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991.
992.
Polygenic load: Earlier disease onset but similar longitudinal progression in Parkinson's disease 下载免费PDF全文
Stefanie Lerche PhD Inga Liepelt‐Scarfone PhD Isabel Wurster MD Claudia Schulte Eva Schäffer MD Benjamin Röben MD Gerrit Machetanz MD Milan Zimmermann MD Selda Akbas Ann‐Kathrin Hauser Thomas Gasser MD Walter Maetzler MD Daniela Berg MD Kathrin Brockmann MD 《Movement disorders》2018,33(8):1349-1353
Objectives: In order to evaluate the influence of the genetic load of 49 genetic variants known to be associated with PD on the age at onset as well as on clinical outcome parameters. Background: PD patients show a large variability in phenotype and progression reflecting interindividual heterogeneity. This might be influenced by a diverse genetic architecture. Methods: Six hundred seventeen PD patients were included in this study and stratified by their “genetic load,” which is based on the weighted odds ratios of 49 genetic variants known to be associated with PD from genome‐wide association studies. Clinical parameters (H & Y, UPDRS‐III, MMSE, and Beck's Depression Inventory) were evaluated cross‐sectionally and in a subgroup longitudinally over 8 years. Results: PD patients with the highest genetic load were younger at disease onset, whereas severity of clinical parameters were similar compared to patients with the lowest genetic load. These findings could be confirmed regarding progression to clinical endpoints in the longitudinal analysis. Conclusion: A high genetic load is associated with a younger age at onset, which, in turn, might possibly promote more effective compensatory mechanisms resulting in a similar rate of disease progression. © 2018 International Parkinson and Movement Disorder Society 相似文献
993.
Introduction
Pre-morbid antecedents in schizophrenia have been studied for some time now more particularly as potential markers of vulnerability. What are the tell-tale signs in some of the patient's childhood? The authors suggest a non-exhaustive review of the literature on this subject.Method
The authors reviewed the literature (English and French) of prospective and retrospective studies.Results
Many fields appear to be impaired during the childhood of some schizophrenic patients, fields such as: developmental abnormalities, speech impairments, social interactions, behaviour, cognitive functioning. The authors also noticed the presence of neurological soft signs and para-clinical abnormalities.Discussion
The authors suggest a critical and synthetic review of existing data: what can be retained of this data? The authors also discuss the evolution of these signs and their interaction with the evolution of the disease itself.Conclusion
Many of these signs were noticed in several children who later developed schizophrenia. For many authors, the more important these signs are, the more severe the disease will be. These pre-morbid antecedents give rise to theoretical questions and open perspectives concerning an early diagnosis of schizophrenia. 相似文献994.
Matthias Wittstock Annette Grossmann Erwin Kunesch Uwe Walter Reiner Benecke Alexander Wolters 《Journal of neurology》2010,257(4):590-597
Callosal dysfunction is known to be evident in a variety of neurodegenerative and inflammatory diseases of the central nervous system. Cerebral microangiopathy (CMA) may also affect callosal pathways by chronic demyelination. The aim of the present study was to investigate callosal function with respect to the extent of CMA. Callosal function was tested by a bimanual tapping task and by analysis of the ipsilateral silent period (iSP) and the transcallosal conduction time (TCT) using transcranial magnetic stimulation. Results were correlated to the extent of CMA measured by cranial magnetic resonance imaging (cMRI) in 44 patients with CMA compared to 10 control subjects. The extent of CMA was quantified by a cMRI score. Additionally, callosal atrophy was quantified by cMRI morphometry. Frequency of pathological iSP findings or disturbed bimanual tapping was significantly correlated to a higher CMA score. Moreover, the extent of CMA was significantly correlated to the degree of callosal atrophy. It is concluded that CMA considerably affects callosal pathways, possibly by chronic demyelination of callosal fibres. As the extent of CMA and atrophy of the corpus callosum is correlated to callosal dysfunction, analysis of the iSP can be used to assess the clinical impact of CMA detected by cMRI. 相似文献
995.
Background
Many heparin-induced thrombocytopenia (HIT) antibodies cause platelet activation in the serotonin release assay (SRA) in the absence of heparin. This in vitro observation may help unravel the mechanism of delayed-onset HIT, where seropositive patients develop thrombocytopenia and associated thrombosis after cessation of heparin.Objective
Studies were conducted to examine the relationship between platelet environment, surface PF4 expression, and the extent of heparin-independent platelet activation in the SRA.Methods
Ex vivo platelets were washed and labeled for SRA, then used either before or after 45 minutes of recovery at 37 °C. HIT antibody-mediated serotonin release in the absence of heparin was compared to the extent of surface staining of the platelets with fluorescent anti-human PF4 antibodies.Results
Handling of platelets for in vitro studies resulted in transient expression of surface PF4, and it was during this interval that platelets were most sensitive to activation by HIT antibodies in the absence of heparin. Heparin-independent platelet activation was attenuated when SRA-positive specimens were retested after platelets were incubated 45 minutes at 37 °C. Surface PF4 expression was diminished on the rested platelets, compared to the same platelets labeled immediately after handling. Thus compared to rested platelets, mildly activated platelets had elevated surface PF4 expression and a higher level of HIT antibody-mediated, heparin-independent platelet activation.Conclusion
Surface expression of PF4 reflects HIT antigen presentation, and varies with the physiological state of platelets. Thus there can be differences in HIT antibody target availability among patients which may explain the variability in consequences of HIT antibody seropositivity. 相似文献996.
Usman Saeed Saira S. Mirza Bradley J. MacIntosh Nathan Herrmann Julia Keith Joel Ramirez Sean M. Nestor Qinggang Yu Jo Knight Walter Swardfager Steven G. Potkin Ekaterina Rogaeva Peter St. George-Hyslop Sandra E. Black Mario Masellis 《Alzheimer's & dementia》2018,14(9):1137-1147
Introduction
Although the apolipoprotein E ε4-allele (APOE-ε4) is a susceptibility factor for Alzheimer's disease (AD) and dementia with Lewy bodies (DLB), its relationship with imaging and cognitive measures across the AD/DLB spectrum remains unexplored.Methods
We studied 298 patients (AD = 250, DLB = 48; 38 autopsy-confirmed; NCT01800214) using neuropsychological testing, volumetric magnetic resonance imaging, and APOE genotyping to investigate the association of APOE-ε4 with hippocampal volume and learning/memory phenotypes, irrespective of diagnosis.Results
Across the AD/DLB spectrum: (1) hippocampal volumes were smaller with increasing APOE-ε4 dosage (no genotype × diagnosis interaction observed), (2) learning performance as assessed by total recall scores was associated with hippocampal volumes only among APOE-ε4 carriers, and (3) APOE-ε4 carriers performed worse on long-delay free word recall.Discussion
These findings provide evidence that APOE-ε4 is linked to hippocampal atrophy and learning/memory phenotypes across the AD/DLB spectrum, which could be useful as biomarkers of disease progression in therapeutic trials of mixed disease. 相似文献997.
998.
Cascio CJ 《Journal of Neurodevelopmental Disorders》2010,2(2):62-69
The purpose of this article is to review the role of somatosensory perception in typical development, its aberration in a range of neurodevelopmental disorders, and the potential relations between tactile processing abnormalities and central features of each disorder such as motor, communication, and social development. Neurodevelopmental disorders that represent a range of symptoms and etiologies, and for which multiple peer-reviewed articles on somatosensory differences have been published, were chosen to include in the review. Relevant studies in animal models, as well as conditions of early sensory deprivation, are also included. Somatosensory processing plays an important, yet often overlooked, role in typical development and is aberrant in various neurodevelopmental disorders. This is demonstrated in studies of behavior, sensory thresholds, neuroanatomy, and neurophysiology in samples of children with Fragile X syndrome, autism spectrum disorders (ASD), attention deficit hyperactivity disorder (ADHD), and cerebral palsy (CP). Impaired somatosensory processing is found in a range of neurodevelopmental disorders and is associated with deficits in communication, motor ability, and social skills in these disorders. Given the central role of touch in early development, both experimental and clinical approaches should take into consideration the role of somatosensory processing in the etiology and treatment of neurodevelopmental disorders. 相似文献
999.
Daniela Berg MD Klaus Seppi MD Inga Liepelt PhD Katherine Schweitzer MD Frank Wollenweber MD Björn Wolf Ulrich Dillmann MD Heike Stockner MD Jana Godau MD Stefan Kiechl MD Alexandra Gaenslen MD Johann Willeit MD Adriana Di Santo Walter Maetzler MD Thomas Gasser MD Werner Poewe MD Stefanie Behnke MD 《Movement disorders》2010,25(10):1464-1469
Enlarged substantia nigra hyperechogenicity (SN+) assessed by transcranial sonography (TCS) may be associated with Parkinson's disease (PD) risk markers such as impaired motor performance and hyposmia. The aim of this multicenter cross‐sectional study was to define the association between SN+ and these risk markers in a large population older than 50 years without the diagnosis of PD. In three centers (Tuebingen, Homburg, and Innsbruck), 1,839 individuals were examined. The echostatus of the SN was assessed by TCS, motor performance by the Unified Parkinson's Disease Rating Scale (UPDRS) motor score, and olfactory function with Sniffin' Sticks. From the 1,603 subjects included in the analysis, 16.2% were SN+, 23.0% scored above zero in the UPDRS motor section, and 28.0% were hyposmic as defined by less than 75% correctly classified Sniffin' Sticks. SN+ was associated with a UPDRS motor score above zero (OR 1.45, 95% CI 1.08–1.96) and with a lower odor identification capability (OR 1.48, 95% CI 1.12–1.96). The combination of these two features (OR 1.98, 95% CI 1.25–3.15) and UPDRS motor scores ≥3 lead to higher OR. It is concluded that SN+, impaired motor performance, and hyposmia are frequently observed in the elderly and in isolation are unspecific and of limited use to predict a subject's risk for PD. Whether the association of SN+ with both impaired motor performance and hyposmia as seen in this study predicts an increased risk for the development of PD needs to be evaluated in the follow‐up investigations. © 2010 Movement Disorder Society 相似文献
1000.
Kathrin Reetz Rebekka Lencer Johannes M. Hagenah Christian Gaser Vera Tadic Uwe Walter Alexander Wolters Susanne Steinlechner Christine Zühlke Katja Brockmann Christine Klein Arndt Rolfs Ferdinand Binkofski 《Cerebellum (London, England)》2010,9(2):210-217
Spinocerebellar ataxia (SCA17) is a rare genetic disorder characterized by a variety of neuropsychiatric symptoms. Recently, using magnetic resonance imaging (MRI) voxel-based morphometry (VBM), several specific functional–structural correlations comprising differential degeneration related to motor and psychiatric symptoms were reported in patients with SCA17. To investigate gray matter volume (GMV) changes over time and its association to clinical neuropsychiatric symptomatology, nine SCA17 mutation carriers and nine matched healthy individuals underwent a detailed neuropsychiatric clinical examination and a high-resolution T1-weighted volume MRI scan, both at baseline and follow-up after 18 months. Follow-up images revealed a progressive GMV reduction in specific degeneration patterns. In contrast to healthy controls, SCA17 patients showed a greater atrophy not only in cerebellar regions but also in cortical structures such as the limbic system (parahippocampus, cingulate) and parietal precuneus. Clinically, progression of motor symptoms was more pronounced than that of psychiatric symptoms. Correlation with the clinical motor scores revealed a progressive reduction of GMV in cerebellar and cerebral motor networks, whereas correlation with psychiatric scores displayed a more widespread GMV impairment in frontal, limbic, parietal, and also cerebellar structures. Interestingly, changes in global functioning were correlated with bilateral atrophy within the para-/hippocampus. While there was a good temporal association between worsening of motor symptoms and progression in cerebral and cortical neurodegeneration, the progression in psychiatric related neurodegeneration seemed to be more widespread and complex, showing progressive atrophy that preceded the further development of clinical psychiatric symptoms. 相似文献