1,721,333 research outputs found
Going Beyond Counting First Authors in Author Co-citation Analysis
Full text linkThe present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation
counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings
are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that
only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into
account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
Mapping the onset and progression of atrophy in familial frontotemporal lobar degeneration
No full textBACKGROUND:
Frontotemporal lobar degeneration (FTLD) may be inherited as an autosomal dominant disease. Studying patients "at risk" for developing FTLD can provide insights into the earliest onset and evolution of the disease.
METHOD:
We carried out approximately annual clinical, MRI, and neuropsychological assessments on an asymptomatic 51 year old "at risk" family member from a family with FTLD associated with ubiquitin-positive and tau-negative inclusion bodies. We used non-linear (fluid) registration of serial MRI to determine areas undergoing significant regional atrophy at different stages of the disease.
RESULTS:
Over the first 26 months of the study, the patient remained asymptomatic, but subsequently developed progressive speech production difficulties, and latterly severe orofacial dyspraxia, dyscalculia, frontal executive impairment, and limb dyspraxia. Regional atrophy was present prior to the onset of symptoms, and was initially centred on the left dorsolateral prefrontal cortex and the left middle frontal gyrus. Latterly, there was increasing asymmetric left frontal and parietal atrophy. Imaging revealed excess and increasing global atrophy throughout the study. Neuropsychological evaluation revealed mild intellectual impairment prior to the onset of these clinical symptoms; frontal executive and left parietal impairment subsequently emerged, culminating in widespread cognitive impairment. Fluid registered MRI allowed the emerging atrophy patterns to be delineated.
CONCLUSION:
We have demonstrated the onset and progressive pattern of in vivo atrophy in familial FTLD using fluid registered MRI and correlated this with the clinical features. Fluid registered MRI may be a useful technique in assessing patterns of focal atrophy in vivo and demonstrating the progression of degenerative diseases
Survival in Alzheimer disease
No full textWe thank Dr Lesser for his comments. We agree that deaths in older populations with AD are often from comorbid conditions, and we would not wish to overinterpret the limited survival data from this study. We also accept that determining symptom onset is an inexact science. However, we would suggest that in this small cohort the disease course of about a decade cannot be considered an aggressive one. Since publication of our study, 2 additional subjects have died 8.9 and 16.8 years after onset thereby increasing the mean time from onset to death to 9.4 years. We agree, however, that further study is required to resolve these issues and in particular to assess genetic factors that may influence the rate of disease progression. Although findings in familial AD may not necessarily generalize to sporadic disease, the study of early-onset pedigrees affords the opportunity to assess progression with fewer confounds of comorbidity
A second family with familial AD and the V717L APP mutation has a later age of onset
No full textFour mutations have been reported at the 717 codon of the amyloid precursor protein (APP), with valine substituted by isoleucine, glycine, phenylalanine, and leucine. While several families with the isoleucine substitution have been described, the other substitutions have been reported in only one family each worldwide.
A family with the V717L APP mutation has been previously reported,1 with a mean age at onset of 38 years (range 35 to 39), based on four affected family members, and a mean age at death of 46 years (range 40 to 50). We have identified a second family with a later mean age at onset of 50 years (range 48 to 57) and mean age at death of 61 years (range 57 to 68)
Variations on the Author
Full text link“Variations on the Author” discusses two of Eduardo Coutinho’s recent films (Um Dia na Vida, from 2010, and Últimas Conversas, posthumously released in 2015) and their contribution to the general question of documentary authorship. The director’s filmography is characterized by a consistent yet self-effacing form of authorial self-inscription: Coutinho often features as an interviewer that rather than express opinions propels discourses; an interviewer that is good at listening. This mode of self-inscription characterizes him as an author who is not expressive but who is nonetheless markedly present on the screen. In Um Dia na Vida, however, Coutinho is completely absent form the image, while Últimas Conversas, on the contrary, includes a confessional prologue that moves the director from the margins to the center of his films. This article examines the ways in which these works stand out in the filmography of a director who offers new insights into the notion of cinematic authorship
A decade of prediagnostic assessment in a case of Familial Alzheimer's disease: tracking progression from asymptomatic to MCI and dementia
No full textLongitudinal and Cross-Sectional Analysis of Atrophy in Alzheimer’s: Cross-Validation of BSI, SIENA and SIENAX
No full textBrain volume loss (atrophy) is widely used as a marker of disease progression. Atrophy has been measured with a variety of methods, some estimating atrophy rate from two temporally separated scans, and others estimating atrophy state from a single scan. Three popular tools for measuring brain atrophy are BSI and SIENA (rate) and SIENAX (state). Previous papers have shown BSI and SIENA to have similar accuracy, but no work has carefully compared both methods using the same data set. Here we compare these methods, using data from patients with Alzheimer's disease and age-matched controls. We also compare the SIENA longitudinal measure with atrophy state estimated by SIENAX using just the earliest scan taken from each subject. We show strong correspondence and similar sensitivity to atrophy between all 3 measures
Tracking progression from pre-MCI to dementia: a decade of pre-diagnostic assessment in a case of Familial Alzheimer's disease
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