Sentidos de viver com depressão na velhice / Meanings of living with depression in old age

Este artigo tem por objetivo analisar os sentidos atribuídos à vivência da depressão por idosos. Trata-se de campo, do tipo transversal e de abordagem qualitativa. Para a caracterização dos participantes foi utilizado um questionário sociodemográfico e para a coleta de dados foi utilizada a Entrevista Narrativa de Doença - McGill Illness Narrative Interview (MINI), entrevista semiestruturada, traduzida, adaptada e validada para o Brasil. Foram analisadas 8 narrativas segundo a metodologia Análise de Conteúdo (Bardin, 2011), e foram sistematizadas as seguintes categorias: (I) A depressão atrelada aos sentidos sociais, agrupando as narrativas que apontam o estigma deste adoecimento psíquico, sendo principalmente relacionando com a loucura; (II) Sentimentos vinculados a depressão e suas repercussões nos laços sociais, incluindo falas sobre a irritabilidade, desânimo e inibição, e necessidade do reconhecimento do outro em relação ao seu sofrimento; e (III) Depressão associada às perdas e lutos de uma vida, havendo correlação entre a depressão na velhice como um acúmulo sucessivas perdas familiares. Os sentidos atrelados a depressão na velhice identificada nessa pesquisa envolvem a dificuldade de nomeação desse sofrimento para além do diagnóstico psiquiátrico e ressalta a necessidade de elaboração de lutos e amparo subjetivo.(AU)

This article aims to analyze the meanings attributed by the elderly to the experience of depression. This is a field research, cross-sectional field study and with a qualitative approach. For the characterization of the participants, a sociodemographic questionnaire was used and for data collection, the Narrative Interview of Disease - McGill Illness Narrative Interview (MINI), semi-structured interview, translated, adapted and validated for Brazil was used. Eight narratives were analyzed according to the Content Analysis methodology (Bardin, 2011), and the following categories were systematized: (I) Depression linked to social senses, grouping the narratives that point out the stigma of this psychic illness, being mainly related to madness ; (II) Feelings linked to depression and their repercussions on social ties, including statements about irritability, discouragement and inhibition, and the need to recognize the other in relation to their suffering; and (III) Depression associated with the losses and mourning of a lifetime, with an association between depression in old age as an accumulation of successive family losses. The meanings linked to depression in old age identified in this research involve the difficulty of naming this suffering beyond the psychiatric diagnosis and emphasizes the need to elaborate grief and subjective support.(AU)

Aging faster: worry and rumination in late life are associated with greater brain age.

Older adults with anxiety have lower gray matter brain volume-a component of accelerated aging. We have previously validated a machine learning model to predict brain age, an estimate of an individual's age based on voxel-wise gray matter images. We investigated associations between brain age and anxiety, depression, stress, and emotion regulation. We recruited 78 participants (≥50 years) along a wide range of worry severity. We collected imaging data and computed voxel-wise gray matter images, which were input into an existing machine learning model to estimate brain age. We conducted a multivariable linear regression between brain age and age, sex, race, education, worry, anxiety, depression, rumination, neuroticism, stress, reappraisal, and suppression. We found that greater brain age was significantly associated with greater age, male sex, greater worry, greater rumination, and lower suppression. Male sex, worry, and rumination are associated with accelerated aging in late life and expressive suppression may have a protective effect. These results provide evidence for the transdiagnostic model of negative repetitive thoughts, which are associated with cognitive decline, amyloid, and tau.

Premature Aging Among Trauma Survivors-The Longitudinal Implications of Sleep Disruptions on Telomere Length and Cognitive Performance.

OBJECTIVES: Sleep is necessary for brain function as well as physical and cognitive processes. Sleep disruptions, common with aging, intensify among trauma survivors. Moreover, former prisoners-of-war (ex-POWs) often experience premature aging. This study investigates the longitudinal effects of sleep disruptions for ex-POWs in relation to cognitive performance and telomere length as well as between cognition and telomeres. METHOD: This study included Israeli veterans from the 1973 Yom Kippur War who participated in four assessments (1991, 2003, 2008, 2015): (a) ex-POWs (n = 99), and (b) veterans who not were captured (controls) (n = 101). Among both groups, sleep disruptions were assessed using a self-report item in all four assessments. Cognitive performance was assessed using the Montreal Cognitive Assessment (MOCA) and telomere length was assessed via total white blood cells (leukocytes) from whole blood samples using Southern blot, both were measured only among ex-POWs in 2015. We conducted descriptive statistics, repeated measures, correlations, and path analyses. RESULTS: Sleep disruptions were related to lower cognitive performance but not to shorter telomeres. Moreover, cognitive performance and telomere length were found to be related when sleep disruptions were taken into consideration. CONCLUSION: Interpersonal trauma was shown to be a unique experience resulting in sleep disruptions over time, leading to cognitive impairment. These findings highlight the importance of viewing trauma survivors at high-risk for sleep disruptions. Therefore, it is imperative to inquire about sleep and diagnose cognitive disorders to help identify and treat premature aging.

Using Facebook to tell stories of premature ageing and sexual and reproductive healthcare across the life course for women with cerebral palsy in the UK and USA.

OBJECTIVE: To enhance understanding of the bodily and lifestyle effects of ageing with cerebral palsy (CP) for women, with a particular focus on experiences with sexual and reproductive healthcare (SRH) services in the UK and North America. DESIGN: A qualitative study underpinned by feminist disability theory and drawing on digital ethnographies to capture health and healthcare experiences for women with CP. SETTING: A global community of 140 women with CP, who are members of the closed international Facebook group, Women Ageing with Cerebral Palsy (WACP). PARTICIPANTS: Forty-five members of WACP who were based in the UK and North America. The women were aged between 21 and 75. METHODS: Messages posted on WACP between January 2018 and October 2018 were collated and underwent thematic analysis to identify themes relating to effects of ageing and experiences of SRH for women with CP at different points over the female life course. RESULTS: The breadth of experiences in relation to the effects of ageing and access to reproductive and sexual healthcare for women with CP can be divided into three themes: (1) bodily effects of ageing; (2) lifestyle effects of ageing; (3) experiences of reproductive and sexual healthcare. CONCLUSIONS: Giving women with CP a platform to 'speak for themselves' in relation to effects of ageing and SRH provides health professionals with an informed knowledge base on which to draw. This might improve treatment for this growing adult patient community whose experiences have not received attention in health discourse or services. Including these experiences in public medical and social discourse can also bring a new knowledge to girls with CP about what ageing could mean for them so plans can be put in place for their future.

Subjective Cognitive Decline Among Sexual and Gender Minorities: Results from a U.S. Population-Based Sample.

The risk of dementia and mild cognitive impairment between older adults in same-sex relationships and those in opposite-sex relationships have been found to be statistically not different. However, studies examining subjective cognitive decline (SCD) among sexual and gender minority populations (SGM) are lacking. The primary objective was to determine if SGM report greater SCD compared to non-SGM populations in a U.S. population-based sample of non-institutionalized adults aged 45 and older. The secondary objective was to assess the association between gender and SCD. Cross-sectional data were obtained from the 2016 Behavioral Risk Factor Surveillance System (n = 36,734). There were 1,094 SGM adults in the sample. Descriptive statistics examined sociodemographic characteristics and their distribution by SCD and SGM status. Crude and multivariable logistic regression models were used to determine the association between SGM status, gender, and SCD. Adjusted models controlled for age, race/ethnicity, income, education, employment, marital status, depression, and diabetes. Statistically significant differences in SGM status and SCD existed by age, race/ethnicity, education, employment, marital status, and depression. Differences in SCD also existed by income and diabetes status. There was no statistically significant association between SGM status and SCD (OR: 0.88; 95% CI: 0.63-1.24). However, men had 64% higher odds (OR: 1.64; 95% CI: 1.44-1.88) of reporting SCD compared to women. Future studies examining the potential reasons for this null association, including resilience and/or premature aging are warranted. Future research assessing potential reasons for gender differences in SCD, whether physiological or environmental, is also needed.

Does education level protect us from rapid ageing? Sirtuin expression versus age and level of education.

PURPOSE: SIR proteins (silent information regulators, sirtuins, SIRT1 - SIRT7, SIR1 - SIR7) belong to NAD+-dependent deacetylases, enzymes taking part in a catalytic reaction of deacetylation, i.e. splitting the rest of acetic acid from protein substrates. Sirtuins play an important role in many cellular processes and are, therefore, involved in the ageing process and in the regulation of cell life. The aim of this paper is to verify the statistical hypothesis assuming the correlation between the age and level of education of examined persons and the expression of selected sirtuins (SIR1 - SIR7, SIRT1 - SIRT7) at the mRNA level in the Polish population. MATERIAL AND METHODS: 197 people, aged M = 38.27 (SD = 13.19), in whom expression at the level of mRNA for SIR1 - SIR7 was determined, took part in the study (99 healthy people with a negative history of mental and somatic diseases and 98 people with diagnosed recurrent depressive disorders). RESULTS: A significant correlation was found in the case of age of the examined individuals and the expression of SIR1 - SIR7 at the mRNA level (p < 0.001). Differences in the expression of SIR1 - SIR7 were also found in relation to the level of education (number of years of education) of the examined population (p < 0.001). CONCLUSIONS: 1. The higher the number of years of education, the higher the level of SIR1 and SIR6 expression, and the lower the level of SIR2, SIR3, SIR4, SIR5 and SIR7 expression. 2. With age, the level of SIR1 and SIR6 expression decreases and the expression of SIR2, SIR3, SIR4, SIR5 and SIR7 increases.

Accelerated aging in serious mental disorders.

PURPOSE OF REVIEW: Clinical, epidemiological, and biological evidence raises the possibility that serious mental disorders (SMDs) are associated with accelerated biological aging. To the extent this is true; SMDs should not simply be considered in terms of mental illness or brain dysfunction, but also as 'whole body' and multisystem illnesses, or else as conditions with significant somatic concomitants. RECENT FINDINGS: The concept of accelerated biological aging in SMDs is supported by reports of accelerated changes in certain biomarkers normally associated with the aging process. SUMMARY: We define and discuss several proposed biological aging markers that have been examined in SMDs, we review the most recent findings, and we conclude with opinions regarding the merits and meanings of these markers, their usefulness in understanding and treating SMDs, and remaining questions and future directions in this area of research.

Marriage and Gut (Microbiome) Feelings: Tracing Novel Dyadic Pathways to Accelerated Aging.

Within a couple, partners influence each other's mental and physical health. This review focuses on how couples' relationships, the partners' individual and joint vulnerabilities, and their health behaviors influence health through changes in the gut microbiota, metabolism, and immune function. Couples' shared stressors and emotions and their intertwined lifestyles and routines serve to promote common disease risks in part through parallel changes in their gut microbiotas. Marital discord, stress, and depression have strong bidirectional links, fueling one another. Chronic marital stress and depression can elevate the risk for obesity, metabolic syndrome, and cardiovascular disease by altering resting energy expenditure, insulin production, and triglyceride responses after unhealthy meals. During stressful times, health behaviors typically suffer-and sleep disturbances, poor diets, and sedentary behavior all influence these metabolic pathways while also promoting gut dysbiosis. Dysbiosis increases intestinal permeability (gut leakiness), providing a mechanistic pathway from marital distress and depression to heightened inflammation and accelerated aging. Age-related changes in the gut microbiota's composition and gut leakiness foster immunosenescence, as well as the progression of inflamm-aging; these age-related risks may be altered by stress and depression, diet, sleep, exercise habits, and developmental shifts in emotion regulation strategies. Consideration of the strong mutual influences that partners have on each other's mood and health behaviors, as well as the biological pathways that underlie these influences, provides a new way to view marriage's health implications.

Social environment improves immune function and redox state in several organs from prematurely aging female mice and increases their lifespan.

Aging is associated with a chronic oxidative stress (increase of oxidants and decrease of antioxidants), which contributes to immunosenescence and therefore shorter longevity. Nevertheless, a positive social network has been related to the adequate maintenance of health and deceleration of aging. Adult prematurely aging mice (PAM) are characterized by their inadequate stress response to a T-maze, showing premature immunosenescence and oxidative stress establishment. These impairments contribute to shorter life spans in comparison to exceptional non-PAM (ENPAM). However, it is not known whether these characteristics of PAM could be prevented by a positive cohabitation. Therefore, the aim of the present work was to determine if the premature immunosenescence and oxidative stress shown by PAM could be avoided by the cohabitation with ENPAM, increasing their life span. Female CD1 PAM and ENPAM were divided into three experimental groups: PAM controls, ENPAM controls and a social environment experimental group, containing in the same cage ENPAM and PAM (proportion 5/2, respectively). After 2 months, mice were sacrificed and spleen, thymus, liver and heart removed. Later, several immune functions as well as oxidative stress parameters were assessed in spleen and thymus leukocytes. Also, several oxidative stress parameters were analyzed in liver and heart. The results showed that PAM, after co-housing with ENPAM, had improved immune functions and redox balance in spleen and thymus leukocytes. This improvement of redox state was also observed in liver and heart. Furthermore, all these positive effects seem to be related to the increased life span of PAM.

Frailty Quantified by the "Valencia Score" as a Potential Predictor of Lifespan in Mice.

The development of frailty scores suitable for mice and which resemble those used in the clinical scenario is of great importance to understand human frailty. The aim of the study was to determine an individual frailty score for each mouse at different ages and analyze the association between the frailty score and its lifespan. For this purpose, the "Valencia Score" for frailty was used. Thus, a longitudinal study in mice was performed analyzing weight loss, running time and speed, grip strength and motor coordination at the late-adult, mature and old ages (40, 56 and 80 weeks old, respectively). These parameters are equivalent to unintentional weight loss, poor endurance, slowness, weakness, and low activity level, respectively, in humans. A cut-off point was used to identify frail mice for each criterion. All the measurements were also performed on chronologically adult prematurely aging mice. The results show that by using the "Valencia Score" for frailty a prematurely aged phenotype can be identified even during the adulthood of animals. This opens up the possibility of carrying out preventive long-term interventions. Moreover, the individual frailty score of a given mouse at the late-adult, mature and old ages is shown to be a relevant predictor of its lifespan.

Sexual Dimorphism in the Behavioral Responses and the Immunoendocrine Status in d-Galactose-Induced Aging.

For almost 20 years, chronic systemic d-galactose, a monosaccharide abundantly present in milk products, fruits, and vegetables, has been used as a tool to achieve models of accelerated aging. Its neurotoxicity, induced by abnormal accumulation of reactive oxygen species and advanced glycation end products, has been widely reported. However, behavioral outcomes are still controversial and little is known about sex-dependent vulnerability. We performed a comprehensive behavioral and multifunctional screening of the chronic effects of low (50 mg/kg) and high (100 mg/kg) doses of d-galactose in 6-month-old male and female gold-standard C57BL/6 mice. Twelve classical tests with convergent validity analyzed sensorimotor, emotional and cognitive domains, indicating the existence of thresholds of response. Distinct vulnerability patterns were found in a selective sex- and dose-dependent manner. In males, d-galactose induced sensorimotor impairment and immunoendocrine senescence, but the low dose resulted in improved learning and memory. Oppositely, d-galactose-treated females exhibited a dose-dependent worse motor and spatial learning, but improved memory. Behavioral outcome items point at distinct neuronal substrates underlying the functional capacity of d-galactose-treated animals to meet task-dependent performance demands. They support that males and females can be regarded as two exceptional natural scenarios to study the functional interplay in the cross talk of homeostatic networks in aging.

Chronic corticosterone-induced depression mediates premature aging in rats.

BACKGROUND: Stress hormones such as corticosterone (CORT) play an essential role in the development of depression. Chronic CORT administration has been shown to induce dysfunction in the hypothalamic-pituitary-adrenal axis leading to depression, which was in turn associated with accelerated aging. However, the effect of CORT administration on aging remains unclear. METHODS: Rats were acclimatized for 1 week and then injected daily with CORT (40mg/kg) or vehicle (n = 10 each) for 21 consecutive days. Age-related indexes were then compared between CORT-treated rats and control rats. RESULTS: CORT induced affective behaviors indicative of depressive-like symptoms in rats, including reduced sucrose preference and increased immobility time in the forced swimming test. CORT-treated rats exhibited telomere shortening, possibly contributing to decreased telomerase activity and down-regulated expression of telomere-binding factor 2, correlated with enhanced oxidative damage. This was associated with inhibition of sirtuin 3 leading to reduced activities of superoxide dismutase 2 and glutathione reductase. CORT-treated rats showed degenerated mitochondrial functions represented by decreased adenosine triphosphate production, decreased nicotinamide adenine dinucleotide+ content, and decreased activity of nicotinamide phosphoribosyltransferase. LIMITATIONS: The group sample sizes were small, and only male rats and a single dose level of CORT were used. CONCLUSION: These findings demonstrate that CORT-induced depression may be involved in mediating the pathophysiology of premature aging in rats.

A prospective analysis of the role of cognition in three models of aging and schizophrenia.

OBJECTIVES: This study uses longitudinal data from a sample of older adults with schizophrenia spectrum disorder (OAS) to examine the role of cognition in 3 models of aging and schizophrenia-accelerated aging, paradoxical aging, and heterogeneity of course-and their clinical relevance. METHODS: The sample consisted of 103 community-dwelling persons aged 55 and over (mean=61years) with early-onset schizophrenia. Mean follow-up was 52.5months (range: 12-116months); 55% were men; 55% were white. We identified 21 potential predictor variables and used the Dementia Rating Scale (DRS) to assess cognition. RESULTS: There were no significant differences in the DRS at baseline (T1) and follow-up (T2). However, 20%, 22% and 58% of persons exhibited >0.5 effect size increase or decrease, or no change in their DRS scores, respectively; 19% were rapid decliners (>-2.11pts/year) and 19% were rapid improvers (>+2.11pts/year). In multivariable analysis, there were 3 predictors of higher DRS (T2): DRS (T1), decline in anxiety score, and race (white). CONCLUSIONS: The heterogeneity model best characterized the trajectory of cognition in later life. The accelerated aging model did not represent typical cognitive trajectories since most individuals were stable or improved. The heterogeneous trajectories made it difficult to generalize about cognition's role in the paradoxical aging model. Despite the paucity of predictors, our findings suggested that it may be clinically productive to enlist remediation strategies that target anxiety and cognition, and direct more attention to non-white OAS.

Cognitive and functional deficits in people with schizophrenia: Evidence for accelerated or exaggerated aging?

Cognitive and functional deficits are commonly seen in people with schizophrenia. The profile of these impairments has a resemblance to the cognitive changes seen in healthy aging. In specific, many of the cognitive ability domains that change the most with aging in healthy people are the most salient of these deficits seen in people with schizophrenia, including prominent deficits in processing speed, working memory, and episodic memory. Functional deficits seen in schizophrenia are also similar to those seen in healthy aging. There is a relationship between multiple psychotic relapses and treatment resistance and longitudinal cognitive and functional changes in schizophrenia, with this relationship starting early in the course of illness. Cognitive performance in people with schizophrenia may be consistent with accelerated or premature aging. People with schizophrenia perform similarly to healthy people who are 3 or more decades older on indices of both cognition and their everyday functional skills. Some people with schizophrenia show exaggerated cognitive changes as well. Cognitive and functional performance worsens at the outset of the illness in schizophrenia compared to premorbid functioning, meaning that these deficits are not due to development disabilities. There are multiple medical and substance abuse comorbidities in schizophrenia and although these comorbidities affect cognitive functioning, they are not completely responsible for age-related changes.

Traumatic Stress and Accelerated Cellular Aging: From Epigenetics to Cardiometabolic Disease.

PURPOSE OF REVIEW: The aim of this paper is to review the recent literature on traumatic stress-related accelerated aging, including a focus on cellular mechanisms and biomarkers of cellular aging and on the clinical manifestations of accelerated biological aging. RECENT FINDINGS: Multiple lines of research converge to suggest that PTSD is associated with accelerated aging in the epigenome, and the immune and inflammation systems, and this may be reflected in premature onset of cardiometabolic and cardiovascular disease. The current state of research paves the way for future work focused on identifying the peripheral and central biological mechanisms linking traumatic stress to accelerated biological aging and medical morbidity, with an emphasis on processes involved in inflammation, immune functioning, oxidative stress, autonomic arousal, and stress response. Ultimately, such work could help reduce the pace of biological aging and improve health and wellness.

[Complex estimation of the state of health, quality of life, level of psychological adaptation and rates of senescence of war veterans, suffering from arterial hypertension].

The article presents some aspects of the health status of the veterans of the Samara region. Intercommunication is marked between the level of social adaptation, quality of life and rate aging combatants. The study shows the effect of chronic posttraumatic stress disorder on the occurrence of psychosomatic pathology and development of senescence combat veterans suffering from arterial hypertension.

Senescence-accelerated OXYS rats: a model of age-related cognitive decline with relevance to abnormalities in Alzheimer disease.

Senescence-accelerated OXYS rats are an experimental model of accelerated aging that was established from Wistar stock via selection for susceptibility to cataractogenic effects of a galactose-rich diet and via subsequent inbreeding of highly susceptible rats. Currently, we have the 102nd generation of OXYS rats with spontaneously developing cataract and accelerated senescence syndrome, which means early development of a phenotype similar to human geriatric disorders, including accelerated brain aging. In recent years, our group found strong evidence that OXYS rats are a promising model for studies of the mechanisms of brain aging and neurodegenerative processes similar to those seen in Alzheimer disease (AD). The manifestation of behavioral alterations and learning and memory deficits develop since the fourth week of age, i.e., simultaneously with first signs of neurodegeneration detectable on magnetic resonance imaging and under a light microscope. In addition, impaired long-term potentiation has been demonstrated in OXYS rats by the age of 3 months. With age, neurodegenerative changes in the brain of OXYS rats become amplified. We have shown that this deterioration happens against the background of overproduction of amyloid precursor protein (AßPP), accumulation of ß-amyloid (Aß), and hyperphosphorylation of the tau protein in the hippocampus and cortex. The development of AMD-like retinopathy in OXYS rats is also accompanied by increased accumulation of Aß in the retina. These published data suggest that the OXYS strain may serve as a spontaneous rat model of AD-like pathology and could help to decipher the pathogenesis of AD.

Comparison of behavioral and biochemical deficits in rats with hereditary defined or D-galactose-induced accelerated senescence: evaluating the protective effects of diosgenin.

One of the important factors in aging is oxidative stress and aging-related disturbances are believed be ameliorated by antioxidants. Diosgenin is a bio-active ingredient of dioscorea that is widely used in Chinese medicine, shows anti-oxidant activity and improves some aging-related deficits in senescent and menopausal animals. We compared alterations in behavior, biochemical parameters (plasma levels of the uric acid, creatinine, calcium, phosphate, total cholesterol, low-density lipoprotein cholesterol and triglycerides, and the plasma activity of aminotransferases AST and ALT), and sperm motility in two models of accelerated senescence (d-galactose-induced (150 mg/kg/day, i.p., 57 days) aging in Wistar rats vs. genetically defined in OXYS rats) and examined the protective effects of diosgenin (10 or 50mg/kg/day, p.o., 57 days). Both models had augmented levels of ALT activity indicating hepatopathology. Compared to d-galactose-treated animals, OXYS rats demonstrated profound biochemical alterations (hypocalcemia, hypophosphatemia, and hypocholesterolemia) and behavioral deficits (impaired object recognition, decreased sexual motivation and locomotor activity, retarded learning) that confirmed the difference in the mechanisms of accelerated senescence in these models. We first showed diminished sperm motility in males of both models of accelerated senescence studied. Chronic diosgenin treatment failed to improve biochemical and behavioral disturbances and had some undesirable side effects on body weight and working memory in OXYS rats. However, diosgenin restored moderately decreased sperm motility in d-galactose-treated Wistar males and might be recommended for treatment of mild age-related reproductive dysfunctions.

ß-Asarone prevents autophagy and synaptic loss by reducing ROCK expression in asenescence-accelerated prone 8 mice.

ß-Asarone is an active component of the Acori graminei rhizome that is a traditional Chinese medicine clinically used in treating dementia in China. However, the cognitive effect of ß-asarone and its mechanism has remained elusive. Here, we used asenescence-accelerated prone 8 (SAMP8) mice, which mimic many of the salient features of Alzheimer׳s disease (AD), to further investigate whether modulation of the ROCK signaling pathway and/or autophagy, synaptic loss is involved in the effects of ß-asarone on learning and memory. SAMP8 mice at the age of 6 months were intragastrically administered by ß-asarone or a vehicle daily for 2 months. Senescence-accelerated-resistant (SAMR1) mice were used as the control. Our results demonstrate that autophagy and ROCK expression were increased significantly in 8 months SAMP8 mice, which were concomitant with that SAMP8 mice at the same age displayed a significant synaptic loss and cognitive deficits. The up-regulation of ROCK expression and autophage in the hippocampus of SAMP8 were significantly reduced by ß-asarone, and prevents synaptic loss and improved cognitive function of the SAMP8 mice. ß-asarone decreased neuronophagia and lipofuscin in the hippocampus of SAMP8 mice, but did not reduce Aß42 levels and malondialdehyde levels and superoxide dismutase activities. Moreover, suppression of ROCK2 by siRNA significantly reduced the effects of ß-asarone on the autophage and synaptic proteins expression in PC12 cells damage induced by Aß1-40. Taken together, ß-asarone prevents autophagy and synaptic loss by reducing ROCK expression in SAMP8 mice.

Knowledge, attitude and beliefs of people in North India regarding blood donation.

BACKGROUND: To develop targeted interventions in the field of donor recruitment, an understanding of existing knowledge, attitudes and beliefs regarding blood donation is required. Recruiters should be aware of variability in different demographic strata when implementing interventions. MATERIAL AND METHODS: A self-administered questionnaire along with a face-to-face interview was conducted in 400 each of voluntary donors, replacement donors and non-donors to assess their knowledge, attitude and beliefs regarding blood donation and their motivations for giving blood. Data were analysed using ANOVA and the c2 test. RESULTS: The most common reason given by non-donors (40.75%) for not donating blood was "no one asked them to give blood". Voluntary donors had a more pleasant blood donation experience compared to replacement donors and, therefore, more of them were willing to donate again (89.5%). The knowledge scores of non-donors were lower than those of donors and, among the latter, voluntary donors had better scores compared to replacement donors. Expectedly, the frequency of false beliefs was highest among non-donors (22.75%), with the most prevalent misbelief being that blood donation is associated with infertility. Television was found to be the most effective medium of communication for raising awareness about blood donation. CONCLUSION: It is recommended that extensive blood donation campaigning should be initiated, targeting the campaigns to eliminate specific misbeliefs and reinforce motivational perceptions. Blood centres should implement strategies to improve donor retention and should aim to provide a pleasant donation experience, regardless of the donor type. The idea of voluntary blood donation needs to be intensively promoted.