Current treatments for Alzheimer's disease are only symptomatic and limited to reduce the progression rate of the mental deterioration. Mild Cognitive Impairment, a transitional stage in which the ...patient is not cognitively normal but do not meet the criteria for specific dementia, is associated with high risk for development of Alzheimer's disease. Thus, non-invasive techniques to predict the individual's risk to develop Alzheimer's disease can be very helpful, considering the possibility of early treatment. Diffusion Tensor Imaging, as an indicator of cerebral white matter integrity, may detect and track earlier evidence of white matter abnormalities in patients developing Alzheimer's disease. Here we performed a voxel-based analysis of fractional anisotropy in three classes of subjects: Alzheimer's disease patients, Mild Cognitive Impairment patients, and healthy controls. We performed Support Vector Machine classification between the three groups, using Fisher Score feature selection and Leave-one-out cross-validation. Bilateral intersection of hippocampal cingulum and parahippocampal gyrus (referred as parahippocampal cingulum) is the region that best discriminates Alzheimer's disease fractional anisotropy values, resulting in an accuracy of 93% for discriminating between Alzheimer's disease and controls, and 90% between Alzheimer's disease and Mild Cognitive Impairment. These results suggest that pattern classification of Diffusion Tensor Imaging can help diagnosis of Alzheimer's disease, specially when focusing on the parahippocampal cingulum.
Cross‐modal plasticity in blind individuals has been reported over the past decades showing that nonvisual information is carried and processed by “visual” brain structures. However, despite multiple ...efforts, the structural underpinnings of cross‐modal plasticity in congenitally blind individuals remain unclear. We mapped thalamocortical connectivity and assessed the integrity of white matter of 10 congenitally blind individuals and 10 sighted controls. We hypothesized an aberrant thalamocortical pattern of connectivity taking place in the absence of visual stimuli from birth as a potential mechanism of cross‐modal plasticity. In addition to the impaired microstructure of visual white matter bundles, we observed structural connectivity changes between the thalamus and occipital and temporal cortices. Specifically, the thalamic territory dedicated to connections with the occipital cortex was smaller and displayed weaker connectivity in congenitally blind individuals, whereas those connecting with the temporal cortex showed greater volume and increased connectivity. The abnormal pattern of thalamocortical connectivity included the lateral and medial geniculate nuclei and the pulvinar nucleus. For the first time in humans, a remapping of structural thalamocortical connections involving both unimodal and multimodal thalamic nuclei has been demonstrated, shedding light on the possible mechanisms of cross‐modal plasticity in humans. The present findings may help understand the functional adaptations commonly observed in congenitally blind individuals.
The absence of visual stimuli from birth changes the pattern of thalamocortical connectivity, specifically between visual, auditory and multimodal structures. Our findings bring new evidence for the possible neural underpinnings of cross‐modal plasticity in blind individuals.
Altered reward processing has been proposed to contribute to the symptoms of attention deficit hyperactivity disorder (ADHD). The neurobiological mechanism underlying this alteration remains unclear. ...We hypothesize that the transfer of dopamine release from reward to reward-predicting cues, as normally observed in animal studies, may be deficient in ADHD. Functional magnetic resonance imaging (fMRI) was used to investigate striatal responses to reward-predicting cues and reward delivery in a classical conditioning paradigm. Data from 14 high-functioning and stimulant-naïve young adults with elevated lifetime symptoms of ADHD (8 males, 6 females) and 15 well-matched controls (8 males, 7 females) were included in the analyses. During reward anticipation, increased blood-oxygen-level-dependent (BOLD) responses in the right ventral and left dorsal striatum were observed in controls, but not in the ADHD group. The opposite pattern was observed in response to reward delivery; the ADHD group demonstrated significantly greater BOLD responses in the ventral striatum bilaterally and the left dorsal striatum relative to controls. In the ADHD group, the number of current hyperactivity/impulsivity symptoms was inversely related to ventral striatal responses during reward anticipation and positively associated with responses to reward. The BOLD response patterns observed in the striatum are consistent with impaired predictive dopamine signaling in ADHD, which may explain altered reward-contingent behaviors and symptoms of ADHD.
Introduction: Irisin is a novel hormone originally identified for its role as a regulator of peripheral metabolism and recently found to protect synapses and rescue memory in mouse models of ...Alzheimer's disease (AD). However, whether and how cerebrospinal fluid (CSF) irisin varies in relation to canonical AD biomarkers and cognition in humans remains unknown.
Methods: We determined CSF levels of irisin and brain‐derived neurotrophic factor (BDNF) and examined their correlations with CSF amyloid beta (Aβ)42, total tau, and Mini‐Mental State Exam (MMSE) scores in a cohort comprising AD patients (n = 14) and non‐demented controls (NDC; n = 25).
Results: CSF irisin correlated positively with BDNF, Aβ42, and MMSE scores, but not with CSF total tau.
Discussion: Results indicate that CSF irisin and BDNF are directly correlated with Aβ pathology and cognition in AD.
Background and purpose
This case illustrates for the first time the clinical and radiological evolution of SARS‐CoV‐2 meningo‐encephalitis.
Methods
A case of a SARS‐CoV‐2 meningo‐encephalitis is ...reported.
Results
A 65‐year‐old man with COVID‐19 presenting with meningo‐encephalitis without respiratory involvement is described. He had fever, diarrhea and vomiting, followed by diplopia, urinary retention and sleepiness. Examination disclosed a convergence strabismus and ataxia. Cerebrospinal fluid (CSF) showed lymphocytic pleocytosis, oligoclonal bands and increased interleukin 6 level. SARS‐CoV‐2 was detected in the CSF through reverse transcriptase polymerase chain reaction, but not in nasopharyngeal, tracheal secretion and rectal samples. Brain magnetic resonance imaging showed lesions on white matter hemispheres, the body and splenium of the corpus callosum and resembling the projection of corticospinal tract, remarkably on cerebellar peduncles.
Conclusions
This demonstrates the challenges in diagnosing COVID‐19 in patients with neurological presentations.
Brain magnetic resonance imaging evolution image of COVID‐19 meningo‐encephalitis.
Introduction
Depression is frequent among older adults and is a risk factor for dementia. Identifying molecular links between depression and dementia is necessary to shed light on shared disease ...mechanisms. Reduced brain‐derived neurotrophic factor (BDNF) and neuroinflammation are implicated in the pathophysiology of depression and dementia. The exercise‐induced hormone, irisin, increases BDNF and improves cognition in animal models of Alzheimer's disease. Lipoxin A4 is a lipid mediator with anti‐inflammatory activity. However, the roles of irisin and lipoxin A4 in depression remain to be determined.
Methods
In the present study, blood and CSF were collected from 61 elderly subjects, including individuals with and without cognitive impairment. Screening for symptoms of depression was performed using the 15‐item Geriatric Depression Scale (GDS‐15).
Results
CSF irisin and lipoxin A4 were positively correlated and reduced, along with a trend of BDNF reduction, in elderly individuals with depression, similar to previous observations in patients with dementia.
Discussion
Our findings provide novel insight into shared molecular signatures connecting depression and dementia.
This manuscript presents the quantification and correlation of three aspects of Alzheimer's Disease evolution, including structural, biochemical, and cognitive assessments. We aimed to test a novel ...structural biomarker for neurodegeneration based on a cortical folding model for mammals. Our central hypothesis is that the cortical folding variable, representative of axonal tension in white matter, is an optimal discriminator of pathological aging and correlates with altered loadings in Cerebrospinal Fluid samples and a decline in cognition and memory. We extracted morphological features from T1w 3T MRI acquisitions using FreeSurfer from 77 Healthy Controls (age = 66 ± 8.4, 69% females), 31 Mild Cognitive Impairment (age = 72 ± 4.8, 61% females), and 13 Alzheimer's Disease patients (age = 77 ± 6.1, 62% females) of recruited volunteers in Brazil to test its discriminative power using optimal cut-point analysis. Cortical folding distinguishes the groups with reasonable accuracy (Healthy Control-Alzheimer's Disease, accuracy = 0.82; Healthy Control-Mild Cognitive Impairment, accuracy = 0.56). Moreover, Cerebrospinal Fluid biomarkers (total Tau, AFormula: see text1-40, AFormula: see text1-42, and Lipoxin) and cognitive scores (Cognitive Index, Rey's Auditory Verbal Learning Test, Trail Making Test, Digit Span Backward) were correlated with the global neurodegeneration in MRI aiming to describe health, disease, and the transition between the two states using morphology.
Background
Attention‐deficit/hyperactivity disorder (ADHD) is a prevalent neurodevelopmental disorder. Neuroanatomic heterogeneity limits our understanding of ADHD’s etiology. This study aimed to ...parse heterogeneity of ADHD and to determine whether patient subgroups could be discerned based on subcortical brain volumes.
Methods
Using the large ENIGMA‐ADHD Working Group dataset, four subsamples of 993 boys with and without ADHD and to subsamples of 653 adult men, 400 girls, and 447 women were included in analyses. We applied exploratory factor analysis (EFA) to seven subcortical volumes in order to constrain the complexity of the input variables and ensure more stable clustering results. Factor scores derived from the EFA were used to build networks. A community detection (CD) algorithm clustered participants into subgroups based on the networks.
Results
Exploratory factor analysis revealed three factors (basal ganglia, limbic system, and thalamus) in boys and men with and without ADHD. Factor structures for girls and women differed from those in males. Given sample size considerations, we concentrated subsequent analyses on males. Male participants could be separated into four communities, of which one was absent in healthy men. Significant case–control differences of subcortical volumes were observed within communities in boys, often with stronger effect sizes compared to the entire sample. As in the entire sample, none were observed in men. Affected men in two of the communities presented comorbidities more frequently than those in other communities. There were no significant differences in ADHD symptom severity, IQ, and medication use between communities in either boys or men.
Conclusions
Our results indicate that neuroanatomic heterogeneity in subcortical volumes exists, irrespective of ADHD diagnosis. Effect sizes of case–control differences appear more pronounced at least in some of the subgroups.
Previous studies have indicated that amputation or deafferentation of a limb induces functional changes in sensory (S1) and motor (M1) cortices, related to phantom limb pain. However, the extent of ...cortical reorganization after lower limb amputation in patients with nonpainful phantom phenomena remains uncertain. In this study, we combined functional magnetic resonance (fMRI) and diffusion tensor imaging (DTI) to investigate the existence and extent of cortical and callosal plasticity in these subjects. Nine "painless" patients with lower limb amputation and nine control subjects (sex- and age-matched) underwent a 3-T MRI protocol, including fMRI with somatosensory stimulation. In amputees, we observed an expansion of activation maps of the stump in S1 and M1 of the deafferented hemisphere, spreading to neighboring regions that represent the trunk and upper limbs. We also observed that tactile stimulation of the intact foot in amputees induced a greater activation of ipsilateral S1, when compared with controls. These results demonstrate a functional remapping of S1 in lower limb amputees. However, in contrast to previous studies, these neuroplastic changes do not appear to be dependent on phantom pain but do also occur in those who reported only the presence of phantom sensation without pain. In addition, our findings indicate that amputation of a limb also induces changes in the cortical representation of the intact limb. Finally, DTI analysis showed structural changes in the corpus callosum of amputees, compatible with the hypothesis that phantom sensations may depend on inhibitory release in the sensorimotor cortex.
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