| 1. |
- Crespi, Ângela Elisa, et al.
(författare)
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Low resistivity amorphous carbon-based thin films employed as anti-reflective coatings on copper
- 2020
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Ingår i: Thin Solid Films. - : Elsevier BV. - 0040-6090 .- 1879-2731. ; 712
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Tidskriftsartikel (refereegranskat)abstract
- Amorphous carbon-based coatings deposited on copper substrates by magnetron sputtering at different target-to-substrate distances were investigated. Films deposited at short distances as 2 cm presented the best results in terms of morphology, density, and resistivity. Ultraviolet near-infrared range spectrometry measurements determined total reflectance and ellipsometry, extinction coefficient, refraction index, and pseudo bandgap. Amorphous carbon films of 150 nm deposited at 2 cm reduced the total reflectance by up to 60 ± 5% in the near-infra-red range when compared to pure copper films. The addition of Fe* boosts the absorption of the coating reducing the total reflectance by up to 70 ± 5% in near-infrared. (Fe*: deposited from stainless-steel target used in direct-current magnetron sputtering). Also, Fe* reduces the electrical resistivity by a factor of 100 compared to that of pure amorphous carbon films. The reduction in total reflectance induced by the presence of the amorphous carbon-based films on copper depends, as expected, on light penetration depth and the absorption coefficient.
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| 2. |
- de Erausquin, Gabriel A, et al.
(författare)
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Chronic neuropsychiatric sequelae of SARS-CoV-2: Protocol and methods from the Alzheimer's Association Global Consortium.
- 2022
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Ingår i: Alzheimer's & dementia (New York, N. Y.). - : Wiley. - 2352-8737. ; 8:1
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Tidskriftsartikel (refereegranskat)abstract
- Coronavirus disease 2019 (COVID-19) has caused >3.5 million deaths worldwide and affected >160 million people. At least twice as many have been infected but remained asymptomatic or minimally symptomatic. COVID-19 includes central nervous system manifestations mediated by inflammation and cerebrovascular, anoxic, and/or viral neurotoxicity mechanisms. More than one third of patients with COVID-19 develop neurologic problems during the acute phase of the illness, including loss of sense of smell or taste, seizures, and stroke. Damage or functional changes to the brain may result in chronic sequelae. The risk of incident cognitive and neuropsychiatric complications appears independent from the severity of the original pulmonary illness. It behooves the scientific and medical community to attempt to understand the molecular and/or systemic factors linking COVID-19 to neurologic illness, both short and long term.This article describes what is known so far in terms of links among COVID-19, the brain, neurological symptoms, and Alzheimer's disease (AD) and related dementias. We focus on risk factors and possible molecular, inflammatory, and viral mechanisms underlying neurological injury. We also provide a comprehensive description of the Alzheimer's Association Consortium on Chronic Neuropsychiatric Sequelae of SARS-CoV-2 infection (CNS SC2) harmonized methodology to address these questions using a worldwide network of researchers and institutions.Successful harmonization of designs and methods was achieved through a consensus process initially fragmented by specific interest groups (epidemiology, clinical assessments, cognitive evaluation, biomarkers, and neuroimaging). Conclusions from subcommittees were presented to the whole group and discussed extensively. Presently data collection is ongoing at 19 sites in 12 countries representing Asia, Africa, the Americas, and Europe.The Alzheimer's Association Global Consortium harmonized methodology is proposed as a model to study long-term neurocognitive sequelae of SARS-CoV-2 infection.The following review describes what is known so far in terms of molecular and epidemiological links among COVID-19, the brain, neurological symptoms, and AD and related dementias (ADRD)The primary objective of this large-scale collaboration is to clarify the pathogenesis of ADRD and to advance our understanding of the impact of a neurotropic virus on the long-term risk of cognitive decline and other CNS sequelae. No available evidence supports the notion that cognitive impairment after SARS-CoV-2 infection is a form of dementia (ADRD or otherwise). The longitudinal methodologies espoused by the consortium are intended to provide data to answer this question as clearly as possible controlling for possible confounders. Our specific hypothesis is that SARS-CoV-2 triggers ADRD-like pathology following the extended olfactory cortical network (EOCN) in older individuals with specific genetic susceptibility.The proposed harmonization strategies and flexible study designs offer the possibility to include large samples of under-represented racial and ethnic groups, creating a rich set of harmonized cohorts for future studies of the pathophysiology, determinants, long-term consequences, and trends in cognitive aging, ADRD, and vascular disease.We provide a framework for current and future studies to be carried out within the Consortium. and offers a "green paper" to the research community with a very broad, global base of support, on tools suitable for low- and middle-income countries aimed to compare and combine future longitudinal data on the topic.The Consortium proposes a combination of design and statistical methods as a means of approaching causal inference of the COVID-19 neuropsychiatric sequelae. We expect that deep phenotyping of neuropsychiatric sequelae may provide a series of candidate syndromes with phenomenological and biological characterization that can be further explored. By generating high-quality harmonized data across sites we aim to capture both descriptive and, where possible, causal associations.
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| 3. |
- Götze, Karl, et al.
(författare)
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Plasma neurofilament light chain in memory clinic practice: Evidence from a real-life study.
- 2023
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Ingår i: Neurobiology of disease. - : Elsevier BV. - 1095-953X .- 0969-9961. ; 176
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Tidskriftsartikel (refereegranskat)abstract
- To explore the accuracy of plasma neurofilament light chain (NfL) as a biomarker for diagnosis and staging of cognitive impairment, in a large cohort with of previously diagnosed patients in clinical practice.Retrospective, cross-sectional, monocentric study, from a tertiary memory clinic. Patients underwent cerebrospinal fluid core Alzheimer's disease (AD) biomarker evaluation using ELISA or Elecsys methods, and plasma NfL analysis using the single molecule array technology. The patients' biomarker data were examined for associations with: i/cognitive status ii/presence of neurodegenerative disease and iii/diagnostic groups. Associations between core CSF biomarkers and plasma NfL were determined.Participants (N=558, mean age=69.2±8.8, 56.5% women) were diagnosed with AD (n=274, considering dementia and MCI stages), frontotemporal dementia (FTD, n=55), Lewy body disease (LBD, n=40, considering MCI and dementia stages), other neurodegenerative diseases, n=57 (e.g Supranuclear Palsy, Corticobasal syndrome), non-neurodegenerative cognitive impairment (NND, n=79, e.g. vascular lesions, epilepsy or psychiatric disorders) or subjective cognitive impairment (SCI, n=53). Mean plasma NfL (log, pg/mL) levels were higher in neurodegenerative than non-neurodegenerative disorders (1.35±0.2 vs 1.16±0.23, p<0.001), higher in all diagnostic groups than in SCI (1.06±0.23) p<0.001), and associated with the stage of cognitive impairment (p<0.001). The addition of plasma NfL to a clinical model (age, MMSE and APOE ε4 carriership) marginally improved the discrimination of degenerative from non-degenerative disorders in ROC analysis (AUC clinical model: 0.81, 95% CI=[0.77;0.85] AUC clinical model + plasma NfL: AUC=0.83 95% CI=[0.78;0.87], delta Akaike information criterion=-11.7).Plasma NfL could help discrimination between degenerative and non-degenerative cognitive disorders, albeit not better than comprehensive clinical evaluation.
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| 4. |
- Öhrfelt, Annika, 1973, et al.
(författare)
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A Novel ELISA for the Measurement of Cerebrospinal Fluid SNAP-25 in Patients with Alzheimer's Disease.
- 2019
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Ingår i: Neuroscience. - : Elsevier BV. - 1873-7544 .- 0306-4522. ; 420, s. 136-144
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Tidskriftsartikel (refereegranskat)abstract
- Synaptic degeneration is central in Alzheimer's disease (AD) pathogenesis and biomarkers to monitor this pathophysiology in living patients are warranted. We developed a novel sandwich enzyme-linked immunosorbent assay (ELISA) for the measurement of the pre-synaptic protein SNAP-25 in cerebrospinal fluid (CSF) and evaluated it as a biomarker for AD. CSF samples included a pilot study consisting of AD (N=26) and controls (N=26), and two independent clinical cohorts of AD patients and controls. Cohort I included CSF samples from patients with dementia due to AD (N=17), patients with mild cognitive impairment (MCI) due to AD (N=5) and controls (N=17), and cohort II CSF samples from patients with dementia due to AD (N=24), patients with MCI due to AD (N=18) and controls (N=36). CSF levels of SNAP-25 were significantly increased in patients with AD compared with controls (P≤0.00001). In both clinical cohorts, CSF levels of SNAP-25 were significantly increased in patients with MCI due to AD (P<0.0001). SNAP-25 could differentiate dementia due to AD (N=41) from controls (N=52) and MCI due to AD (N=23) from controls (N=52) with areas under the curve of 0.967 (P<0.0001) and 0.948 (P<0.0001), respectively. CSF SNAP-25 is a promising AD biomarker that differentiates AD patients in different clinical stages of the disease from controls with excellent diagnostic accuracy. Future studies should address the specificity of the CSF SNAP-25 against common differential diagnoses to AD, as well as how the biomarker changes in response to treatment with disease-modifying drug candidates.
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