study.

Correlation of auditory network hyperconnectivity with P3a amplitude and set-shifting in individuals with autism spectrum disorder.

The Desegregation of Neural Networks During Worry Induction in Late Life: An Effective Connectivity Analysis.

Anterior cingulate cortex-related functional dysconnectivity in adolescents with major depressive disorder with and without severe loneliness.

Progressive supranuclear palsy (PSP) is a clinically heterogeneous neurodegenerative disorder with unclear pathophysiology. This study aimed to uncover clinically relevant metabolic networks derived from 18F-fluorodeoxyglucose (FDG) positron emission tomography (PET) in PSP. FDG and dopaminergic transporter PET data from 72 PSP patients and 70 healthy controls were analyzed, with an independent test set of 24 PSP patients. All patients underwent comprehensive neuropsychiatric assessments. Using spatial independent component analysis, the study identified independent metabolic networks and examined their correlations with clinical features and striatal dopaminergic binding. Three distinct metabolic networks were identified in PSP: The first network demonstrated hypometabolism in dorsomedial thalamus (dmT), medial prefrontal cortex (mPFC) and midbrain, termed the dmT-mPFC network, negatively correlating with disease severity, functional disability and duration, and associating with gait/midline disturbances and ocular dysfunction. The second network displayed posterior cingulate cortex (PCC) and lateral prefrontal hypometabolism (LPFC), named the PCC-LPFC network, linking to disease severity, cognitive impairment, and parkinsonism. The third network exhibited preserved putamen metabolism with ventrolateral thalamus and sensorimotor cortex hypermetabolism, inversely relating to disease duration. Both dmT-mPFC and PCC-LPFC networks strongly correlated with striatal dopaminergic degeneration. The test set showed strong associations between cognitive impairment and the PCC-LPFC network, and between functional disability and the dmT-mPFC network, along with potential trends linking disease severity to these networks. The robust clinical and dopaminergic-related independent metabolic networks offer novel insights into disease pathophysiology, whereas their qualitative weighting offers a potential tool for staging disease severity. © 2025 International Parkinson and Movement Disorder Society.

Abstract Although the classifications of “past, ” “present, ” and “future” are considered abstract concepts, we naturally understand them. Those classifications were named “A-series” time by McTaggart in 1908. Alzheimer's disease (AD) is the most common type of dementia, with initial symptoms generally including temporal disorientation. This study aims to (1) elucidate the impairment process of temporal cognition in AD by administering A-series temporal tasks to individuals with AD, mild cognitive impairment (MCI), and healthy controls, and (2) clarify the relationship between temporal cognition at each stage of impairment and cerebral blood flow (CBF). A diagnosis of AD (n=37), MCI (n=10), and no dementia (ND) (n=10) took part. The “A-series” task consisted of eleven short sentences that were grammatically correct using seven-time qualifiers (last week, yesterday, today, now, tomorrow, this week, or next week). The participants were required to respond when the events in the sentences happened or would happen in nine stages. We compared the pattern of their responses, the scores of the Japanese version of the Mini-Mental State Examination (MMSE-J), and the regional CBFs performed by 99mTc-ethyl cysteinate dimer Single Photon Emission Computed Tomography. We found that ND was intact in the ability to distinguish between the past, present, and future, on the other hand, AD and MCI showed a diminished ability in temporal orientation when we sorted the 11 sentences in the ascending order of the mean response scores among the ND participants, they were generally ordered according to the time represented by adverbs of time. We also found that the participants could be best classified into three clusters. All ND participants (10/10) and half of the MCI participants (5/10) belonged to Cluster 1, whereas only 19% of the AD participants belonged to the cluster (7/37). Cluster 2 was contributed by three MCI participants (3/10) and 30% of the AD participants (11/37). Finally, most of the AD participants (51%) belonged to cluster 3 (19/37) with a few MCI participants (2/10). We compared CBFs across the three clusters and found the CBF in the pairs of the left and the right pericallosal region could predict whether a participant belonged to either cluster at the largest hit rate of 75%. Our findings suggest that the bilateral pericallosal region, including the posterior cingulate gyrus and precuneus cortex, is associated with temporal orientation.

ABSTRACTPreclinical detection of Alzheimer's disease (AD) is crucial to efficiently recruit clinical trial participants for examining AD‐modifying drugs and ultimately yield clinical benefits for at‐risk individuals. Cerebral amyloidosis precedes synaptic dysfunction and neurodegeneration markers, followed by the onset of AD‐related cognitive impairment. To improve early AD‐biomarker detection accuracy, patient data is, however, often collected via invasive procedures such as a lumbar puncture or intravenous injection of active radiopharmaceuticals. This coupled health risk is small yet significant and can be avoided by generating equally predictive or superior AD‐risk staging proxy biomarkers derived from noninvasive neuroimaging modalities. In addition, using neuroimaging can provide richer insights into regional distributions of brain biomarkers of AD. Motivated by that, here we train neural networks to optimally generate latent structural MRI (sMRI) representations as proxies for cerebrospinal fluid (CSF) biomarker status on multiple classification and prediction contexts, an approach that we demonstrate has the potential to be clinically useful in screening and diagnosing AD and predicting AD progression. We found that the amygdala, hippocampus, parahippocampus, posterior and middle cingulate gyrus, middle and inferior temporal gyrus, angular gyrus, precuneus, and inferior parietal lobe regions revealed maximum attribution, thereby implying the highest prognostic value for AD risk. The proposed approach of predicting amyloid and/or tau pathology biomarkers from MRI data and subsequently transferring the MRI‐derived amyloid and/or tau pathology models to predict future risk of AD progression may be useful to assist in disease screening, triage of patients for invasive testing, and efficiently determining suitability for clinical trial recruitment.

Serial order memory, a key type of episodic representation, requires the encoding of map-like context information (interitem relationships) to facilitate recall. In rodent models, both spatial and nonspatial order memory depend heavily on the hippocampus. However, in humans, lesional and neurophysiological data also implicate extrahippocampal areas, especially the orbital frontal cortex and medial parietal regions, in these mnemonic abilities. To investigate the neurophysiological mechanisms of order information in human memory, we used direct brain recordings from hippocampal-cortical circuits as neurosurgical patients performed a serial recall task. Our unique dataset included simultaneous acquisition of data from the hippocampus, orbitofrontal cortex, and posterior cingulate regions. Focusing on ripple events, we demonstrate distinct interregional dynamics during successful order memory encoding using temporally precise, simultaneous recordings across these circuits. The relative timing of co-rippling events implicates theta oscillations in cross-regional integration, particularly between the hippocampus and PCC, and we show that ripple rate, but not ripple duration, is correlated with the quantity of encoded order information. Notably, we find evidence for theta phase coding of serial position for early list items. We link our findings with computational and anatomical models of episodic memory processing as well as general theories of temporal binding facilitated by co-rippling events. These results point toward complementary mechanisms for order representation across hippocampal circuits and suggest the potential of anatomically specific approaches for neuromodulation that alter mnemonic neurophysiology.

Deficits in cortical thickness have been a replicated finding in BD. Greater brain serotonin 1 A receptor (5HT1AR) binding has also been reported in BD, consistent with a disruption in serotonin signaling. Serotonin can cause a trophic effect on the cerebral cortex. 31 depressed participants with BD and 49 healthy volunteers (HVs) were included. PET imaging with [11C]WAY100635 was obtained with a metabolite-corrected arterial input function. Radiotracer binding potential (BPF) values were quantified within cortical regions. T1-weighted MRI scans were processed through Freesurfer 7.1.1, and cortical thickness values were quantified within a right caudal middle frontal region that had previously been shown to have deficits in BD. The previous results were replicated here, with lower cortical thickness in BD relative to HV’s in the region. Cortical thickness in that region was inversely associated with BPF of [11C]WAY100635 in BD (F = 4.77; df = 1, 28; p = 0.037), but no association was found in HVs (F = 0.62; df = 1, 46; p = 0.44). Whole brain exploratory analyses were performed to examine vertex-wise associations between BPF values and cortical thickness. Within BD participants, BPF of [11C]WAY100635 was inversely associated with right superior parietal cortical thickness, and positively associated in the right posterior cingulate cortex and the left entorhinal cortex. Mean cortical thickness values in the significant clusters did not differ between BD and HV groups. Within HVs, no clusters were associated between cortical thickness and BPF of [11C]WAY100635. These data are consistent with a model wherein disruptions in serotonin signaling lead to a loss of trophic effect on cortical tissue in BD. Associations between 5HT1AR binding and cortical thickness in BD are not limited to areas of cortical thickness deficits.