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En este trabajo desarrollamos un breve estudio sobre la función cuantil y su estimación según un determinado método en el caso de utilizar información auxiliar. Presentamos el método de estimación de la función cuantil que va acompañado de la estimación de la función de distribución. Consideradas dos características de esa población, definimos un estimador ratio simple de la función cuantil que nos va a servir para poder analizar la relación de proporcionalidad que pueda existir entre ambas, observando que cuanto mayor es esta relación más se aproxima el estimador ratio a la función cuantil de la población, coincidiendo ambas en el caso de que esta relación de proporcionalidad sea total. Se acompaña dicho estudio de una simulación realizada sobre una población donde hemos analizado las dos características.

Esta comunicaación pretende cuantificar en unidades monetarias el riesgo inherentes a las operaciones financieras aleatorias y logicamente, dicha cantidad estará referida al momento de su disponibilidad. Por lo tanto el análisis y valoración del riesgo, que clásicamente se hace a través de las desviaciones típicas, lo completamos mediante la valoración de dichas desviaciones mediante una ley finanicera; para ello utilizamos como función de distribución la función de desviación típica de los procesos estocásticos de prestación y contraprestación.

Objective Neuropsychiatric symptoms (NPS) are common clinical features of patients with Parkinson's disease (PD). However, such symptoms in non-demented PD patients have scarcely been investigated. To address this issue, we describe the neuropsychiatric profile in PD patients with and without Mild Cognitive Impairment (MCI). Participants and Method Eighty non-demented PD patients were included. The patients were divided into two groups depending on the presence or absence of MCI (PD-MCI and PD-nMCI, respectively). MCI diagnosis was made according to the Movement Disorder Society Task Force Level I criteria. NPS were evaluated using the Neuropsychiatric Inventory (NPI). For each domain, the presence and magnitude of symptoms (frequency x severity) was calculated. The total NPI score was also computed, in which higher scores suggest greater behavioral disturbance. Results PD-nMCI (n = 59, 74%) and PD-MCI (n = 21, 26%) groups were similar in the disease stage and years since diagnosis. In contrast with the PD-nMCI group, participants in the PD-MCI group were older. Fourteen PD-MCI (66%) and 45 PD-nMCI (76%) patients reported at least one neuropsychiatric symptom in the previous month. In both groups, the most frequent NPS were sleep disorders, depression, anxiety, apathy, irritability, and disinhibition. Additionally, the proportion of these symptoms between groups did not differ significantly (p > 0.05). There was only a tendency of greater score in the disinhibition subscale in PD-MCI group (p < 0.02). In both groups, NPS were not associated with clinical variables (years since diagnosis, Unified Parkinson's Disease Rating Scale -III) after adjusting for age. Conclusions Preliminary findings suggest that NPS are frequent in PD patients independent of the degree of cognitive impairment, and they may encompass non-motor features of the clinical spectrum of the disease. Further longitudinal investigations are needed to determine whether such symptoms may predict the cognitive decline in these patients. [ABSTRACT FROM AUTHOR]

Here, ERPs were employed to characterise the residual face processing of FE, a patient with extensive damage to the ventral temporal-occipital cortex and a dense prosopagnosia. Alarge N170 was present in FE and he performed well in tests of face structural processing. Covert recognition of the faces of personal acquaintances was demonstrated with P300 oddball experiments. The onset latency of the P300 effect was normal, indicating fast availability of covert memory. The scalp topography of this component in FE was different from that of the P3b, presenting a centro-frontal maximum. FE also presented larger skin conductance responses to familiar than to unfamiliar faces. The amplitudes of both the single-trial P300s and the SCRs triggered by familiar faces were positively correlated with the degree of person-familiarity that FE had for the poser. He performed at chance when asked to select between the face of a familiar person and that of an unfamiliar person on the basis of explicit recognition, whereas he selected more the previously known face if the forced choice was based on trustworthiness or a vague sense of familiarity. The results suggest that in FE, early face processing was relatively intact and covert recognition was fast. Neural structures involved in the processing of emotional or social cues possibly mediate the covert recognition present in FE. [ABSTRACT FROM AUTHOR]

Objective: The purpose of this research was to identify environmental and personal factors that could be related to the variability in the age of onset of familial Alzheimer's disease (FAD) (36-62 years).Methods: A sample was taken of 49 subjects with FAD and with the mutation E280A in the presenilin-1 gene on chromosome 14; the sample was divided into two subgroups: 27 individuals with age of onset of the disease between 36 and 46 years (early onset) and 22 individuals whose disease began between 47 and 62 years (late onset). Information on environmental and personal factors was collected by means of a questionnaire answered by the patients if their clinical condition allowed it, or by their relatives; such information was organized in a categorical way. Comparisons between the two groups for each categorical variable were done by means of the chi-square test. Noncollinear variables that showed statistical significance were included as independent variables in a logistic regression analysis to predict their association with early onset of the disease.Results: Only 5 of the 140 studied variables were different between the two groups in univariate analysis: education, surgical history, type of stressful event, depression, and affective losses. The logistic regression model was constituted by education, depression, and affective losses. High-level education had approximately 15 times more probability of association with an early onset of the disease; both the history of affective losses and depressive symptoms had 4 times more probability of a similar association.Conclusions: The association of high-level education and early onset of the disease could be related to an earlier detection of symptoms, in turn determined by greater intellectual and environmental demands. The occurrence of depression and affective losses has been considered a prodromic manifestation of the disease. Our findings are evidence of high clinical heterogeneity even in a genetically homogeneous group. [ABSTRACT FROM AUTHOR]

In Antioquia, Colombia, investigators have recently discovered the largest family with the E280A mutation in the presenilin 1 gene that causes one type of familial Alzheimer's disease (FAD). The current study compares two groups within this family: those diagnosed with Alzheimer's disease (AD) in its early stage (nine subjects) and relatives (carriers) who did not show any signs of dementia (nine subjects). A battery of the following neuropsychological tests was administered to subjects in both groups: the Consortium to Establish a Registry for Alzheimer's Disease (CERAD), a Phonological Verbal Fluency test, the Visual 'A' Cancellation Test, memory of three phrases, the Rey-Osterrieth Complex Figure, and the Trail Making Test Part A. Statistical analyses of the average test scores of each group showed that the AD group scored significantly (p < 0.01 or p < 0.05) lower on 29 of the 43 neuropsychological variables measured (67 percent). Therefore, this specific battery was useful in discriminating subjects with AD from their healthy relatives who are carriers of the disease. The AD group as a whole presented slight dementia with predominant deficits in memory, language, praxis, and attention. This profile is similar to those reported in subjects with sporadic AD in its early stage and confirms the findings found in other neuropsychological studies of subjects with FAD linked to mutations in chromosome 14. [ABSTRACT FROM AUTHOR]

Recent studies have shown that the missense mutation in presenilin-1 [E280A] increases deposition of amyloid-beta (Abeta) and neurofibrillary tangle (NFT) formation. Indeed, we only observed 10 out of 48 FAD brain sections displaying TUNEL (+) labeling, and none with the classical apoptotic morphology. These results may indicate that DNA fragmentation is not a generalized phenomenon in early-onset FAD PS1 [E280A] patients or that neuronal cells are dying by a different mechanism of cell death. Taking together these findings suggest that Abeta and NFTs are not per se a causative factor to damage neuronal cells but their damage could be more related with individual neuronal vulnerability and brain aging [ABSTRACT FROM AUTHOR]

Recent studies have shown that the missense mutation in presenilin-1 [E280A] increases deposition of amyloid-â (Aâ[1-42/43]) producing severe cerebellar pathology.  Although Aâ has been involved as a neurotoxic peptide, its role in neuronal loss in PS-1 [E280A] patients has not yet been established.  This study investigated terminal fluorescein 12-dUTP nick-end labeling (TUNEL)-positive cells (neuron, glia and microglial cells) and thioflavine S-stained Aâ-plaques and neurofibrillary tangles in the frontal, parietal, temporal, occipital, hippocampus and cerebellum cortices of 3 normal aging and 8 familial Alzheimer's disease patients with the presenilin-1 [E280A] mutation.  Using these approaches, we found no obvious correlation between DNA fragmentation and the severity of amyloid-â deposition (Aâ) and neurofibrillary tangle (NFT) formation.  Indeed, we only observed 10 out of 48 FAD brain sections displaying TUNEL (+) labeling, and none with the classical apoptotic morphology.  These results may indicate that DNA fragmentation is not a generalized phenomenon in early-onset FAD PS1 [E280A] patients or that neuronal cells are dying by a different mechanism of cell death.  Taking together these findings suggest that Aâ and NFTs are not per se a causative factor to damage neuronal cells but their damage could be more related with individual neuronal vulnerability and brain aging. [ABSTRACT FROM AUTHOR]