TY  - JOUR
AB  - BACKGROUND: Elevated low-frequency activity (4-12 Hz) within the globus pallidus internus (GPi) has been consistently associated with dystonia. However, the impacts of the genetic etiology of dystonia on low-frequency GPi activity remain unclear; yet it holds importance for adaptive deep brain stimulation (DBS) treatment. METHODS: We compared the properties of GPi electrophysiology acquired from 70 microelectrode recordings (MER) trajectories of DYT-GNAL, DYT-KMT2B, DYT-SGCE, DYT-THAP1, DYT-TOR1A, DYT-VPS16, and idiopathic dystonia (iDYT) patients who underwent GPi-DBS surgery across standard frequency bands. RESULTS: DYT-SGCE patients exhibited significantly lower alpha band activity (2.97%) compared to iDYT (4.44%, p = 0.006) and DYT-THAP1 (4.51%, p = 0.011). Additionally, theta band power was also significantly reduced in DYT-SGCE (4.42%) compared to iDYT and DYT-THAP1 (7.91% and 7.00%, p < 0.05). Instead, the genetic etiology of dystonia did not affect the spatial characteristics of GPi electrophysiology along MER trajectories. CONCLUSION: Considering the genetic etiology of dystonia in closed-loop DBS treatments and utilizing theta and alpha activity for GPi stimulation may optimize clinical outcomes. MER-based DBS lead placement can proceed independently of the underlying genetic cause.
AU  - Kaymak, A.*
AU  - Romito, L.M.*
AU  - Colucci, F.*
AU  - Andreasi, N.G.*
AU  - Telese, R.*
AU  - Rinaldo, S.*
AU  - Levi, V.*
AU  - Zorzi, G.*
AU  - Israel, Z.*
AU  - Arkadir, D.*
AU  - Bergman, H.*
AU  - Carecchio, M.*
AU  - Prokisch, H.
AU  - Zech, M.
AU  - Garavaglia, B.*
AU  - Mazzoni, A.*
AU  - Eleopra, R.*
C1  - 73638
C2  - 57151
CY  - 111 River St, Hoboken 07030-5774, Nj Usa
TI  - Genetic etiology influences the low-frequency components of globus pallidus internus electrophysiology in dystonia.
JO  - Eur. J. Neurol.
VL  - 32
IS  - 3
PB  - Wiley
PY  - 2025
SN  - 1351-5101
ER  - 

TY  - JOUR
AB  - BACKGROUND: Skin biopsies and seed amplification assays (SAA) provide a sensitive and potentially quantitative method to detect alpha-synuclein (a-syn) aggregation in peripheral nerve fibers in Parkinson's disease (PD). Relating to the previously published hypothesis that PD may either originate in the peripheral (body-first) or central (brain-first) nervous system, we investigated whether patients with clinical features that have been reported to be associated with a suspected body-first subtype of PD exhibit higher levels of a-syn aggregation in dermal nerve fibers compared to those without these features. Patients with isolated REM sleep behavior disorder (iRBD) representing a suspected premotor stage of body-first PD were studied in comparison to the PD cohort. METHODS: Patients were categorized on the basis of clinical features, and SAA parameters such as lag time, number of positive curves, and titers were analyzed and correlated with clinical features. RESULTS: Although patients with clinical features of suspected body-first PD showed slightly higher titers, significant differences were mainly observed between iRBD patients and PD patients. CONCLUSIONS: Our data suggest that widespread α-syn aggregation in advanced PD limits the use of SAA in skin biopsies for subtype differentiation.
AU  - Vieregge, M.*
AU  - Kuzkina, A.*
AU  - Janzen, A.*
AU  - Oertel, W.H.
AU  - Sommerauer, M.*
AU  - Volkmann, J.*
AU  - Doppler, K.*
C1  - 76160
C2  - 58442
TI  - Dermal alpha-synuclein aggregation in seed amplification assays for parkinson's disease subtype differentiation.
JO  - Eur. J. Neurol.
VL  - 32
IS  - 12
PY  - 2025
SN  - 1351-5101
ER  - 

TY  - JOUR
AB  - BACKGROUND: Understanding the adverse effects of proton pump inhibitors (PPIs) is important due to their widespread use, but the available evidence for an increased dementia risk among patients taking PPIs is inconclusive. The present study aimed to estimate the causal effect of PPIs on the risk of dementia by target trial emulation and time-varying exposure modeling. METHODS: Using claims data of 2,698,176 insured people of a large German statutory health insurer, we conceptualized a target trial in which individuals aged 40 years and older were classified as PPI initiators or non-initiators between 2008 and 2018, and followed until diagnosis of dementia, death, loss to follow-up or end of study. Incidence of dementia (ICD-10 codes F00, F01, F03, F05.1, G30, G31.0, G31.1, G31.9, and F02.8+G31.82) was defined applying a 1-year lag window. We used weighted Cox models to estimate the effect of PPI initiation vs. non-initiation on dementia risk and weighted pooled logistic regression to estimate the effect of time-varying use vs. non-use. RESULTS: 29,746 PPI initiators (4.4%) and 26,830 non-initiators (1.3%) were diagnosed with dementia. Comparing PPI initiation with no initiation, the hazard ratio (HR) for dementia was 1.54 (95% confidence interval [CI]: 1.51-1.58). The HR for time-dependent PPI use vs. non-use was 1.56 (95% CI: 1.50-1.63). Differentiated subtypes, including unspecified dementia, Alzheimer's disease (AD), and vascular dementia (VaD), showed increased risk by PPI initiation and time-varying PPI use. CONCLUSIONS: This study suggests that PPI initiation and time-varying PPI use may increase overall dementia risk.
AU  - Ahn, N.*
AU  - Nolde, M.*
AU  - Günter, A.*
AU  - Güntner, F.*
AU  - Gerlach, R.*
AU  - Tauscher, M.*
AU  - Amann, U.
AU  - Linseisen, J.
AU  - Meisinger, C.*
AU  - Rückert-Eheberg, I.-M.
AU  - Baumeister, S.E.*
C1  - 64361
C2  - 52208
CY  - 111 River St, Hoboken 07030-5774, Nj Usa
SP  - 1335-1343
TI  - Emulating a target trial of proton pump inhibitors and dementia risk using claims data.
JO  - Eur. J. Neurol.
VL  - 29
IS  - 5
PB  - Wiley
PY  - 2022
SN  - 1351-5101
ER  - 

TY  - JOUR
AB  - BACKGROUND: Diabetic sensorimotor peripheral neuropathy (DSPN) is usually considered to affect predominantly the lower limbs (LL-N), while the impact of upper limb neuropathy (UL-N) on hand functional performance and quality of life (QoL) has not been evaluated systematically. This study aims to investigate the prevalence and characteristics of UL-N and its functional and psychosocial consequences in type 2 diabetes. METHODS: Individuals with type 2 diabetes (n=141) and an age- and sex-matched control group (n=73) underwent comprehensive assessment of neuropathy, hand functional performance and psychosocial status. RESULTS: The prevalence of UL-N was 30.5% in patients with diabetes and that of LL-N 49.6%, with 25.5% exhibiting both. Patients with diabetes showed similar sensory phenotype regarding both large and small fiber functions in hands and feet. Patients with UL-N showed reduced manual dexterity, but normal hand grip force. Additionally, there was a correlation between reduced dexterity and sensory deficits. Patients with UL-N had reduced estimates of psychosocial health including health-related QoL compared to control subjects and patients without UL-N. UL-N correlated with the severity of LL-N, but not with duration of diabetes, glycaemia, age, or sex. CONCLUSIONS: This study points to a substantial prevalence of UL-N in type 2 diabetes. The sensory phenotype of patients with UL-N was similar to LL-N and was characterized by loss of sensory function. Our study demonstrated an association of UL-N with impaired manual dexterity and reduced health-related QoL. Thus, upper limb sensorimotor functions should be assessed early in patients with diabetes.
AU  - Kender, Z.*
AU  - Groener, J.B.*
AU  - Jende, J.M.E.*
AU  - Kurz, F.T.*
AU  - Fleming, T.*
AU  - Sulaj, A.*
AU  - Schuh-Hofer, S.*
AU  - Treede, R.D.*
AU  - Bendszus, M.*
AU  - Szendroedi, J.
AU  - Nawroth, P.P.
AU  - Kopf, S.*
C1  - 65431
C2  - 52677
SP  - 3081-3091
TI  - Diabetic neuropathy is a generalized phenomenon with impact on hand functional performance and quality of life.
JO  - Eur. J. Neurol.
VL  - 29
IS  - 10
PY  - 2022
SN  - 1351-5101
ER  - 

TY  - JOUR
AB  - BACKGROUND: Hereditary myopathies with limb-girdle muscular weakness (LGW) are a genetically heterogeneous group of disorders, in which molecular diagnosis remains challenging. Our aim was to present a detailed clinical and genetic characterisation of a large cohort of patients with LGW. METHODS: This nationwide cohort study included patients with LGW suspected to be associated with hereditary myopathies. Parameters associated with specific genetic aetiologies were evaluated, and we further assessed how they predicted the detection of causative variants by genetic analyses. RESULTS: Molecular diagnoses were identified in 62.0% (75/121) of the cohort, with a higher proportion of patients diagnosed by next-generation sequencing (NGS) than by single gene testing (77.3% vs. 22.7% of solved cases). Median time from onset to genetic diagnosis was 8.9 years (IQR 3.7-19.9) and 17.8 years (IQR 7.9-27.8) for single gene testing and NGS, respectively. The most common diagnoses were myopathies associated with variants in CAPN3 (n = 9), FKRP (n = 9), ANO5 (n = 8), DYSF (n = 8) and SGCA (n = 5), together accounting for 32.2% of the cohort. Younger age at disease onset (p = 0.043), >10x elevated CK activity levels (p = 0.024) and myopathic electromyography findings (p = 0.007) were significantly associated with the detection of causative variants. CONCLUSIONS: Our findings suggest an earlier use of NGS in patients with LGW to avoid long diagnostic delays. We further present parameters predictive of a molecular diagnosis that may help to select patients for genetic analyses, especially in centres with limited access to sequencing.
AU  - Krenn, M.*
AU  - Tomschik, M.*
AU  - Wagner, M.
AU  - Zulehner, G.*
AU  - Weng, R.*
AU  - Rath, J.*
AU  - Klotz, S.*
AU  - Gelpi, E.*
AU  - Bsteh, G.*
AU  - Keritam, O.*
AU  - Colonna, I.*
AU  - Paternostro, C.*
AU  - Jäger, F.*
AU  - Lindeck-Pozza, E.*
AU  - Iglseder, S.*
AU  - Grinzinger, S.*
AU  - Schönfelder, M.*
AU  - Hohenwarter, C.*
AU  - Freimüller, M.*
AU  - Embacher, N.*
AU  - Wanschitz, J.*
AU  - Topakian, R.*
AU  - Töpf, A.*
AU  - Straub, V.*
AU  - Quasthoff, S.*
AU  - Zimprich, F.*
AU  - Löscher, W.N.*
AU  - Cetin, H.*
C1  - 64521
C2  - 52249
CY  - 111 River St, Hoboken 07030-5774, Nj Usa
SP  - 1815-1824
TI  - Clinico-genetic spectrum of limb-girdle muscular weakness in Austria: A multi-centre cohort study.
JO  - Eur. J. Neurol.
VL  - 29
IS  - 6
PB  - Wiley
PY  - 2022
SN  - 1351-5101
ER  - 

TY  - JOUR
AB  - BACKGROUND: An incremental number of cases of acute transverse myelitis (ATM) in individuals with ongoing or recent coronavirus disease 2019 (COVID-19) have been reported. METHODS: We performed a systematic review of cases of ATM described in the context of severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection by screening both articles published and in preprint. RESULTS: Twenty cases were identified. There was a slight male predominance (60.0%) and the median age was 56 years. Neurological symptoms first manifested after a mean of 10.3 days from the first onset of classical, mostly respiratory symptoms of COVID-19. Overall, COVID-19 severity was relatively mild. PCR of CSF for SARS-CoV-2 was negative in all 14 cases examined. Cerebrospinal fluid findings reflected an inflammatory process in most instances (77.8%). Aquaporin-4 and myelin oligodendrocyte protein (tested in 10 and 9 cases, respectively) antibodies in serum were negative. On MRI, the spinal cord lesions spanned a mean of 9.8 vertebral segments, necrotic-hemorrhagic transformation was present in three cases and two individuals had additional acute motor axonal neuropathy. More than half of the patients received a second immunotherapy regimen. Over a limited follow-up period of several weeks, 90% of individuals recovered either partially or near fully. CONCLUSION: Although causality cannot readily be inferred, it is possible that cases of ATM occur para- or post-infectiously in COVID-19. All identified reports are anecdotal and case descriptions are heterogenous. Whether the condition and the observed radiological characteristics are specific to SARS-CoV-2 infection needs to be clarified.
AU  - Schulte, E.C.
AU  - Hauer, L.*
AU  - Kunz, A.B.*
AU  - Sellner, J.*
C1  - 62212
C2  - 50735
CY  - 111 River St, Hoboken 07030-5774, Nj Usa
SP  - 3230-3244
TI  - Systematic review of cases of acute myelitis in individuals with COVID-19.
JO  - Eur. J. Neurol.
VL  - 28
IS  - 10
PB  - Wiley
PY  - 2021
SN  - 1351-5101
ER  - 

TY  - JOUR
AB  - Background and purpose Next-generation sequencing has greatly improved the diagnostic success rates for genetic neuromuscular disorders (NMDs). Nevertheless, most patients still remain undiagnosed, and there is a need to maximize the diagnostic yield. Methods A retrospective study was conducted on 72 patients with NMDs who underwent exome sequencing (ES), partly followed by genotype-guided diagnostic reassessment and secondary investigations. The diagnostic yields that would have been achieved by appropriately chosen narrow and comprehensive gene panels were also analysed. Results The initial diagnostic yield of ES was 30.6% (n = 22/72 patients). In an additional 15.3% of patients (n = 11/72) ES results were of unknown clinical significance. After genotype-guided diagnostic reassessment and complementary investigations, the yield was increased to 37.5% (n = 27/72). Compared to ES, targeted gene panels (<25 kilobases) reached a diagnostic yield of 22.2% (n = 16/72), whereas comprehensive gene panels achieved 34.7% (n = 25/72). Conclusion Exome sequencing allows the detection of pathogenic variants missed by (narrowly) targeted gene panel approaches. Diagnostic reassessment after genetic testing further enhances the diagnostic outcomes for NMDs.
AU  - Krenn, M.*
AU  - Tomschik, M.*
AU  - Rath, J.*
AU  - Cetin, H.*
AU  - Grisold, A.*
AU  - Zulehner, G.*
AU  - Milenkovic, I.*
AU  - Stogmann, E.*
AU  - Zimprich, A.*
AU  - Strom, T.M.
AU  - Meitinger, T.
AU  - Wagner, M.
AU  - Zimprich, F.*
C1  - 56744
C2  - 47277
CY  - 111 River St, Hoboken 07030-5774, Nj Usa
SP  - 51-61
TI  - Genotype-guided diagnostic reassessment after exome sequencing in neuromuscular disorders: Experiences with a two-step approach.
JO  - Eur. J. Neurol.
VL  - 27
IS  - 1
PB  - Wiley
PY  - 2020
SN  - 1351-5101
ER  - 

TY  - JOUR
AU  - Krenn, M.*
AU  - Rath, J.*
AU  - Zulehner, G.*
AU  - Wagner, M.*
AU  - Strom, T.M.
AU  - Stoegmann, E.*
AU  - Zimprich, F.*
C1  - 53937
C2  - 45102
CY  - Po Box 211, 1000 Ae Amsterdam, Netherlands
SP  - 549-549
TI  - Clinical whole-exome sequencing for the diagnosis of Mendelian neuromuscular disorders.
JO  - Eur. J. Neurol.
VL  - 25
PB  - Elsevier Science Bv
PY  - 2018
SN  - 1351-5101
ER  - 

TY  - JOUR
AU  - Tan, J.*
AU  - Wagner, M.
AU  - Stenton, S.
AU  - Strom, T.M.
AU  - Prokisch, H.
AU  - Klopstock, T.*
C1  - 53940
C2  - 45105
CY  - Po Box 211, 1000 Ae Amsterdam, Netherlands
SP  - 31-31
TI  - Estimated lifetime prevalences of autosomal mitochondrial disorders based on allele frequencies of pathogenic variants in exome databases.
JO  - Eur. J. Neurol.
VL  - 25
PB  - Elsevier Science Bv
PY  - 2018
SN  - 1351-5101
ER  - 

TY  - JOUR
AB  - BACKGROUND AND PURPOSE: Aseptic infections of the central nervous system (CNS) are frequently observed in Germany. However, no study has systematically addressed the spectrum of aseptic CNS infections in Germany. METHODS: Data on 191 adult patients diagnosed from January 2007 to December 2014 with aseptic meningitis or encephalitis/meningoencephalitis at our hospital were collected by chart review and analyzed for demographic, clinical and laboratory findings. Patients were stratified according to the causative virus and findings were compared between groups. RESULTS: In our cohort, meningitis was caused in 36% by enterovirus (EV), 15% by herpes simplex virus (HSV), 12% by varicella zoster virus (VZV) and 5% by tick borne encephalitis (TBE). Encephalitis/meningoencephalitis was caused in 13% by HSV, 13% by VZV, and three out of 11 tested patients were positive for TBE. The highest incidence of EV infections was between 25 and 35 years and of HSV infections between 30 and 60 years. VZV infections had a bimodal distribution peaking below 30 and above 70 years. VZV and EV infections were more frequently observed during summer, whereas HSV infections showed no seasonal preference. Inflammatory changes in cerebrospinal fluid (CSF) were highest in HSV and lowest in EV infections. CONCLUSIONS: Polymerase chain reaction tests for HSV, VZV and EV in CSF and TBE serology determined the causative virus in over 60% of tested patients. The age of affected patients, seasonal distribution, disease course and inflammatory changes in CSF differ between groups of patients affected by the most common viral infections.
AU  - Kaminski, M.*
AU  - Grummel, V.*
AU  - Hoffmann, D.
AU  - Berthele, A.*
AU  - Hemmer, B.*
C1  - 51383
C2  - 43196
CY  - Hoboken
SP  - 1062-1070
TI  - The spectrum of aseptic central nervous system infections in southern Germany - demographic, clinical and laboratory findings.
JO  - Eur. J. Neurol.
VL  - 24
IS  - 8
PB  - Wiley
PY  - 2017
SN  - 1351-5101
ER  - 

TY  - JOUR
AB  - Background and purpose: Hereditary spastic paraplegia is a clinically and genetically heterogeneous group of rare, inherited disorders causing an upper motor neuron syndrome with (complex) or without (pure) additional neurological symptoms. Mutations in the KIF1A gene have already been associated with recessive and dominant forms of hereditary spastic paraplegia (SPG30) in a few cases. Methods: All family members included in the study were examined neurologically. Whole-exome sequencing was used in affected individuals to identify the responsible candidate gene. Conventional Sanger sequencing was conducted to validate familial segregation. Results: A family of Macedonian origin with two affected siblings, one with slowly progressive and the other one with a more complex and rapidly progressing hereditary spastic paraplegia is reported. In both affected individuals, two novel pathogenic mutations outside the motor domain of the KIF1A gene were found (NM_001244008.1:c.2909G>A, p.Arg970His and c.1214dup, p.Asn405Lysfs*40) that segregate with the disease within the family establishing the diagnosis of autosomal recessive SPG30. Conclusions: This report provides the first evidence that mutations outside the motor domain of the gene can cause (recessive) SPG30 and extends the genotype-phenotype association for KIF1A-related diseases.
AU  - Krenn, M.*
AU  - Zulehner, G.*
AU  - Hotzy, C.*
AU  - Rath, J.*
AU  - Stogmann, E.*
AU  - Wagner, M.
AU  - Haack, T.B.*
AU  - Strom, T.M.
AU  - *
AU  - Zimprich, F.*
C1  - 50933
C2  - 42962
CY  - Hoboken
SP  - 741-747
TI  - Hereditary spastic paraplegia caused by compound heterozygous mutations outside the motor domain of the KIF1A gene.
JO  - Eur. J. Neurol.
VL  - 24
IS  - 5
PB  - Wiley
PY  - 2017
SN  - 1351-5101
ER  - 

TY  - JOUR
AB  - BACKGROUND AND PURPOSE: Although the genetic contribution to stroke risk is well known, it remains unclear if young-onset stroke has a stronger genetic contribution than old-onset stroke. This study aims to compare the heritability of ischaemic stroke risk between young and old, using common genetic variants from whole-genome array data in population-based samples. METHODS: This analysis included 4050 ischaemic stroke cases and 5765 controls from six study populations of European ancestry; 47% of cases were young-onset stroke (age < 55 years). To quantify the heritability for stroke risk in these unrelated individuals, the pairwise genetic relatedness was estimated between individuals based on their whole-genome array data using a mixed linear model. Heritability was estimated separately for young-onset stroke and old-onset stroke (age ≥ 55 years). RESULTS: Heritabilities for young-onset stroke and old-onset stroke were estimated at 42% (±8%, P < 0.001) and 34% (±10%, P < 0.001), respectively. CONCLUSIONS: Our data suggest that the genetic contribution to the risk of stroke may be higher in young-onset ischaemic stroke, although the difference was not statistically significant.
AU  - Bluher, A.*
AU  - Devan, W.J.*
AU  - Holliday, E.G.*
AU  - Nalls, M.*
AU  - Parolo, S.*
AU  - Bione, S.*
AU  - Giese, A.K.*
AU  - Boncoraglio, G.B.*
AU  - Maguire, J.M.*
AU  - Müller-Nurasyid, M.
AU  - Gieger, C.
AU  - Meschia, J.F.*
AU  - Rosand, J.*
AU  - Rolfs, A.*
AU  - Kittner, S.J.*
AU  - Mitchell, B.D.*
AU  - O'Connell, J.R.*
AU  - Cheng, Y.C.*
C1  - 46772
C2  - 37802
SP  - 1488-1491
TI  - Heritability of young- and old-onset ischaemic stroke.
JO  - Eur. J. Neurol.
VL  - 22
IS  - 11
PY  - 2015
SN  - 1351-5101
ER  - 

TY  - JOUR
AU  - Kuepper, C.*
AU  - Gallenmueller, C.*
AU  - Mueller-Felber, W.*
AU  - Haack, T.B.
AU  - Strom, T.M.
AU  - Meitinger, T.
AU  - Klopstock, T.*
C1  - 47334
C2  - 40564
SP  - 30
TI  - Familial dyskinesia with facial myokymia due to ADCY5 mutation: Treatment with propranolol.
JO  - Eur. J. Neurol.
VL  - 22
PY  - 2015
SN  - 1351-5101
ER  - 

TY  - JOUR
AB  - Background and purpose: Platelet collagen receptor glycoprotein VI (GPVI) contributes significantly to platelet adhesion and thrombus formation. We aimed to investigate GPVI in patients presenting with symptoms of acute cerebrovascular disease and to define GPVI as biomarker for acute stroke. Methods: We consecutively evaluated 205 patients, who admitted the stroke unit with symptoms for stroke. Surface expression of the platelet activation markers (GPVI, CD62P, GPIb) was determined by two-color whole blood flow cytometry. Results: Patients with transient ischemic attack (TIA) (n = 18; 8.8%) as well as with stroke (n = 133; 64.9%) showed a significantly enhanced GPVI expression (mean fluorescence intensity ± SD) on admission compared to patients with non-ischemic (NI) events (n = 54; 26.3%) (TIA: 20.9 ± 7.1 vs. NI: 16.2 ± 3.9; P = 0.002; stroke: 20.4 ± 5.7 vs. NI; P = 0.002). Neither CD62P nor GPIb surface expression showed a significant difference. Logistic regression analysis revealed that on admission GPVI was associated with stroke independent of conventional laboratory markers such as C-reactive protein, blood glucose, and creatine kinase. Using a receiver operating characteristic curve on GPVI, we have determined the cut off value of 18.2 for stroke. Thus, patients with enhanced GPVI expression levels (≥18.2) had a 2.4-fold relative risk for stroke. Patients with elevated platelet GPVI expression level had a poorer clinical outcome in cumulative event-free survival for stroke, myocardial infarction, and cerebro-/cardiovascular death at 3-month follow-up (log rank; P = 0.045). Conclusions: These findings indicate that platelet GPVI surface expression is significantly enhanced in patients with TIA and stroke compared to patients with NI events. Determination of platelet-specific GPVI may be useful as an early biomarker for cerebral ischemia.
AU  - Bigalke, B.*
AU  - Stellos, K.*
AU  - Geisle, T.*
AU  - Kremmer, E.
AU  - Seize, P.*
AU  - Ma, A.E.*
AU  - Lindemann, S.*
AU  - Melms, A.*
AU  - Luft, A.*
AU  - Gawaz, M.*
C1  - 293
C2  - 26684
SP  - 111-117
TI  - Expression of platelet glycoprotein VI is associated with transient ischemic attack and stroke.
JO  - Eur. J. Neurol.
VL  - 17
IS  - 1
PB  - Wiley-Blackwell
PY  - 2009
SN  - 1351-5101
ER  -