Within the framework of Friederici's (2002) neurocognitive model of sentence processing, the early left anterior negativity (ELAN) in event-related potentials (ERPs) has been claimed to be a brain marker of syntactic first-pass parsing. As ELAN components seem to be exclusively elicited by word category violations (phrase structure violations), they have been taken as strong empirical support for syntax-first models of sentence processing and have gained considerable impact on psycholinguistic theory in a variety of domains. The present article reviews relevant ELAN studies and raises a number of serious issues concerning the reliability and validity of the findings. We also discuss how baseline problems and contextual factors can contribute to early ERP effects in studies examining word category violations. We conclude that--despite the apparent wealth of ELAN data--the functional significance of these findings remains largely unclear. The present paper does not claim to have falsified the existence of ELANs or syntax-related early frontal negativities. However, by separating facts from myths, the paper attempts to make a constructive contribution to how future ERP research in the area of syntax processing may better advance our understanding of online sentence comprehension.
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http://dx.doi.org/10.1016/j.bandl.2011.07.001 | DOI Listing |
Diagnostics (Basel)
November 2024
Department of Medicine, Cumming School of Medicine, University of Calgary, 2500 University Drive NW, Calgary, AB T2N 1N4, Canada.
The disruption of the intestinal epithelial barrier leads to increased intestinal permeability (IP), allowing endotoxins and pathogens to enter the bloodstream contributing to chronic inflammation. Western diets are associated with increased IP, while diets rich in polyphenols, fiber, and omega-3 fats are linked to decreased IP. The relationship between diet, disease activity, and IP in ulcerative colitis (UC) is poorly understood.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Dementia Research Centre, Department of Neurodegenerative Disease, UCL Queen Square Institute of Neurology, Queen Square, London, UK.
Alzheimers Dement
November 2024
Department of Pathology and Immunology, Washington University School of Medicine, Saint Louis, Missouri, USA.
Introduction: Biomarkers for Alzheimer's disease neuropathologic change (ADNC) have been instrumental in developing effective disease-modifying therapeutics. However, to prevent/treat dementia effectively, we require biomarkers for non-AD neuropathologies; for this, neuropathologic examinations and annotated tissue samples are essential.
Methods: We conducted clinicopathologic correlation for the first 100 Alzheimer's Disease Neuroimaging Initiative (ADNI) Neuropathology Core (NPC) cases.
J Pers Med
September 2024
Department of Plastic and Hand Surgery and Laboratory for Tissue Engineering and Regenerative Medicine, University Hospital Erlangen, Friedrich-Alexander University Erlangen-Nürnberg (FAU), 91054 Erlangen, Germany.
Background: The Autotaxin (ATX)-lysophosphatidic acid (LPA) axis is involved in decreasing radiation sensitivity of breast tumor cells. This study aims to further elucidate the effect of irradiation on the ATX-LPA axis and cytokine secretion in different breast cancer cell lines to identify suitable breast cancer subtypes for targeted therapies.
Methods: Different breast cancer cell lines (MCF-7 (luminal A), BT-474 (luminal B), SKBR-3 (HER2-positive), MDA-MB-231 and MDA-MB-468 (triple-negative)) and the breast epithelial cell line MCF-10A were irradiated.
Alzheimers Dement
November 2024
Clinical Memory Research Unit, Department of Clinical Sciences Malmö, Lund University, Lund, Sweden.
Introduction: We examined the relations of misfolded alpha synuclein (α-synuclein) with Alzheimer's disease (AD) biomarkers in two large independent cohorts.
Methods: We included Biomarkers for Identifying Neurodegenerative Disorders Early and Reliably Two (BioFINDER-2) and Alzheimer's Disease Neuroimaging Initiative (ADNI) participants (n = 2315, cognitively unimpaired, mild cognitive impairment, AD dementia) who had cross-sectional cerebrospinal fluid (CSF) α-synuclein measurement from seed-amplification assay as well as cross-sectional and longitudinal amyloid beta (Aβ) and tau levels (measured in CSF and/or by positron emission tomography). All analyses were adjusted for age, sex, and cognitive status.
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