36 research outputs found

    Data_Sheet_1_Autonomic function predicts cognitive decline in mild cognitive impairment: Evidence from power spectral analysis of heart rate variability in a longitudinal study.docx

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    BackgroundDespite the emerging clinical relevance of heart rate variability (HRV) as a potential biomarker of cognitive decline and as a candidate target for intervention, there is a dearth of research on the prospective relationship between HRV and cognitive change. In particular, no study has addressed this issue in subjects with a diagnosis of cognitive status including cognitive impairment.ObjectiveTo investigate HRV as a predictor of cognitive decline in subjects with normal cognition (NC) or Mild Cognitive Impairment (MCI). Specifically, we tested the literature-based hypothesis that the HRV response to different physical challenges would predict decline in different cognitive domains.MethodsThis longitudinal study represents the approximately 3-year follow-up of a previous cross-sectional study enrolling 80 older outpatients (aged ≥ 65). At baseline, power spectral analysis of HRV was performed on five-minute electrocardiographic recordings at rest and during a sympathetic (active standing) and a parasympathetic (paced breathing) challenge. We focused on normalized HRV measures [normalized low frequency power (LFn) and the low frequency to high frequency power ratio (LF/HF)] and on their dynamic response from rest to challenge (Δ HRV). Extensive neuropsychological testing was used to diagnose cognitive status at baseline and to evaluate cognitive change over the follow-up via annualized changes in cognitive Z-scores. The association between Δ HRV and cognitive change was explored by means of linear regression, unadjusted and adjusted for potential confounders.ResultsIn subjects diagnosed with MCI at baseline a greater response to a sympathetic challenge predicted a greater decline in episodic memory [adjusted model: Δ LFn, standardized regression coefficient (β) = −0.528, p = 0.019; Δ LF/HF, β = −0.643, p = 0.001] whereas a greater response to a parasympathetic challenge predicted a lesser decline in executive functioning (adjusted model: Δ LFn, β = −0.716, p ConclusionOur findings provide novel insight into the link between HRV and cognition in MCI. They contribute to a better understanding of the heart-brain connection, but will require replication in larger cohorts.</p

    RELATEC : Revista latinoamericana de tecnología educativa

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    Resumen en inglésResumen basado en el de la publicaciónSe presentan las principales aportaciones de un estudio realizado sobre la utilización de diferentes medios tecnológicos realizada por una muestra de profesores y profesoras universitarias. Entre las categorías que ayudan a entender los usos de dichas herramientas en las prácticas docentes está la finalidad instructiva o formativa de los mismos, las estrategias organizativas utilizadas en los centros para ubicar los medios y, finalmente, la formación y apoyo técnico disponible en las mencionadas instituciones de enseñanza superiorES

    Spontaneous confabulations in amnestic-mild cognitive impairment due to Alzheimer’s disease: a new (yet old) atypical variant?

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    <p>Confabulation may be present in Alzheimer’s disease (AD), but usually it is not a primary feature of either its typical or atypical variants. In this report, we describe the case of an AD patient who showed an unusual and enduring neuropsychiatric phenotype characterized by early and prominent spontaneous confabulation. Surprisingly, such atypical AD presentation bears a striking resemblance to presbyophrenia, a subtype of dementia which was described at the beginning of the twentieth century and then sank into oblivion. In discussion, we speculate on the “return” of presbyophrenia as an unrecognized neuropsychiatric variant of AD and its possible neuroanatomical substrates.</p

    Peaks combination for the generation of models for blind samples.

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    <p>Models were constructed by Quick Classifier module of ClinProTools software by combining the peaks with the most robust statistics. For each combination, the name of the model, sensitivity, specificity and false negatives are shown.</p

    Protein signature in cerebrospinal fluid and serum of Alzheimer’s disease patients: The case of apolipoprotein A-1 proteoforms

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    <div><p>In the diagnosis of Alzheimer’s disease (AD) total tau (T-tau), tau phosphorylated at threonine 181 (P-tau181), and the 42 amino acid isoform of alpha β-amyloid (Aβ) are well established surrogate CSF markers. However, there is a constant need for new diagnostic markers to identify the disease at a very early stage. The identification of new molecules for AD diagnosis and monitoring in CSF is hampered by several “confounding” factors including intra- and inter-individual, pre-analytical and analytical variabilities. In an attempt to partially overcome patient’s variability and to determine new molecules significantly dysregulated in CSF, we assessed the proteome profile of low molecular weight protein species in CSF and serum of the same patients. CSFs and sera from 36 ADs, 32 iNPHs (idiopathic normal pressure hydrocephalus) and 12 controls were compared by MALDI profiling (non-parametric statistics, CV<20%, AUC>0.750). After protein identification by mass spectrometry, the proteoform composition was assessed by 2-D DIGE/MS. Results indicated that CSF of iNPH can be used as control. Serum and CSF of AD patients shows a specific protein profile compared to iNPH samples. A variation (p<0.01) of Apo A-1 levels in AD, together with a specific dysregulation of Apo A-1 proteoforms was observed. The profiling of CSF and serum of the same patients, suggests that the decrement of total Apo A-1 occurs specifically in CSF. Serum and CSF of AD shows a characteristic Apo A-1 proteoform pattern suggesting it as potential marker which can support the clinical workflow adopted for AD diagnosis and progression.</p></div

    Additional file 2: of Efficacy of ultra-micronized palmitoylethanolamide (um-PEA) in geriatric patients with chronic pain: study protocol for a series of N-of-1 randomized trials

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    CENT 2015 checklist*; CONSORT 2010 checklist items with modifications or additions for individual or series of N-of-1 trials; empty items in the CENT 2015 column indicate no modification from the CONSORT 2010 item. (DOCX 97.2 kb

    CSF MALDI profiling of AD <i>vs</i> iNPHs.

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    <p>Representative MALDI profiling spectrum of CSF from AD (average spectrum, red line) and iNPH patients (average spectrum, green line). Samples were spotted onto the AnchorChip target (Bruker Daltonics) using DHAP matrix as described in method section. The corresponding PCA plot showed a good separation between the considered classes (AD, red circles; iNPH, green circles).</p

    PCA score plot relating to healthy controls <i>vs</i> iNPHs comparison.

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    <p>PCA plot is based on the CSF profiling of healthy subjects (black circles) and iNPH patients (grey circles). The analysis, performed by using ClinProTools software showed the absence of clusterization of the two classes.</p
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