Vilket stöd behövde närstående från sjuksköterskor inom akutsjukvård och intensivvård vid anhörigs sjukdom och vilket stöd trodde sjuksköterskor att närstående hade behov av : En litteraturöversikt

Syfte: Att undersöka vilket stöd närstående haft behov av från sjuksköterskor inom akutsjukvård och intensivvård vid anhörigs sjukdom och vilket stöd sjuksköterskor trodde att närstående hade behov av. Metod: Studien genomfördes som en litteraturöversikt. Artiklar söktes i databaserna PubMed och Cinahl. I studiens resultat ingick 13 artiklar med både kvalitativ(n=7) och kvantitativ(n=6) ansats som sammanställdes under olika teman. Resultat: Redovisades i fyra teman; CCFNI, Information, Delaktighet och Bemötande. Närstående och sjuksköterskor ansåg att de mest centrala behoven innefattade information, delaktighet och bemötande. Att få rak och ärlig information och att närstående var delaktiga samt att de blev bemötta med respekt och empati visade sig vara det viktigaste från både närstående och sjuksköterskors perspektiv. Slutsats: Vid anhörigs sjukdom behöver närstående stöd framför allt i form av information, bra bemötande och att få känna sig delaktiga i vården av den anhörige. Denna uppfattning delas av sjuksköterskor inom akutsjukvård och intensivvård. Som sjuksköterska bör man tänka på att ge rak och ärlig information, låta närstående vara delaktiga i den mån de själva vill samt att alltid ge så bra bemötande som möjligt.

Sjuksköterskor verksamma inom den somatiska sjukvårdens upplevelser av att vårda patienter med psykisk sjukdom

Syfte: Var att beskriva sjuksköterskors upplevelser av att vårda patienter med psykisk sjukdom inom den somatiska sjukvården.Design: Studien genomfördes som en litteraturstudie.Metod: Litteratur som publicerats mellan 2003-2013 söktes i databaser PubMed CINAHL, PsykInfo, PsykArticles och ERIC. Tolv vetenskapliga artiklar utgjorde grunden för resultatet, dessa artiklar blev kvalitetsgranskade innan de användes.Resultat: Sjuksköterskor kände rädsla, oförutsägbarhet, osäkerhet samt frustation och hopplöshet i vården av psykiskt sjuka patienter då de saknade kunskap. Bristen av kunskap upplevdes som det största hindret i vården av denna patientgrupp. De upplevde osäkerhet till en följd av egna värderingar och fördomar till dessa patienter, vilket ledde till att sjuksköterskor undvek denna patientgrupp. Sjuksköterskor beskrev avsaknad av handledning och samarbete med psykiatriska kliniker då denna patientgrupp vårdades på somatiska avdelningar.Slutsats: Med en utökad kunskap inom psykiatri kan sjuksköterskor få möjlighet att minimera fördomar och rädsla i mötet med psykiskt sjuka patienter.

Unga reumatikers upplevelser av sin sjukdom : En kvalitativ intervjustudie av unga kvinnor och män med reumatism

Syftet med den här studien är att få en inblick i hur unga kvinnor och män med reumatismupplever sin sjukdom. Vi vill jämföra dessa upplevelser mellan män och kvinnor genomatt undersöka om det finns skillnader och likheter i återgivna beskrivningar ochupplevelser. Vi vill undersöka om könsspecifika skillnader på upplevelser kringreumatism skulle kunna kopplas till det faktum att fler kvinnor än män diagnostiseras.Vidare vill vi undersöka om samhällets bemötande av individer med reumatism kankopplas till att fler kvinnor än män diagnostiseras. För att finna svar på studiensfrågeställningar har sex stycken personer med en reumatisk diagnos eller reumatiskabesvär intervjuats. Studiens resultat visar på att upplevelserna kring reumatism skiljer sigmer mellan könen än inom dem. Männen tycks inte identifiera sig som sjuka i sammautsträckning som kvinnorna och kvinnorna verkar ha upplevt större motstånd frånsjukvården. Resultatet visar dessutom att männen har större benägenhet att dölja sindiagnos från sin omgivning medan kvinnorna ställer sig mer positiva till att prata om den.

Graph analysis of verbal fluency test discriminate between patients with Alzheimer’s disease, Mild Cognitive Impairment and normal elderly controls

Verbal fluency is the ability to produce a satisfying sequence of spoken words during a given time interval. The core of verbal fluency lies in the capacity to manage the executive aspects of language. The standard scores of the semantic verbal fluency test are broadly used in the neuropsychological assessment of the elderly, and different analytical methods are likely to extract even more information from the data generated in this test. Graph theory, a mathematical approach to analyze relations between items, represents a promising tool to understand a variety of neuropsychological states. This study reports a graph analysis of data generated by the semantic verbal fluency test by cognitively healthy elderly (NC), patients with Mild Cognitive Impairment – subtypes amnestic(aMCI) and amnestic multiple domain (a+mdMCI) - and patients with Alzheimer’s disease (AD). Sequences of words were represented as a speech graph in which every word corresponded to a node and temporal links between words were represented by directed edges. To characterize the structure of the data we calculated 13 speech graph attributes (SGAs). The individuals were compared when divided in three (NC – MCI – AD) and four (NC – aMCI – a+mdMCI – AD) groups. When the three groups were compared, significant differences were found in the standard measure of correct words produced, and three SGA: diameter, average shortest path, and network density. SGA sorted the elderly groups with good specificity and sensitivity. When the four groups were compared, the groups differed significantly in network density, except between the two MCI subtypes and NC and aMCI. The diameter of the network and the average shortest path were significantly different between the NC and AD, and between aMCI and AD. SGA sorted the elderly in their groups with good specificity and sensitivity, performing better than the standard score of the task. These findings provide support for a new methodological frame to assess the strength of semantic memory through the verbal fluency task, with potential to amplify the predictive power of this test. Graph analysis is likely to become clinically relevant in neurology and psychiatry, and may be particularly useful for the differential diagnosis of the elderly.

Cortical correlates of affective syndrome in dementia due to Alzheimer’s disease

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Sulforaphane as a multifunctional neuroprotective molecule to prevent and slow down the progression of Alzheimer’s disease

Oxidative stress has been implicated in the pathogenesis of a number of diseases including neurodegenerative disorders, cancer, ischemia, etc. Alzheimer’s disease (AD) is histopathologically characterized by the presence of extracellular senile plaque (SP), predominantly consisting of fibrillar amyloid-peptide (Aβ), intracellular neurofibrillary tangles (NFTs), composed of hyperphosphorylated tau protein, and cell loss in the selected regions of the brain. However, the pathogenesis of AD remains largely unknown, but a number of hypothesis were proposed for AD mechanisms, which include: the amyloid cascade, excitotoxicity, oxidative stress and inflammation hypothesis, and all of them are based, to some extent on the role of A. Accumulated evidence indicates that the increased levels of ROS may act as important mediators of synaptic loss and eventually promote formation of neurofibrillary tangles and senile plaques. Therefore a vicious circle between ROS and Aaccumulation may accelerate progression of AD. For these reasons, growing attention has focused on oxidative mechanism of Atoxicity as well as the search for novel neuroprotective agents. A strategy to prevent the oxidative stress in neurons may be the use of chemopreventive agents as inducers of antioxidant and phase 2 enzymes. Sulforaphane (SF), derived from corresponding glucoraphanin, glucosinolate found in abundance in cruciferous vegetables, has recently gained attention as a potential neuroprotective compound inducer of antioxidant phase 2 enzymes. Consistent with this evidence, the study is aimed at identifying the SF ability to prevent and counteract the oxidative damage inducted by oligomers of Aβ (1-42) in terms of impairment in the intracellular redox state and cellular death in differentiated human neuroblastoma and microglia primary cultures. In addition we will evaluated the mechanism underlying the SF neuroprotection activity.

Human herpes virus and Alzheimer’s disease

Alzheimer’s disease (AD) is a chronic and progressive neurodegenerative disorder and according to the WHO it is estimated that 36 millions of people worldwide currently suffer from AD. Genetic and environmental factors interact in a complex interplay that might affect pathogenic mechanisms leading to age-related neurodegeneration. The hypothesis is that the presence of allelic polymorphisms in selected genes affecting individual brain susceptibility to infection by the herpes virus family during aging, may contribute to neuronal loss, inflammation and amyloid deposition. Herpes virus family show features relevant to AD, since they infect a large proportion of human population, develop a latent form persisting for several years, are difficult to eliminate by immune responses especially when latency has been established and are able to infect neurons. The association between AD and herpes viruses infection has been investigated. In particular the investigation focused on CMV, EBV and HHV-6 in DNA samples from peripheral blood of a large cohort of patients with clinical diagnosis of AD and age matched CTR, from a longitudinal population study, and DNA samples from brain tissue of patients with neuropathological diagnosis of definitive AD. An association between the presence of EBV and HHV-6 DNA from PBL positivity with the cognitive deterioration and progression to AD has been focused. Moreover, IgG plasma levels in CTR and AD to these viruses were tested. CMV and EBV IgG plasma levels were higher in elderly subjects that developed clinical AD at the end of the five year follow up. Our findings support the notion that persistent cycles of latency and reactivation of herpes viruses may contribute to impair systemic immune response and induce altered inflammatory process that in turn affect cognitive decline during aging.

Biomolecular studies in Alzheimer’s Disease models: investigations in vitro and in vivo

The Alzheimer’s disease (AD), the most prevalent form of age-related dementia, is a multifactorial and heterogeneous neurodegenerative disease. The molecular mechanisms underlying the pathogenesis of AD are yet largely unknown. However, the etiopathogenesis of AD likely resides in the interaction between genetic and environmental risk factors. Among the different factors that contribute to the pathogenesis of AD, amyloid-beta peptides and the genetic risk factor apoE4 are prominent on the basis of genetic evidence and experimental data. ApoE4 transgenic mice have deficits in spatial learning and memory associated with inflammation and brain atrophy. Evidences suggest that apoE4 is implicated in amyloid-beta accumulation, imbalance of cellular antioxidant system and in apoptotic phenomena. The mechanisms by which apoE4 interacts with other AD risk factors leading to an increased susceptibility to the dementia are still unknown. The aim of this research was to provide new insights into molecular mechanisms of AD neurodegeneration, investigating the effect of amyloid-beta peptides and apoE4 genotype on the modulation of genes and proteins differently involved in cellular processes related to aging and oxidative balance such as PIN1, SIRT1, PSEN1, BDNF, TRX1 and GRX1. In particular, we used human neuroblastoma cells exposed to amyloid-beta or apoE3 and apoE4 proteins at different time-points, and selected brain regions of human apoE3 and apoE4 targeted replacement mice, as in vitro and in vivo models, respectively. All genes and proteins studied in the present investigation are modulated by amyloid-beta and apoE4 in different ways, suggesting their involvement in the neurodegenerative mechanisms underlying the AD. Finally, these proteins might represent novel potential diagnostic and therapeutic targets in AD.

THE MOLECULAR INTERACTION BETWEEN TYPE II DIABETES AND ALZHEIMER’S DISEASE THROUGH CROSS-SEEDING OF PROTEIN MISFOLDING

With the population of the world aging, the prominence of diseases such as Type II Diabetes (T2D) and Alzheimer’s disease (AD) are on the rise. In addition, patients with T2D have an increased risk of developing AD compared to age-matched individuals, and the number of AD patients with T2D is higher than among aged-matched non-AD patients. AD is a chronic and progressive dementia characterized by amyloid-beta (Aβ) plaques, neurofibrillary tangles (NFTs), neuronal loss, brain inflammation, and cognitive impairment. T2D involves the dysfunctional use of pancreatic insulin by the body resulting in insulin resistance, hyperglycemia, hyperinsulinemia, pancreatic beta cell (β-cell) death, and other complications. T2D and AD are considered protein misfolding disorders (PMDs). PMDs are characterized by the presence of misfolded protein aggregates, such as in T2D pancreas (islet amyloid polypeptide - IAPP) and in AD brain (amyloid– Aβ) of affected individuals. The misfolding and accumulation of these proteins follows a seeding-nucleation model where misfolded soluble oligomers act as nuclei to propagate misfolding by recruiting other native proteins. Cross-seeding occurs when oligomers composed by one protein seed the aggregation of a different protein. Our hypothesis is that the pathological interactions between T2D and AD may in part occur through cross-seeding of protein misfolding. To test this hypothesis, we examined how each respective aggregate (Aβ or IAPP) affects the disparate disease pathology through in vitro and in vivo studies. Assaying Aβ aggregates influence on T2D pathology, IAPP+/+/APPSwe+/- double transgenic (DTg) mice exhibited exacerbated T2D-like pathology as seen in elevated hyperglycemia compared to controls; in addition, IAPP levels in the pancreas are highest compared to controls. Moreover, IAPP+/+/APPSwe+/- animals demonstrate abundant plaque formation and greater plaque density in cortical and hippocampal areas in comparison to controls. Indeed, IAPP+/+/APPSwe+/- exhibit a colocalization of both misfolded proteins in cerebral plaques suggesting IAPP may directly interact with Aβ and aggravate AD pathology. In conclusion, these studies suggest that cross-seeding between IAPP and Aβ may occur, and that these protein aggregates exacerbate and accelerate disease pathology, respectively. Further mechanistic studies are necessary to determine how these two proteins interact and aggravate both pancreatic and brain pathologies.