Publications
282 results found
Schmitt J, Palleis C, Sauerbeck J, et al., 2021, Dual-Phase β-Amyloid PET Captures Neuronal Injury and Amyloidosis in Corticobasal Syndrome, FRONTIERS IN AGING NEUROSCIENCE, Vol: 13, ISSN: 1663-4365
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- Citations: 8
Palleis C, Sauerbeck J, Beyer L, et al., 2021, In Vivo Assessment of Neuroinflammation in 4-Repeat Tauopathies, MOVEMENT DISORDERS, Vol: 36, Pages: 883-894, ISSN: 0885-3185
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- Citations: 22
Haeckert J, Brendel M, Beyer L, et al., 2021, Effective Valproic Acid Treatment in a Patient With Delusional Parasitosis Due to Corticobasal Syndrome and Alzheimer Disease, JOURNAL OF CLINICAL PSYCHOPHARMACOLOGY, Vol: 41, Pages: 335-337, ISSN: 0271-0749
Wesselman LMPD, van Lent DM, Schroeder A, et al., 2021, Dietary patterns are related to cognitive functioning in elderly enriched with individuals at increased risk for Alzheimer's disease, EUROPEAN JOURNAL OF NUTRITION, Vol: 60, Pages: 849-860, ISSN: 1436-6207
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- Citations: 25
Kreuzer A, Sauerbeck J, Scheifele M, et al., 2021, Detection Gap of Right-Asymmetric Neuronal Degeneration by CERAD Test Battery in Alzheimer's Disease, FRONTIERS IN AGING NEUROSCIENCE, Vol: 13, ISSN: 1663-4365
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- Citations: 2
Frederiksen KS, Nielsen TR, Appollonio I, et al., 2021, Biomarker counseling, disclosure of diagnosis and follow-up in patients with mild cognitive impairment: A European Alzheimer's disease consortium survey, INTERNATIONAL JOURNAL OF GERIATRIC PSYCHIATRY, Vol: 36, Pages: 324-333, ISSN: 0885-6230
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- Citations: 15
Franzmeier N, Ren J, Damm A, et al., 2021, The <i>BDNF</i><sub><i>Val66Met</i></sub> SNP modulates the association between beta-amyloid and hippocampal disconnection in Alzheimer's disease, MOLECULAR PSYCHIATRY, Vol: 26, Pages: 614-628, ISSN: 1359-4184
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- Citations: 43
Alexopoulos P, Papanastasiou AD, Economou P, et al., 2021, Associations between APOE-, COMT Val108/158Met-and BDNF Val66Met polymorphisms and variations in depressive and anxiety symptoms, sense of coherence and vital exhaustion in the real-life setting of mandatory basic military training, JOURNAL OF NEURAL TRANSMISSION, Vol: 128, Pages: 105-114, ISSN: 0300-9564
Beyer L, Meyer-Wilmes J, Schoenecker S, et al., 2021, Cognitive reserve hypothesis in frontotemporal dementia: A FDG-PET study, NEUROIMAGE-CLINICAL, Vol: 29, ISSN: 2213-1582
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- Citations: 10
Sannemann L, Schild A-K, Altenstein S, et al., 2020, Neuropsychiatric symptoms in at-risk groups for AD dementia and their association with worry and AD biomarkers-results from the DELCODE study, ALZHEIMERS RESEARCH & THERAPY, Vol: 12
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- Citations: 14
Palleis C, Sauerbeck J, Beyer L, et al., 2020, 18kDa Translocator Protein PET in 4-Repeat Tauopathies - A Cross-Sectional Single Center Study, Movement-Disorder-Society (MDS) International Virtual Congress, Publisher: WILEY, Pages: S507-S507, ISSN: 0885-3185
Brendel M, Palleis C, Prix C, et al., 2020, <SUP>18</SUP>F-PI-2620 Tau-PET in Corticobasal Syndrome, 33rd Annual Congress of the European-Association-of-Nuclear-Medicine (EANM), Publisher: SPRINGER, Pages: S93-S93, ISSN: 1619-7070
Gao Y, Wang T, Yu X, et al., 2020, Mendelian randomization implies no direct causal association between leukocyte telomere length and amyotrophic lateral sclerosis, SCIENTIFIC REPORTS, Vol: 10, ISSN: 2045-2322
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- Citations: 3
Rauchmann B-S, Ghaseminejad F, Mekala S, et al., 2020, Cerebral Microhemorrhage at MRI in Mild Cognitive Impairment and Early Alzheimer Disease: Association with Tau and Amyloid β at PET Imaging, RADIOLOGY, Vol: 296, Pages: 134-142, ISSN: 0033-8419
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- Citations: 2
Saller T, MacLullich AMJ, Perneczky R, 2020, The 4AT - an instrument for delirium detection for older patients in the post-anaesthesia care unit (vol 75, pg 410, 2020), ANAESTHESIA, Vol: 75, Pages: 684-684, ISSN: 0003-2409
Frederiksen KS, Nielsen R, Appollonio I, et al., 2020, Biomarker counseling, disclosure of diagnosis and follow-up in patients with mild cognitive impairment: a European survey of EADC centers, 6th Congress of the European-Academy-of-Neurology (EAN), Publisher: WILEY, Pages: 105-105, ISSN: 1351-5101
Huber M, Beyer L, Prix C, et al., 2020, Metabolic correlates of dopaminergic loss in dementia with lewy bodies, MOVEMENT DISORDERS, Vol: 35, Pages: 595-605, ISSN: 0885-3185
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- Citations: 34
Saller T, MacLullich AMJ, Perneczky R, 2020, The 4AT-an instrument for delirium detection for older patients in the post-anaesthesia care unit, ANAESTHESIA, Vol: 75, Pages: 410-410, ISSN: 0003-2409
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- Citations: 9
von Siemens M, Perneczky R, Vogelmeier C, et al., 2020, The association of cognitive functioning as measured by the DemTect with clinical and functional characteristics of COPD, Publisher: GEORG THIEME VERLAG KG, Pages: S83-S84, ISSN: 0934-8387
Schoeberl F, Pradhan C, Irving S, et al., 2020, Real-space navigation testing differentiates between amyloid-positive and -negative aMCI, NEUROLOGY, Vol: 94, Pages: E861-E873, ISSN: 0028-3878
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- Citations: 12
Rauchmann B-S, Sadlon A, Perneczky R, 2020, Soluble TREM2 and Inflammatory Proteins in Alzheimer's Disease Cerebrospinal Fluid, JOURNAL OF ALZHEIMERS DISEASE, Vol: 73, Pages: 1615-1626, ISSN: 1387-2877
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- Citations: 24
Garibotto V, Trombella S, Antelmi L, et al., 2020, A Comparison of Two Statistical Mapping Tools for Automated Brain FDG-PET Analysis in Predicting Conversion to Alzheimer's Disease in Subjects with Mild Cognitive Impairment, CURRENT ALZHEIMER RESEARCH, Vol: 17, Pages: 1186-1194, ISSN: 1567-2050
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- Citations: 3
von Siemens SM, Perneczky R, Vogelmeier CF, et al., 2019, The association of cognitive functioning as measured by the DemTect with functional and clinical characteristics of COPD: results from the COSYCONET cohort, RESPIRATORY RESEARCH, Vol: 20
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- Citations: 12
Takousis P, Sadlon A, Schulz J, et al., 2019, Differential expression of microRNAs in Alzheimer's disease brain, blood, and cerebrospinal fluid, Alzheimers & Dementia, Vol: 15, Pages: 1468-1477, ISSN: 1552-5260
INTRODUCTION: Several microRNAs (miRNAs) have been implicated in Alzheimer's disease pathogenesis, but the evidence from individual case-control studies remains inconclusive. METHODS: A systematic literature review was performed, followed by standardized multistage data extraction, quality control, and meta-analyses on eligible data for brain, blood, and cerebrospinal fluid specimens. Results were compared with miRNAs reported in the abstracts of eligible studies or recent qualitative reviews to assess novelty. RESULTS: Data from 147 independent data sets across 107 publications were quantitatively assessed in 461 meta-analyses. Twenty-five, five, and 32 miRNAs showed studywide significant differential expression (α < 1·08 × 10-4) in brain, cerebrospinal fluid, and blood-derived specimens, respectively, with 5 miRNAs showing differential expression in both brain and blood. Of these 57 miRNAs, 13 had not been reported in the abstracts of previous original or review articles. DISCUSSION: Our systematic assessment of differential miRNA expression is the first of its kind in Alzheimer's disease and highlights several miRNAs of potential relevance.
Schumann C, Alexopoulos P, Perneczky R, 2019, Determinants of self- and carer-rated quality of life and caregiver burden in Alzheimer disease, INTERNATIONAL JOURNAL OF GERIATRIC PSYCHIATRY, Vol: 34, Pages: 1378-1385, ISSN: 0885-6230
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- Citations: 27
Sadlon A, Takousis P, Alexopoulos P, et al., 2019, miRNAs identify shared pathways in Alzheimer's and Parkinson's Diseases, Trends in Molecular Medicine, Vol: 25, Pages: 662-672, ISSN: 1471-4914
Despite the identification of several dozens of common genetic variants associated with Alzheimer’s disease (AD) and Parkinson’s disease (PD), most of the genetic risk remains uncharacterised. Therefore, it is important to understand the role of regulatory elements, such as miRNAs. Dysregulated miRNAs are implicated in AD and PD, with potential value in dissecting the shared pathophysiology between the two disorders. miRNAs relevant to both neurodegenerative diseases are related to axonal guidance, apoptosis, and inflammation, therefore, AD and PD likely arise from similar underlying biological pathway defects. Furthermore, pathways regulated by APP, L1CAM, and genes of the caspase family may represent promising therapeutic miRNA targets in AD and PD since they are targeted by dysregulated miRNAs in both disorders.
Miebach L, Wolfsgruber S, Polcher A, et al., 2019, Which features of subjective cognitive decline are related to amyloid pathology? Findings from the DELCODE study, ALZHEIMERS RESEARCH & THERAPY, Vol: 11, ISSN: 1758-9193
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- Citations: 68
Bonham LW, Steele NZR, Karch CM, et al., 2019, Genetic variation across RNA metabolism and cell death gene networks is implicated in the semantic variant of primary progressive aphasia, SCIENTIFIC REPORTS, Vol: 9, ISSN: 2045-2322
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- Citations: 6
Schulz J, Takousis P, Wohlers I, et al., 2019, Meta-analyses identify differentially expressed microRNAs in Parkinson's disease, Annals of Neurology, Vol: 85, Pages: 835-851, ISSN: 0364-5134
Objective: MicroRNA-mediated (dys)regulation of gene expression has been implicated in Parkinson's disease (PD), although results of microRNA expression studies remain inconclusive. We aimed to identify microRNAs that show consistent differential expression across all published expression studies in PD.Mathods: We performed a systematic literature search on microRNA expression studies in PD and extracted data from eligible publications. After stratification for brain, blood, and cerebrospinal fluid (CSF)-derived specimen we performed meta-analyses across microRNAs assessed in three or more independent datasets. Meta-analyses were performed using effect-size and p-value based methods, as applicable.Results: After screening 599 publications we identified 47 datasets eligible for meta-analysis. On these, we performed 160 meta-analyses on microRNAs quantified in brain (n=125), blood (n=31), or CSF samples (n=4). Twenty-one meta-analyses were performed using effect sizes. We identified 13 significantly (Bonferroni-adjusted α=3.13x10-4 ) differentially expressed microRNAs in brain (n=3) and blood (n=10) with consistent effect directions across studies. The most compelling findings were with hsa-miR-132-3p (p=6.37x10-5 ), hsa-miR-497-5p (p=1.35x10-4 ), and hsa-miR-133b (p=1.90x10-4 ) in brain, and with hsa-miR-221-3p (p=4.49x10-35 ), hsa-miR-214-3p (p=2.00x10-34 ), and hsa-miR-29c-3p (p=3.00x10-12 ) in blood. No significant signals were found in CSF. Analyses of GWAS data for target genes of brain microRNAs showed significant association (α=9.40x10-5 ) of genetic variants in nine loci.Interpretation: We identified several microRNAs that showed highly significant differential expression in PD. Future studies may assess the possible role of the identified brain miRNAs in pathogenesis and disease progression as well as the potential of the top blood microRNAs as biomarkers for diagnosis, progression or prediction of PD.
Gallo V, Vineis P, Cancellieri M, et al., 2019, Exploring causality of the association between smoking and Parkinson's disease, International Journal of Epidemiology, Vol: 48, Pages: 912-925, ISSN: 1464-3685
Background: The aim of this paper is to investigate the causality of the inverse association between cigarette smoking and Parkinson's disease (PD). The main suggested alternatives include a delaying effect of smoking, reverse causality or an unmeasured confounding related to a low-risk-taking personality trait. Methods: A total of 715 incident PD cases were ascertained in a cohort of 220 494 individuals from NeuroEPIC4PD, a prospective European population-based cohort study including 13 centres in eight countries. Smoking habits were recorded at recruitment. We analysed smoking status, duration, and intensity and exposure to passive smoking in relation to PD onset. Results: Former smokers had a 20% decreased risk and current smokers a halved risk of developing PD compared with never smokers. Strong dose-response relationships with smoking intensity and duration were found. Hazard ratios (HRs) for smoking <20 years were 0.84 [95% confidence interval (CI) 0.67-1.07], 20-29 years 0.73 (95% CI 0.56-0.96) and >30 years 0.54 (95% CI 0.43-0.36) compared with never smokers. The proportional hazard assumption was verified, showing no change of risk over time, arguing against a delaying effect. Reverse causality was disproved by the consistency of dose-response relationships among former and current smokers. The inverse association between passive smoking and PD, HR 0.70 (95% CI 0.49-0.99) ruled out the effect of unmeasured confounding. Conclusions: These results are highly suggestive of a true causal link between smoking and PD, although it is not clear which is the chemical compound in cigarette smoking responsible for the biological effect.
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