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[PMID]: 29524833
[Au] Autor:Zhu K; Yuan B; Hu M; Li CJ; Xu JH; Feng GF; Liu Y; Liu JX
[Ad] Address:Institute of Neurobiology, School of Basic Medical Sciences, Xi'an Jiaotong University Health Science Center, 76 West Yanta Road, Xi'an city, 710061, China.
[Ti] Title:Ablation of aberrant neurogenesis fails to attenuate cognitive deficit of chronically epileptic mice.
[So] Source:Epilepsy Res;142:1-8, 2018 Mar 03.
[Is] ISSN:1872-6844
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Pilocarpine-induced acute seizures strongly induce aberrant hippocampal neurogenesis, characterized by increased proliferation of neural progenitors and abnormal integrations of newly generated granule cells - hilar ectopic granule cells (EGCs), mossy fibre sprouting (MFS), and hilar basal dendrites (HBDs), which may disturb hippocampal neuronal circuits and thus contribute to cognitive impairment in temporal lobe epilepsy (TLE) patients and animal models. Previous studies via ablating hippocampal neurogenesis after acute seizures produced inconsistent results regarding the development of long-term cognitive impairment. Furthermore, a sufficient decrease of subsequent abnormal integrations in chronically epileptic hippocampus was not well-established in these studies. Therefore, the link between seizure-induced aberrant hippocampal neurogenesis and cognitive decline associated with epilepsy is still in need to be clarified. In this study, the mice were injected with methylazoxymethanol acetate (MAM) both before and after pilocarpine-induced status epilepticus (SE) to achieve an overall ablation of newborn cells contributing to the pathological recruitment. In addition, a protracted time point was chosen for behavioral testing considering it takes a fairly long time for newborn granule cells to adequately develop abnormal integrations, especially MFS. Although an overall reduction of abnormal integrations, including EGCs, MFS and HBDs was confirmed following the ablation regime, the performance of ablated and non-ablated mice in the Morris Water Maze (MWM) task did not differ. The current findings therefore provide novel evidences that ablation of neurogenesis with an overall decrease of abnormal integrations cannot attenuate subsequent cognitive impairment at least in the model used in this study.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  2 / 48066 MEDLINE  
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[PMID]: 29524710
[Au] Autor:Roessler K; Kasper BS; Coras R; Arinrad S; Scholz M; Hamer HH; Blümcke I; Buchfelder M
[Ad] Address:Neurosurgical Clinic. Electronic address: Karl.Roessler@uk-erlangen.de.
[Ti] Title:Technical modification of amygdalo-hippocampectomy (AHE) in temporal lobe epilepsy surgery to further reduce severe neurological complications. A clinical- anatomical study.
[So] Source:World Neurosurg;, 2018 Mar 07.
[Is] ISSN:1878-8769
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND: Temporal lobe resection (TLR) including amygdalo-hippocampectomy (AHE) is the most frequent performed procedure in epilepsy surgery. Due to close anatomical relationship of the mesial temporal structures and the midbrain and choroidal fissure, the risk of severe complications like postoperative stroke is up to 2.5%. METHODS: We developed a modification of the classical technique for AHE by early entering the choroidal fissure for identification of crus cerebri, posterior cerebri artery and oculomotor nerve via the anterior part of the fronto- mesial temporal horn cleft. Uncus and amygdala were removed second step after visualization of the cleavage plane between midbrain and middle cerebral artery. RESULTS: Altogether, 81 patients (47 females, 34 males, mean age 40 years at surgery) had temporal lobe epilepsy surgery including AHE for heterogeneous pathologies using this surgical modification (45 hippocampal sclerosis, 11 ganglioglioma, 2 dysembryoplastic neuroepithelioma (DNET), 2 diffuse glioma 21 other pathologies like cavernoma, scar tissue or mild cortical dysplasia). All patients had anterior temporal resection including AHE by using our modified technique. Seizure outcome was favorable after a mean follow up of 27 (from 3 to 56) months: 64% were completely seizure free (Engel Class 1A) and 75% had Engel Class 1 outcome. There was no mortality, 0% permanent severe neurological and 3.7% surgical complications. CONCLUSION: The newly described modification for AHE demonstrated low complication rates in surgery of medically refractory temporal lobe epilepsy. Its attention especially contributes to avoid permanent severe complications.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

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[PMID]: 29524639
[Au] Autor:Zhang Z; Zhang D; Wang Z; Li J; Lin Y; Chang S; Huang R; Liu M
[Ad] Address:Center for the Study of Applied Psychology, Key Laboratory of Mental Health and Cognitive Science of Guangdong Province, School of Psychology, South China Normal University, Guangzhou, China; Department of Special Education and Communication Disorders, University of Nebraska, Lincoln, 68583, United
[Ti] Title:Intrinsic neural linkage between primary visual area and default mode network in human brain: Evidence from visual mental imagery.
[So] Source:Neuroscience;, 2018 Mar 07.
[Is] ISSN:1873-7544
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Previous studies have reported the essence of the sensory-based properties of human brain function, in which mental imagery is of great importance. In this study, we explored the association between the activities of two special regions, i.e., the primary visual area (PVA), which is the classically dominant sensory region, and the default mode network (DMN), which is the classical supra-sensory region, with a focus on their linkage in visual mental imagery. For this purpose, we collected fMRI data from 30 healthy participants (15 males; 22.37 ± 2.52 years) during the resting state and a mental rotation task state. By using a critical time point analysis (CTPA), we investigated the association between the activities of the PVA and the DMN. As the results showed, there existed a PVA-related (i.e., prefrontal cortex, DMN, sensorimotor areas and medial temporal lobe) and a DMN-related neural association pattern (i.e., PVA, prefrontal cortex and the medial temporal lobe) in the human brain. Furthermore, the results showed the steady and tight intrinsic association between the activities of the PVA and the DMN, with the prefrontal cortex and the medial temporal lobe regions being found to be consistently involved in the resting state brain. It also was suggested that the observed association between the PVA and the DMN was highly reproducible for the mental rotation task. Together, these observations, from the perspective of visual mental imagery, provided experimental evidence for the robustness and stability of the detailed map of the associations between the activities of the PVA and the DMN.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

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[PMID]: 29506554
[Au] Autor:Vizuete AFK; Hansen F; Negri E; Leite MC; de Oliveira DL; Gonçalves CA
[Ad] Address:Department of Biochemistry, Instituto de Ciências Básicas da Saúde, Universidade Federal do Rio Grande do Sul, Ramiro Barcelos, 2600-Anexo, Porto Alegre, RS, 90035-003, Brazil. adrianavizuete@gmail.com.
[Ti] Title:Effects of dexamethasone on the Li-pilocarpine model of epilepsy: protection against hippocampal inflammation and astrogliosis.
[So] Source:J Neuroinflammation;15(1):68, 2018 Mar 05.
[Is] ISSN:1742-2094
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: Temporal lobe epilepsy (TLE) is the most common form of partial epilepsy and is accompanied, in one third of cases, by resistance to antiepileptic drugs (AED). Most AED target neuronal activity modulated by ionic channels, and the steroid sensitivity of these channels has supported the use of corticosteroids as adjunctives to AED. Assuming the importance of astrocytes in neuronal activity, we investigated inflammatory and astroglial markers in the hippocampus, a key structure affected in TLE and in the Li-pilocarpine model of epilepsy. METHODS: Initially, hippocampal slices were obtained from sham rats and rats subjected to the Li-pilocarpine model of epilepsy, at 1, 14, and 56 days after status epilepticus (SE), which correspond to the acute, silent, and chronic phases. Dexamethasone was added to the incubation medium to evaluate the secretion of S100B, an astrocyte-derived protein widely used as a marker of brain injury. In the second set of experiments, we evaluated the in vivo effect of dexamethasone, administrated at 2 days after SE, on hippocampal inflammatory (COX-1/2, PGE2, and cytokines) and astroglial parameters: GFAP, S100B, glutamine synthetase (GS) and water (AQP-4), and K (Kir 4.1) channels. RESULTS: Basal S100B secretion and S100B secretion in high-K medium did not differ at 1, 14, and 56 days for the hippocampal slices from epileptic rats, in contrast to sham animal slices, where high-K medium decreased S100B secretion. Dexamethasone addition to the incubation medium per se induced a decrease in S100B secretion in sham and epileptic rats (1 and 56 days after SE induction). Following in vivo dexamethasone administration, inflammatory improvements were observed, astrogliosis was prevented (based on GFAP and S100B content), and astroglial dysfunction was partially abrogated (based on Kir 4.1 protein and GSH content). The GS decrease was not prevented by dexamethasone, and AQP-4 was not altered in this epileptic model. CONCLUSIONS: Changes in astroglial parameters emphasize the importance of these cells for understanding alterations and mechanisms of epileptic disorders in this model. In vivo dexamethasone administration prevented most of the parameters analyzed, reinforcing the importance of anti-inflammatory steroid therapy in the Li-pilocarpine model and possibly in other epileptic conditions in which neuroinflammation is present.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Data-Review
[do] DOI:10.1186/s12974-018-1109-5

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[PMID]: 29501554
[Au] Autor:Taylor AJ; Kim JH; Ress D
[Ad] Address:Department of Neuroscience, Core for Advanced MRI, Baylor College of Medicine, Houston, TX, 77030, USA.
[Ti] Title:Characterization of the hemodynamic response function across the majority of human cerebral cortex.
[So] Source:Neuroimage;173:322-331, 2018 Mar 01.
[Is] ISSN:1095-9572
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:A brief (<4 s) period of neural activation evokes a stereotypical sequence of vascular and metabolic events to create the hemodynamic response function (HRF) measured using functional magnetic resonance imaging (fMRI). Linear analysis of fMRI data requires that the HRF be treated as an impulse response, so the character and temporal stability of the HRF are critical issues. Here, a simple audiovisual stimulus combined with a fast-paced task was used to evoke a strong HRF across a majority, ∼77%, of cortex during a single scanning session. High spatiotemporal resolution (2-mm voxels, 1.25-s acquisition time) was used to focus HRF measurements specifically on the gray matter for whole brain. The majority of activated cortex responds with positive HRFs, while ∼27% responds with negative (inverted) HRFs. Spatial patterns of the HRF response amplitudes were found to be similar across subjects. Timing of the initial positive lobe of the HRF was relatively stable across the cortical surface with a mean of 6.1 ±â€¯0.6 s across subjects, yet small but significant timing variations were also evident in specific regions of cortex. The results provide guidance for linear analysis of fMRI data. More importantly, this method provides a means to quantify neurovascular function across most of the brain, with potential clinical utility for the diagnosis of brain pathologies such as traumatic brain injury.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  6 / 48066 MEDLINE  
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[PMID]: 29365066
[Au] Autor:Whelan CD; Altmann A; Botía JA; Jahanshad N; Hibar DP; Absil J; Alhusaini S; Alvim MKM; Auvinen P; Bartolini E; Bergo FPG; Bernardes T; Blackmon K; Braga B; Caligiuri ME; Calvo A; Carr SJ; Chen J; Chen S; Cherubini A; David P; Domin M; Foley S; França W; Haaker G; Isaev D; Keller SS; Kotikalapudi R; Kowalczyk MA; Kuzniecky R; Langner S; Lenge M; Leyden KM; Liu M; Loi RQ; Martin P; Mascalchi M; Morita ME; Pariente JC; Rodríguez-Cruces R; Rummel C; Saavalainen T; Semmelroch MK; Severino M; Thomas RH; Tondelli M; Tortora D; Vaudano AE; Vivash L; von Podewils F
[Ad] Address:Imaging Genetics Center, Mark and Mary Stevens Neuroimaging and Informatics Institute, University of Southern California, Los Angeles, California, USA.
[Ti] Title:Structural brain abnormalities in the common epilepsies assessed in a worldwide ENIGMA study.
[So] Source:Brain;141(2):391-408, 2018 Feb 01.
[Is] ISSN:1460-2156
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Progressive functional decline in the epilepsies is largely unexplained. We formed the ENIGMA-Epilepsy consortium to understand factors that influence brain measures in epilepsy, pooling data from 24 research centres in 14 countries across Europe, North and South America, Asia, and Australia. Structural brain measures were extracted from MRI brain scans across 2149 individuals with epilepsy, divided into four epilepsy subgroups including idiopathic generalized epilepsies (n =367), mesial temporal lobe epilepsies with hippocampal sclerosis (MTLE; left, n = 415; right, n = 339), and all other epilepsies in aggregate (n = 1026), and compared to 1727 matched healthy controls. We ranked brain structures in order of greatest differences between patients and controls, by meta-analysing effect sizes across 16 subcortical and 68 cortical brain regions. We also tested effects of duration of disease, age at onset, and age-by-diagnosis interactions on structural measures. We observed widespread patterns of altered subcortical volume and reduced cortical grey matter thickness. Compared to controls, all epilepsy groups showed lower volume in the right thalamus (Cohen's d = -0.24 to -0.73; P < 1.49 × 10-4), and lower thickness in the precentral gyri bilaterally (d = -0.34 to -0.52; P < 4.31 × 10-6). Both MTLE subgroups showed profound volume reduction in the ipsilateral hippocampus (d = -1.73 to -1.91, P < 1.4 × 10-19), and lower thickness in extrahippocampal cortical regions, including the precentral and paracentral gyri, compared to controls (d = -0.36 to -0.52; P < 1.49 × 10-4). Thickness differences of the ipsilateral temporopolar, parahippocampal, entorhinal, and fusiform gyri, contralateral pars triangularis, and bilateral precuneus, superior frontal and caudal middle frontal gyri were observed in left, but not right, MTLE (d = -0.29 to -0.54; P < 1.49 × 10-4). Contrastingly, thickness differences of the ipsilateral pars opercularis, and contralateral transverse temporal gyrus, were observed in right, but not left, MTLE (d = -0.27 to -0.51; P < 1.49 × 10-4). Lower subcortical volume and cortical thickness associated with a longer duration of epilepsy in the all-epilepsies, all-other-epilepsies, and right MTLE groups (beta, b < -0.0018; P < 1.49 × 10-4). In the largest neuroimaging study of epilepsy to date, we provide information on the common epilepsies that could not be realistically acquired in any other way. Our study provides a robust ranking of brain measures that can be further targeted for study in genetic and neuropathological studies. This worldwide initiative identifies patterns of shared grey matter reduction across epilepsy syndromes, and distinctive abnormalities between epilepsy syndromes, which inform our understanding of epilepsy as a network disorder, and indicate that certain epilepsy syndromes involve more widespread structural compromise than previously assumed.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Data-Review
[do] DOI:10.1093/brain/awx341

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[PMID]: 29228211
[Au] Autor:Irwin DJ; McMillan CT; Xie SX; Rascovsky K; Van Deerlin VM; Coslett HB; Hamilton R; Aguirre GK; Lee EB; Lee VMY; Trojanowski JQ; Grossman M
[Ad] Address:Penn Frontotemporal Degeneration Center, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.
[Ti] Title:Asymmetry of post-mortem neuropathology in behavioural-variant frontotemporal dementia.
[So] Source:Brain;141(1):288-301, 2018 Jan 01.
[Is] ISSN:1460-2156
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Antemortem behavioural and anatomic abnormalities have largely been associated with right hemisphere disease in behavioural-variant frontotemporal dementia, but post-mortem neuropathological examination of bilateral hemispheres remains to be defined. Here we measured the severity of post-mortem pathology in both grey and white matter using a validated digital image analysis method in four cortical regions sampled from each hemisphere in 26 patients with behavioural-variant frontotemporal dementia, including those with frontotemporal degeneration (i.e. tau = 9, TDP-43 = 14, or FUS = 1 proteinopathy) or Alzheimer's pathology (n = 2). We calculated an asymmetry index based on the difference in measured pathology from each left-right sample pair. Analysis of the absolute value of the asymmetry index (i.e. degree of asymmetry independent of direction) revealed asymmetric pathology for both grey and white matter in all four regions sampled in frontototemporal degeneration patients with tau or TDP-43 pathology (P ≤ 0.01). Direct interhemispheric comparisons of regional pathology measurements within-subjects in the combined tauopathy and TDP-43 proteinopathy group found higher pathology in the right orbitofrontal grey matter compared to the left (P < 0.01) and increased pathology in ventrolateral temporal lobe grey matter of the left hemisphere compared to the right (P < 0.02). Preliminary group-wise comparisons between tauopathy and TDP-43 proteinopathy groups found differences in patterns of interhemispheric burden of grey and white matter regional pathology, with greater relative white matter pathology in tauopathies. To test the association of pathology measurement with ante-mortem observations, we performed exploratory analyses in the subset of patients with imaging data (n = 15) and found a direct association for increasing pathologic burden with decreasing cortical thickness in frontotemporal regions on ante-mortem imaging in tauopathy (P = 0.001) and a trend for TDP-43 proteinopathy (P = 0.06). Exploratory clinicopathological correlations demonstrated an association of socially-inappropriate behaviours with asymmetric right orbitofrontal grey matter pathology, and reduced semantically-guided category naming fluency was associated asymmetric white matter pathology in the left ventrolateral temporal region. We conclude that pathologic disease burden is distributed asymmetrically in behavioural-variant frontotemporal dementia, although not universally in the right hemisphere, and this asymmetry contributes to the clinical heterogeneity of the disorder. The basis for this asymmetric profile is enigmatic but may reflect distinct species or strains of tau and TDP-43 pathologies with propensities to spread by distinct cell- and region-specific mechanisms. Patterns of region-specific pathology in the right hemisphere as well as the left hemisphere may play a role in antemortem clinical observations, and these observations may contribute to antemortem identification of molecular pathology in frontotemporal degeneration.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1712
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Data-Review
[do] DOI:10.1093/brain/awx319

  8 / 48066 MEDLINE  
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[PMID]: 29228180
[Au] Autor:Tetzloff KA; Duffy JR; Clark HM; Strand EA; Machulda MM; Schwarz CG; Senjem ML; Reid RI; Spychalla AJ; Tosakulwong N; Lowe VJ; Jack CR; Josephs KA; Whitwell JL
[Ad] Address:Department of Radiology, Mayo Clinic, Rochester, MN, USA.
[Ti] Title:Longitudinal structural and molecular neuroimaging in agrammatic primary progressive aphasia.
[So] Source:Brain;141(1):302-317, 2018 Jan 01.
[Is] ISSN:1460-2156
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:The agrammatic variant of primary progressive aphasia affects normal grammatical language production, often occurs with apraxia of speech, and is associated with left frontal abnormalities on cross-sectional neuroimaging studies. We aimed to perform a detailed assessment of longitudinal change on structural and molecular neuroimaging to provide a complete picture of neurodegeneration in these patients, and to determine how patterns of progression compare to patients with isolated apraxia of speech (primary progressive apraxia of speech). We assessed longitudinal structural MRI, diffusion tensor imaging and 18F-fluorodeoxyglucose PET in 11 agrammatic aphasia subjects, 20 primary progressive apraxia of speech subjects, and 62 age and gender-matched controls with two serial assessments. Rates of change in grey matter volume and hypometabolism, and white matter fractional anisotropy, mean diffusivity, radial diffusivity and axial diffusivity were assessed at the voxel-level and for numerous regions of interest. The greatest rates of grey matter atrophy in agrammatic aphasia were observed in inferior, middle, and superior frontal gyri, premotor and motor cortices, as well as medial temporal lobe, insula, basal ganglia, and brainstem compared to controls. Longitudinal decline in metabolism was observed in the same regions, with additional findings in medial and lateral parietal lobe. Diffusion tensor imaging changes were prominent bilaterally in inferior and middle frontal white matter and superior longitudinal fasciculus, as well as right inferior fronto-occipital fasciculus, superior frontal and precentral white matter. More focal patterns of degeneration of motor and premotor cortex were observed in primary progressive apraxia of speech. Agrammatic aphasia showed greater rates of grey matter atrophy, decline in metabolism, and white matter degeneration compared to primary progressive apraxia of speech in the left frontal lobe, predominantly inferior and middle frontal grey and white matter. Correlations were also assessed between rates of change on neuroimaging and rates of clinical decline. Progression of aphasia correlated with rates of degeneration in frontal and temporal regions within the language network, while progression of parkinsonism and limb apraxia correlated with degeneration of motor cortex and brainstem. These findings demonstrate that disease progression in agrammatic aphasia is associated with widespread neurodegeneration throughout regions of the language network, as well as connecting white matter tracts, but also with progression to regions outside of the language network that are responsible for the development of motor symptoms. The fact that patterns of progression differed from primary progressive apraxia of speech supports the clinical distinction of these syndromes.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1712
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Data-Review
[do] DOI:10.1093/brain/awx293

  9 / 48066 MEDLINE  
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[PMID]: 29228111
[Au] Autor:Roswandowitz C; Kappes C; Obrig H; von Kriegstein K
[Ad] Address:Max Planck Institute for Human Cognitive and Brain Sciences, Stephanstraße 1a, 04103 Leipzig, Germany.
[Ti] Title:Obligatory and facultative brain regions for voice-identity recognition.
[So] Source:Brain;141(1):234-247, 2018 Jan 01.
[Is] ISSN:1460-2156
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Recognizing the identity of others by their voice is an important skill for social interactions. To date, it remains controversial which parts of the brain are critical structures for this skill. Based on neuroimaging findings, standard models of person-identity recognition suggest that the right temporal lobe is the hub for voice-identity recognition. Neuropsychological case studies, however, reported selective deficits of voice-identity recognition in patients predominantly with right inferior parietal lobe lesions. Here, our aim was to work towards resolving the discrepancy between neuroimaging studies and neuropsychological case studies to find out which brain structures are critical for voice-identity recognition in humans. We performed a voxel-based lesion-behaviour mapping study in a cohort of patients (n = 58) with unilateral focal brain lesions. The study included a comprehensive behavioural test battery on voice-identity recognition of newly learned (voice-name, voice-face association learning) and familiar voices (famous voice recognition) as well as visual (face-identity recognition) and acoustic control tests (vocal-pitch and vocal-timbre discrimination). The study also comprised clinically established tests (neuropsychological assessment, audiometry) and high-resolution structural brain images. The three key findings were: (i) a strong association between voice-identity recognition performance and right posterior/mid temporal and right inferior parietal lobe lesions; (ii) a selective association between right posterior/mid temporal lobe lesions and voice-identity recognition performance when face-identity recognition performance was factored out; and (iii) an association of right inferior parietal lobe lesions with tasks requiring the association between voices and faces but not voices and names. The results imply that the right posterior/mid temporal lobe is an obligatory structure for voice-identity recognition, while the inferior parietal lobe is only a facultative component of voice-identity recognition in situations where additional face-identity processing is required.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1712
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Data-Review
[do] DOI:10.1093/brain/awx313

  10 / 48066 MEDLINE  
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[PMID]: 29523926
[Au] Autor:Fan Z; Dani M; Femminella GD; Wood M; Calsolaro V; Veronese M; Turkheimer F; Gentleman S; Brooks DJ; Hinz R; Edison P
[Ad] Address:Department of Medicine, Neurology Imaging Unit, Imperial College London, London, W12 0NN, UK.
[Ti] Title:Parametric mapping using spectral analysis for C-PBR28 PET reveals neuroinflammation in mild cognitive impairment subjects.
[So] Source:Eur J Nucl Med Mol Imaging;, 2018 Mar 09.
[Is] ISSN:1619-7089
[Cp] Country of publication:Germany
[La] Language:eng
[Ab] Abstract:PURPOSE: Neuroinflammation and microglial activation play an important role in amnestic mild cognitive impairment (MCI) and Alzheimer's disease. In this study, we investigated the spatial distribution of neuroinflammation in MCI subjects, using spectral analysis (SA) to generate parametric maps and quantify C-PBR28 PET, and compared these with compartmental and other kinetic models of quantification. METHODS: Thirteen MCI and nine healthy controls were enrolled in this study. Subjects underwent C-PBR28 PET scans with arterial cannulation. Spectral analysis with an arterial plasma input function was used to generate C-PBR28 parametric maps. These maps were then compared with regional C-PBR28 V (volume of distribution) using a two-tissue compartment model and Logan graphic analysis. Amyloid load was also assessed with F-Flutemetamol PET. RESULTS: With SA, three component peaks were identified in addition to blood volume. The C-PBR28 impulse response function (IRF) at 90 min produced the lowest coefficient of variation. Single-subject analysis using this IRF demonstrated microglial activation in five out of seven amyloid-positive MCI subjects. IRF parametric maps of C-PBR28 uptake revealed a group-wise significant increase in neuroinflammation in amyloid-positive MCI subjects versus HC in multiple cortical association areas, and particularly in the temporal lobe. Interestingly, compartmental analysis detected group-wise increase in C-PBR28 binding in the thalamus of amyloid-positive MCI subjects, while Logan parametric maps did not perform well. CONCLUSIONS: This study demonstrates for the first time that spectral analysis can be used to generate parametric maps of C-PBR28 uptake, and is able to detect microglial activation in amyloid-positive MCI subjects. IRF parametric maps of C-PBR28 uptake allow voxel-wise single-subject analysis and could be used to evaluate microglial activation in individual subjects.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher
[do] DOI:10.1007/s00259-018-3984-5


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