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Homocysteine (Hcy) is a cardiovascular risk factor implicated in cognitive impairment and cerebrovascular disease but has also been associated with Alzheimer's disease. In 160 healthy older adults (mean age = 69.66 ± 9.95 years), we sought to investigate the association of cortical brain volume with white matter hyperintensity (WMH) burden and a previously identified Hcy-related multivariate network pattern showing reductions in subcortical gray matter (SGM) volumes of hippocampus and nucleus accumbens with relative preservation of basal ganglia. We additionally evaluated the potential role of these brain imaging markers as a series of mediators in a vascular brain pathway leading to age-related cognitive dysfunction in healthy aging. We found reductions in parietal lobar gray matter associated with the Hcy-SGM pattern, which was further associated with WMH burden. Mediation analyses revealed that slowed processing speed related to aging, but not executive functioning or memory, was mediated sequentially through increased WMH lesion volume, greater Hcy-SGM pattern expression, and then smaller parietal lobe volume. Together, these findings suggest that volume reductions in parietal gray matter associated with a pattern of Hcy-related SGM volume differences may be indicative of slowed processing speed in cognitive aging, potentially linking cardiovascular risk to an important aspect of cognitive dysfunction in healthy aging. [ABSTRACT FROM AUTHOR]

Introduction: Prior MRI studies have shown that patients with subcortical ischemic vascular disease (SIVD) exhibited white matter damage, gray matter atrophy and memory impairment, but the specific characteristics and interrelationships of these abnormal changes have not been fully elucidated. Materials and methods: We collected the MRI data and memory scores from 29 SIVD patients with cognitive impairment (SIVD-CI), 29 SIVD patients with cognitive unimpaired (SIVD-CU) and 32 normal controls (NC). Subsequently, the thicknesses and volumes of the gray matter regions that are closely related to memory function were automatically assessed using FreeSurfer software. Then, the volume, fractional anisotropy (FA), mean diffusivity (MD), amplitude of low-frequency fluctuation (ALFF) and regional homogeneity (ReHo) values of white matter hyperintensity (WMH) region and normal-appearing white matter (NAWM) were obtained using SPM, DPARSF, and FSL software. Finally, the analysis of covariance, spearman correlation and mediation analysis were used to analyze data. Results: Compared with NC group, patients in SIVD-CI and SIVD-CU groups showed significantly abnormal volume, FA, MD, ALFF, and ReHo values of WMH region and NAWM, as well as significantly decreased volume and thickness values of gray matter regions, mainly including thalamus, middle temporal gyrus and hippocampal subfields such as cornu ammonis (CA) 1. These abnormal changes were significantly correlated with decreased visual, auditory and working memory scores. Compared with the SIVD-CU group, the significant reductions of the left CA2/3, right amygdala, right parasubiculum and NAWM volumes and the significant increases of the MD values in the WMH region and NAWM were found in the SIVD-CI group. And the increased MD values were significantly related to working memory scores. Moreover, the decreased CA1 and thalamus volumes mediated the correlations between the abnormal microstructure indicators in WMH region and the decreased memory scores in the SIVD-CI group. Conclusion: Patients with SIVD had structural and functional damages in both WMH and NAWM, along with specific gray matter atrophy, which were closely related to memory impairment, especially CA1 atrophy and thalamic atrophy. More importantly, the volumes of some temporomesial regions and the MD values of WMH regions and NAWM may be potentially helpful neuroimaging indicators for distinguishing between SIVD-CI and SIVD-CU patients. [ABSTRACT FROM AUTHOR]

BackgroundAlzheimer’s disease (AD) is one of the most severe neurodegenerative diseases leading to dementia in the elderly. Cerebral atrophy and hypoperfusion are two important pathophysiological characteristics. However, it is still unknown about the area-specific causal pathways between regional gray matter atrophy, cerebral hypoperfusion, and cognitive impairment in AD patients.MethodForty-two qualified AD patients and 49 healthy controls (HC) were recruited in this study. First, we explored voxel-wise inter-group differences in gray matter volume (GMV) and arterial spin labeling (ASL) -derived cerebral blood flow (CBF). Then we explored the voxel-wise associations between GMV and Mini-Mental State Examination (MMSE) score, GMV and CBF, and CBF and MMSE to identify brain targets contributing to cognitive impairment in AD patients. Finally, a mediation analysis was applied to test the causal pathways among atrophied GMV, hypoperfusion, and cognitive impairment in AD.ResultsVoxel-wise permutation test identified that the left middle temporal gyrus (MTG) had both decreased GMV and CBF in the AD. Moreover, the GMV of this region was positively correlated with MMSE and its CBF, and CBF of this region was also positively correlated with MMSE in AD (p

ObjectiveThis study explored the structural imaging changes in patients with subcortical ischemic vascular disease (SIVD)-vascular cognitive impairment no dementia (VCIND) and the correlation between the changes in gray matter volume and the field of cognitive impairment to provide new targets for early diagnosis and treatment.MethodsOur study included 15 patients with SIVD-normal cognitive impairment (SIVD-NCI), 63 with SIVD-VCIND, 26 with SIVD-vascular dementia (SIVD-VD), and 14 normal controls (NC). T1-weighted images of all participants were collected, and DPABI and SPM12 software were used to process the gray matter of the four groups based on voxels. Fisher’s exact test, one-way ANOVA and Kruskal-Wallis H test were used to evaluate all clinical and demographic data and compare the characteristics of diencephalic gray matter atrophy in each group. Finally, the region of interest (ROI) of the SIVD-VCIND was extracted, and Pearson correlation analysis was performed between the ROI and the results of the neuropsychological scale.ResultsCompared to the NC, changes in gray matter atrophy were observed in the bilateral orbitofrontal gyrus, right middle temporal gyrus, superior temporal gyrus, and precuneus in the SIVD-VCIND. Gray matter atrophy was observed in the left cerebellar region 6, cerebellar crural region 1, bilateral thalamus, right precuneus, and calcarine in the SIVD-VD. Compared with the SIVD-VCIND, gray matter atrophy changes were observed in the bilateral thalamus in the SIVD-VD (p

Poststroke depression (PSD), affecting about one-third of stroke survivors, exerts significant impact on patients' functional outcome and mortality. Great efforts have been made since the 1970s to unravel the neuroanatomical substrate and the brain-behavior mechanism of PSD. Thanks to advances in neuroimaging and computational neuroscience in the past two decades, new techniques for uncovering the neural basis of symptoms or behavioral deficits caused by focal brain damage have been emerging. From the time of lesion analysis to the era of brain networks, our knowledge and understanding of the neural substrates for PSD are increasing. Pooled evidence from traditional lesion analysis, univariate or multivariate lesion-symptom mapping, regional structural and functional analyses, direct or indirect connectome analysis, and neuromodulation clinical trials for PSD, to some extent, echoes the frontal-limbic theory of depression. The neural substrates of PSD may be used for risk stratification and personalized therapeutic target identification in the future. In this review, we provide an update on the recent advances about the neural basis of PSD with the clinical implications and trends of methodology as the main features of interest. [ABSTRACT FROM AUTHOR]

Objective: Previous studies have reliably identified iron deposition in the motor cortex as potential pathogenesis of amyotrophic lateral sclerosis (ALS). Here, we intended to investigate iron deposition, gray matter (GM) atrophy, and their associations with disease severity in the motor cortex and the thalamus in patients with ALS. Methods: A total of 34 patients with ALS (age 51.31 ± 8.24 years, 23 males) and 34 nonneurological controls (age 50.96 ± 9.35 years, 19 males) were enrolled between 2018 and 2020. The Revised ALS Functional Rating Scale (ALSFRS-R) and the Penn upper motor neuron (UMN) score were measured. MRI data included quantitative susceptibility mapping (QSM) for iron deposition and three-dimensional (3D) T1 for gray matter volume. After a between-group comparison, Pearson's correlation coefficient was used for identifying correlations of iron deposition, GM volume, and clinical measurements. Results: The two-sample t -tests revealed increased iron deposition in the left precentral gyrus (peak voxel T = 4.78, P SVC = 0.03) and the thalamus (peak voxel: right: T = 6.38, P SVC < 0.001; left: T = 4.64, P SVC = 0.02) in patients with ALS. GM volume of the precentral gyrus (T = −2.42, P = 0.02) and the bilateral thalamus (T = −4.10, P < 0.001) were reduced. Negative correlations were found between the increased QSM values and the decreased GM volume (P < 0.04, one-tailed) in patients with ALS. Iron deposition in the left precentral gyrus was positively correlated with the UMN score (R = 0.40, P = 0.02) and the GM volume was negatively correlated with the UMN score (R = −0.48, P = 0.004). Negative correlation between thalamic iron deposition and the ALSFRS-R (R = −0.36, P = 0.04) score was observed. Discussion: Iron deposition in the thalamus, in addition to the motor cortex, is accompanied by GM atrophy and is associated with disease severity in patients with ALS, indicating that the thalamus is also a pathological region in patients with ALS. [ABSTRACT FROM AUTHOR]

Poststroke depression (PSD), affecting about one-third of stroke survivors, exerts significant impact on patients’ functional outcome and mortality. Great efforts have been made since the 1970s to unravel the neuroanatomical substrate and the brain-behavior mechanism of PSD. Thanks to advances in neuroimaging and computational neuroscience in the past two decades, new techniques for uncovering the neural basis of symptoms or behavioral deficits caused by focal brain damage have been emerging. From the time of lesion analysis to the era of brain networks, our knowledge and understanding of the neural substrates for PSD are increasing. Pooled evidence from traditional lesion analysis, univariate or multivariate lesion-symptom mapping, regional structural and functional analyses, direct or indirect connectome analysis, and neuromodulation clinical trials for PSD, to some extent, echoes the frontal-limbic theory of depression. The neural substrates of PSD may be used for risk stratification and personalized therapeutic target identification in the future. In this review, we provide an update on the recent advances about the neural basis of PSD with the clinical implications and trends of methodology as the main features of interest.

ObjectivePrevious studies have reliably identified iron deposition in the motor cortex as potential pathogenesis of amyotrophic lateral sclerosis (ALS). Here, we intended to investigate iron deposition, gray matter (GM) atrophy, and their associations with disease severity in the motor cortex and the thalamus in patients with ALS.MethodsA total of 34 patients with ALS (age 51.31 ± 8.24 years, 23 males) and 34 nonneurological controls (age 50.96 ± 9.35 years, 19 males) were enrolled between 2018 and 2020. The Revised ALS Functional Rating Scale (ALSFRS-R) and the Penn upper motor neuron (UMN) score were measured. MRI data included quantitative susceptibility mapping (QSM) for iron deposition and three-dimensional (3D) T1 for gray matter volume. After a between-group comparison, Pearson's correlation coefficient was used for identifying correlations of iron deposition, GM volume, and clinical measurements.ResultsThe two-sample t-tests revealed increased iron deposition in the left precentral gyrus (peak voxel T = 4.78, PSVC = 0.03) and the thalamus (peak voxel: right: T = 6.38, PSVC < 0.001; left: T = 4.64, PSVC = 0.02) in patients with ALS. GM volume of the precentral gyrus (T = −2.42, P = 0.02) and the bilateral thalamus (T = −4.10, P < 0.001) were reduced. Negative correlations were found between the increased QSM values and the decreased GM volume (P < 0.04, one-tailed) in patients with ALS. Iron deposition in the left precentral gyrus was positively correlated with the UMN score (R = 0.40, P = 0.02) and the GM volume was negatively correlated with the UMN score (R = −0.48, P = 0.004). Negative correlation between thalamic iron deposition and the ALSFRS-R (R = −0.36, P = 0.04) score was observed.DiscussionIron deposition in the thalamus, in addition to the motor cortex, is accompanied by GM atrophy and is associated with disease severity in patients with ALS, indicating that the thalamus is also a pathological region in patients with ALS.

Background and Objective: Brain atrophy and cognitive impairment in neurodegenerative diseases are influenced by sex. We aimed to investigate sex differences in brain atrophy and cognition in de novo Parkinson's disease (PD) patients.Methods: Clinical, neuropsychological and T1-weighted MRI data from 205 PD patients (127 males: 78 females) and 69 healthy controls (40 males: 29 females) were obtained from the PPMI dataset.Results: PD males had a greater motor and rapid eye movement sleep behavior disorder symptomatology than PD females. They also showed cortical thinning in postcentral and precentral regions, greater global cortical and subcortical atrophy and smaller volumes in thalamus, caudate, putamen, pallidum, hippocampus, and brainstem, compared with PD females. Healthy controls only showed reduced hippocampal volume in males compared to females. PD males performed worse than PD females in global cognition, immediate verbal recall, and mental processing speed. In both groups males performed worse than females in semantic verbal fluency and delayed verbal recall; as well as females performed worse than males in visuospatial function.Conclusions: Sex effect in brain and cognition is already evident in de novo PD not explained by age per se, being a relevant factor to consider in clinical and translational research in PD.

Introduction: Integrating brain imaging with large scale omics data may identify novel mechanisms of mild cognitive impairment (MCI) and early Alzheimer's disease (AD). We integrated and analyzed brain magnetic resonance imaging (MRI) with cerebrospinal fluid (CSF) metabolomics to elucidate metabolic mechanisms and create a "metabolic map" of the brain in prodromal AD. Methods: In 145 subjects (85 cognitively normal controls and 60 with MCI), we derived voxel-wise gray matter volume via whole-brain structural MRI and conducted high-resolution untargeted metabolomics on CSF. Using a data-driven approach consisting of partial least squares discriminant analysis, a multiomics network clustering algorithm, and metabolic pathway analysis, we described dysregulated metabolic pathways in CSF mapped to brain regions associated with MCI in our cohort. Results: The multiomics network algorithm clustered metabolites with contiguous imaging voxels into seven distinct communities corresponding to the following brain regions: hippocampus/parahippocampal gyrus (three distinct clusters), thalamus, posterior thalamus, parietal cortex, and occipital lobe. Metabolic pathway analysis indicated dysregulated metabolic activity in the urea cycle, and many amino acids (arginine, histidine, lysine, glycine, tryptophan, methionine, valine, glutamate, beta-alanine, and purine) was significantly associated with those regions (P < 0.05). Conclusion: By integrating CSF metabolomics data with structural MRI data, we linked specific AD-susceptible brain regions to disrupted metabolic pathways involving nitrogen excretion and amino acid metabolism critical for cognitive function. Our findings and analytical approach may extend drug and biomarker research toward more multiomics approaches. [ABSTRACT FROM AUTHOR]

Background and Objective: Brain atrophy and cognitive impairment in neurodegenerative diseases are influenced by sex. We aimed to investigate sex differences in brain atrophy and cognition in de novo Parkinson's disease (PD) patients. Methods: Clinical, neuropsychological and T1-weighted MRI data from 205 PD patients (127 males: 78 females) and 69 healthy controls (40 males: 29 females) were obtained from the PPMI dataset. Results: PD males had a greater motor and rapid eye movement sleep behavior disorder symptomatology than PD females. They also showed cortical thinning in postcentral and precentral regions, greater global cortical and subcortical atrophy and smaller volumes in thalamus, caudate, putamen, pallidum, hippocampus, and brainstem, compared with PD females. Healthy controls only showed reduced hippocampal volume in males compared to females. PD males performed worse than PD females in global cognition, immediate verbal recall, and mental processing speed. In both groups males performed worse than females in semantic verbal fluency and delayed verbal recall; as well as females performed worse than males in visuospatial function. Conclusions: Sex effect in brain and cognition is already evident in de novo PD not explained by age per se , being a relevant factor to consider in clinical and translational research in PD. [ABSTRACT FROM AUTHOR]

Objective: Extensive research using water-diffusion MRI reported age-related modifications of cerebral White Matter (WM). Moreover, water-diffusion parameter modifications have been frequently associated with cognitive performances in the elderly sample, reinforcing the idea of aging inducing microstructural disconnection of the brain which in turn impacts cognition. However, only few studies really assessed over-time modifications of these parameters and their relationship with episodic memory outcome of elderly.Materials and Methods: One-hundred and thirty elderly subjects without dementia (74.1 ± 4.1 years; 47% female) were included in this study. Diffusion tensor imaging (DTI) was performed at two-time points (3.49 ± 0.68 years apart), allowing the assessment of changes in water-diffusion parameters over time using a specific longitudinal pipeline. White matter hyperintensity (WMH) burden and gray matter (GM) atrophy were also measured on FLAIR and T1-weighted sequences collected during these two MRI sessions. Free and cued verbal recall scores assessed at the last follow-up of the cohort were used as episodic memory outcome. Changes in water-diffusion parameters over time were included in serial linear regression models to predict retrieval or storage ability of elderly.Results: GM atrophy and an increase in mean diffusivity (MD) and WMH load between the two-time points were observed. The increase in MD was significantly correlated with WMH load and the different memory scores. In models accounting for the baseline cognitive score, GM atrophy, or WMH load, MD changes still significantly predict free verbal recall, and not total verbal recall, suggesting the specific association with the retrieval deficit in healthy aging.Conclusion: In elderly, microstructural WM changes are good predictors of lower free verbal recall performances. Moreover, this contribution is not only driven by WMH load increase. This last observation is in line with studies reporting early water-diffusion modification in WM tissue during aging, resulting lately in the appearance of WMH on conventional MRI.

Objective : Extensive research using water-diffusion MRI reported age-related modifications of cerebral White Matter (WM). Moreover, water-diffusion parameter modifications have been frequently associated with cognitive performances in the elderly sample, reinforcing the idea of aging inducing microstructural disconnection of the brain which in turn impacts cognition. However, only few studies really assessed over-time modifications of these parameters and their relationship with episodic memory outcome of elderly. Materials and Methods : One-hundred and thirty elderly subjects without dementia (74.1 ± 4.1 years; 47% female) were included in this study. Diffusion tensor imaging (DTI) was performed at two-time points (3.49 ± 0.68 years apart), allowing the assessment of changes in water-diffusion parameters over time using a specific longitudinal pipeline. White matter hyperintensity (WMH) burden and gray matter (GM) atrophy were also measured on FLAIR and T1-weighted sequences collected during these two MRI sessions. Free and cued verbal recall scores assessed at the last follow-up of the cohort were used as episodic memory outcome. Changes in water-diffusion parameters over time were included in serial linear regression models to predict retrieval or storage ability of elderly. Results : GM atrophy and an increase in mean diffusivity (MD) and WMH load between the two-time points were observed. The increase in MD was significantly correlated with WMH load and the different memory scores. In models accounting for the baseline cognitive score, GM atrophy, or WMH load, MD changes still significantly predict free verbal recall, and not total verbal recall, suggesting the specific association with the retrieval deficit in healthy aging. Conclusion : In elderly, microstructural WM changes are good predictors of lower free verbal recall performances. Moreover, this contribution is not only driven by WMH load increase. This last observation is in line with studies reporting early water-diffusion modification in WM tissue during aging, resulting lately in the appearance of WMH on conventional MRI. [ABSTRACT FROM AUTHOR]

While the aging process is a universal phenomenon, people perceive and experience one’s aging considerably differently. Subjective age (SA), referring to how individuals experience themselves as younger or older than their actual age, has been highlighted as an important predictor of late-life health outcomes. However, it is unclear whether and how SA is associated with the neurobiological process of aging. In this study, 68 healthy older adults underwent a SA survey and magnetic resonance imaging (MRI) scans. T1-weighted brain images of open-access datasets were utilized to construct a model for age prediction. We utilized both voxel-based morphometry (VBM) and age-prediction modeling techniques to explore whether the three groups of SA (i.e., feels younger, same, or older than actual age) differed in their regional gray matter (GM) volumes, and predicted brain age. The results showed that elderly individuals who perceived themselves as younger than their real age showed not only larger GM volume in the inferior frontal gyrus and the superior temporal gyrus, but also younger predicted brain age. Our findings suggest that subjective experience of aging is closely related to the process of brain aging and underscores the neurobiological mechanisms of SA as an important marker of late-life neurocognitive health.

While the aging process is a universal phenomenon, people perceive and experience one's aging considerably differently. Subjective age (SA), referring to how individuals experience themselves as younger or older than their actual age, has been highlighted as an important predictor of late-life health outcomes. However, it is unclear whether and how SA is associated with the neurobiological process of aging. In this study, 68 healthy older adults underwent a SA survey and magnetic resonance imaging (MRI) scans. T1-weighted brain images of open-access datasets were utilized to construct a model for age prediction.We utilized both voxel-based morphometry (VBM) and age-prediction modeling techniques to explore whether the three groups of SA (i.e., feels younger, same, or older than actual age) differed in their regional gray matter (GM) volumes, and predicted brain age. The results showed that elderly individuals who perceived themselves as younger than their real age showed not only larger GM volume in the inferior frontal gyrus and the superior temporal gyrus, but also younger predicted brain age. Our findings suggest that subjective experience of aging is closely related to the process of brain aging and underscores the neurobiological mechanisms of SA as an important marker of late-life neurocognitive health. [ABSTRACT FROM AUTHOR]

Gray matter alterations are typical features of brain disorders. However, they do not impact on the brain randomly. Indeed, it has been suggested that neuropathological processes can selectively affect certain assemblies of neurons, which typically are at the center of crucial functional networks. Because of their topological centrality, these areas form a core set that is more likely to be affected by neuropathological processes. In order to identify and study the pattern formed by brain alterations in patients’ with Alzheimer’s disease (AD), we devised an innovative meta-analytic method for analyzing voxel-based morphometry data. This methodology enabled us to discover that in AD gray matter alterations do not occur randomly across the brain but, on the contrary, follow identifiable patterns of distribution. This alteration pattern exhibits a network-like structure composed of coaltered areas that can be defined as coatrophy network. Within the coatrophy network of AD, we were able to further identify a core subnetwork of coaltered areas that includes the left hippocampus, left and right amygdalae, right parahippocampal gyrus, and right temporal inferior gyrus. In virtue of their network centrality, these brain areas can be thought of as pathoconnectivity hubs.

Gray matter alterations are typical features of brain disorders. However, they do not impact on the brain randomly. Indeed, it has been suggested that neuropathological processes can selectively affect certain assemblies of neurons, which typically are at the center of crucial functional networks. Because of their topological centrality, these areas form a core set that is more likely to be affected by neuropathological processes. In order to identify and study the pattern formed by brain alterations in patients' with Alzheimer's disease (AD), we devised an innovative meta-analytic method for analyzing voxel-based morphometry data. This methodology enabled us to discover that in AD gray matter alterations do not occur randomly across the brain but, on the contrary, follow identifiable patterns of distribution. This alteration pattern exhibits a network-like structure composed of coaltered areas that can be defined as coatrophy network. Within the coatrophy network of AD, we were able to further identify a core subnetwork of coaltered areas that includes the left hippocampus, left and right amygdalae, right parahippocampal gyrus, and right temporal inferior gyrus. In virtue of their network centrality, these brain areas can be thought of as pathoconnectivity hubs. [ABSTRACT FROM AUTHOR]

Structural brain changes underlying mild cognitive impairment (MCI) have been wellresearched, but most previous studies required subjective cognitive complaints (SCC) as a diagnostic criterion, diagnosed MCI based on a single screening test or lacked analyses in relation to neuropsychological impairment. This longitudinal voxel-based morphometry study aimed to overcome these limitations: The relationship between regional gray matter (GM) atrophy and behavioral performance was investigated over the course of 3 years in individuals unaware of cognitive decline, identified as amnestic MCI based on an extensive neuropsychological test battery. Region of interest analyses revealed GM atrophy in the left amygdala, hippocampus, and parahippocampus in MCI individuals compared to normally aging participants, which was specifically related to verbal memory impairment and evident already at the first measurement point. These findings demonstrate that GM atrophy is detectable in individuals with amnestic MCI despite unawareness of beginning cognitive decline. Thus, individuals with GM atrophy in regions associated with verbal memory impairment do not necessarily need to experience SCC before meeting neuropsychological criteria for MCI. These results have important implications for future research and diagnostic procedures of MCI. [ABSTRACT FROM AUTHOR]

Background: Several neuroimaging studies revealed widespread neurodegeneration in Parkinson's disease but only few considered the asymmetrical clinical presentation. Objective: To investigate gray matter (GM) atrophy in Parkinson Disease considering the side of motor symptom onset. Methods: Sixty patients (57.87± 10.27 years) diagnosed according to the Brain Bank criteria, 26 with right-sided disease onset (RDO) and 34 with left-sided disease onset (LDO), were compared to 80 healthy controls (HC) (57.1± 9.47 years). T1-weighted images were acquired on a 3T scanner. VBM8 (SPM8/Dartel) on Matlab R2012b platform processed and analyzed the images. Statistics included a two-sample test (FWE p

White matter hyperintensities (WMHs) and brain atrophy often coexist in the elderly. Additionally, WMH is often observed as occipital periventricular hyperintensities (OPVHs) with low-grade periventricular white matter lesions and is usually confined within an anatomical structure. However, the effects of OPVHs on gray matter atrophy remain largely unknown. In this study, we investigated gray matter atrophy in OPVHs patients and explored the relationship between such atrophy and clinical risk factors. T1-weighted and T2-weighted MRI were acquired, and voxel-based morphometry (VBM) analysis was applied. The clinical (demographic and cardiovascular) risk factors of the OPVHs patients and healthy controls were then compared. Lastly, scatter plots and correlation analysis were applied to explore the relationship between the MRI results and clinical risk factors in the OPVHs patients. OPVHs patients had significantly reduced gray matter in the right supramarginal gyrus, right angular gyrus, right middle temporal gyrus, right anterior cingulum and left insula compared to healthy controls. Additionally, OPVHs patients had gray matter atrophy in the left precentral gyrus and left insula cortex, and such atrophy is associated with a reduction in low-density lipoprotein cholesterol and apolipoprotein-B.

Abnormal structures in the cortical and subcortical regions have been identified in subcortical vascular cognition impairment (SVCI). However, little is known about the functional alterations in SVCI, and no study refers to the functional connectivity in the prefrontal and subcortical regions in this context. The medial prefrontal cortex (MPFC) is an important region of the executive network and default mode network (DMN), and the subcortical thalamus plays vital roles in mediating or modulating these two networks. To investigate both thalamus- and MPFC-related functional connectivity as well as its relationship with cognition in SVCI, 32 SVCI patients and 23 control individuals were administered neuropsychological assessments. They also underwent structural and functional magnetic resonance imaging (MRI) scans. Voxel-based morphometry (VBM) and functional connectivity analysis were performed to detect gray matter (GM) atrophy and to characterize the functional alterations in the thalamus and the MPFC. For structural data, we observed that GM atrophy was distributed in both cortical regions and subcortical areas. For functional data, we observed that the thalamus functional connectivity in SVCI was significantly decreased in several cortical regions (i.e., the orbitofrontal lobe (OFL)), which are mainly involved in executive function and memory function. However, connectivity was increased in several frontal regions (i.e., the inferior frontal gyrus (IFG)), which may be induced by the compensatory recruitment of the decreased functional connectivity. The MPFC functional connectivity was also decreased in executive- and memory-related regions (i.e., the anterior cingulate cortex (ACC)) along with a motor region (i.e., the supplementary motor region (SMA)). In addition, the cognitive performance was closely correlated with functional connectivity between the left thalamus and the left OFL in SVCI. The present study thus provides evidence for an association between structural and functional alterations and sheds light on the underlying neural mechanisms of executive dysfunction in SVCI.

Background: Imaging studies have revealed widespread neurodegeneration in Parkinson’s disease (PD), but only a few considered the issue of asymmetrical clinical presentations. Objective: To investigate if the side of onset influences the pattern of gray matter (GM) atrophy in PD. Methods: Sixty patients (57.87 ± 10.27 years) diagnosed with idiopathic PD according to the U.K. Brain Bank criteria, 26 with right-sided disease onset (RDO) and 34 with left-sided disease onset (LDO), were compared to 80 healthy controls (HC) (57.1 ± 9.47 years). We acquired T1-weighted images on a 3 T scanner. Images were processed and analyzed with VBM8 (SPM8/Dartel) on Matlab R2012b platform. Statistic assessments included a two-sample test (family-wise error p < 0.05) with extent threshold of 20 voxels. Results: Compared to HC, LDO patients had GM atrophy in the insula, putamen, anterior cingulate, frontotemporal cortex, and right caudate, while the RDO group showed atrophy at the anterior cingulate, insula, frontotemporal, and occipital cortex. Conclusion: This study revealed widespread GM atrophy in PD, predominantly in the left hemisphere, regardless of the side of onset. Future investigations should also consider handedness and side of onset to better characterize cerebral involvement and its progression in PD. [ABSTRACT FROM AUTHOR]