Publications by authors named "Krugers H"

Article Synopsis
  • Alzheimer's Disease is influenced by genetic, environmental, and lifestyle factors, including exercise, diet, education, and early life stress, which can affect its onset and progression.
  • Recent research has identified crucial biological processes, like stress hormones and neuroinflammation, that may link early life stress to an increased risk of developing Alzheimer's Disease.
  • Gaining insights into how early life experiences shape brain health could lead to new prevention and treatment strategies to counteract the impact of stress and reduce dementia risk.
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The ability to learn and remember, which is fundamental for behavioral adaptation, is susceptible to stressful experiences during the early postnatal period, such as abnormal levels of maternal care. The exact mechanisms underlying these effects still remain elusive. This study examined whether early life stress (ELS) alters memory and brain activation patterns in male mice.

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The early postnatal period is a sensitive time window that is characterized by several neurodevelopmental processes that define neuronal architecture and function later in life. Here, we examined in young adult mice, using an auditory fear conditioning paradigm, whether stress during the early postnatal period 1) impacts fear acquisition and memory consolidation in male and female mice; 2) alters the fear responsiveness to corticosterone and 3) whether effects of early-life stress (ELS) can be prevented by treating mice with a glucocorticoid (GR) antagonist at adolescence. Male and female mice were exposed to a limited nesting and bedding model of ELS from postnatal day (PND) 2-9 and injected i.

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Introduction: Early-life stress (ES) increases the risk for Alzheimer's disease (AD). We and others have shown that ES aggravates amyloid-beta (Aβ) pathology and promotes cognitive dysfunction in APP/PS1 mice, but underlying mechanisms remain unclear.

Methods: We studied how ES affects the hippocampal synaptic proteome in wild-type (WT) and APP/PS1 mice at early and late pathological stages, and validated hits using electron microscopy and immunofluorescence.

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Background: Exposure to stress early in life increases the susceptibility to Alzheimer's disease (AD) pathology in aged AD mouse models. So far, the underlying mechanisms have remained elusive.

Objective: To investigate 1) effects of early life stress (ELS) on early functional signs that precede the advanced neuropathological changes, and 2) correlate synaptosomal protein content with cognition to identify neural correlates of AD.

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Stress modulates the activity of various memory systems and can thereby guide behavioral interaction with the environment in an adaptive or maladaptive manner. At the cellular level, a large body of evidence indicates that (nor)adrenaline and glucocorticoid release induced by acute stress exposure affects synapse function and synaptic plasticity, which are critical substrates for learning and memory. Recent evidence suggests that memories are supported in the brain by sparsely distributed neurons within networks, termed engram cell ensembles.

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Early postnatal life is a sensitive period of development that shapes brain structure and function later in life. Exposure to stress during this critical time window can alter brain development and may enhance the susceptibility to psychopathology and neurodegenerative disorders later in life. The developmental effects of early life stress (ELS) on synaptic function are not fully understood, but could provide mechanistic insights into how ELS modifies later brain function and disease risk.

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Background: Successful aging is often linked to individual's ability to demonstrate resilience: the maintenance or quick recovery of functional ability, well-being, and quality of life despite losses or adversity. A crucial element of resilience is behavioral adaptability, which refers to the adaptive changes in behavior in accordance with internal or external demands. Age-related degradation of executive functions can, however, lead to volition problems that compromise flexible adjustment of behavior.

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Glucocorticoids are potent memory modulators that can modify behavior in an adaptive or maladaptive manner. Elevated glucocorticoid levels after learning promote memory consolidation at recent time points, but their effects on remote time points are not well established. Here we set out to assess whether corticosterone (CORT) given after learning modifies remote fear memory.

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The COVID-19 pandemic brought ageism to the forefront of public discourse. Negative ageism incurs more negative self-perceptions of aging, which affects physical and mental functioning. Whether negative ageism as perceived and experienced by older adults has worsened as the pandemic lingered, and how such changes impact quality of life (QoL) and mental well-being (MWB), remain urgent questions.

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Ageism as perceived by older individuals has been recognized as a potential risk factor for physical and mental health. We aimed to develop a comprehensive scale that can quantify perceived ageism among aging individuals (55+), including both positive and negative stereotypes, prejudices, and discriminations. This effort resulted in an 8-item Perceived Ageism Questionnaire (PAQ-8), with good psychometric properties and a two-factor structure distinguishing a positive (3 items) and negative (5 items) subscale (Analysis 1; = 500).

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While aging is an important risk factor for neurodegenerative disorders such as Alzheimer's disease and Parkinson's disease, age-related cognitive decline can also manifest without apparent neurodegenerative changes. In this review, we discuss molecular, cellular, and network changes that occur during normal aging in the absence of neurodegenerative disease. Emerging findings reveal that these changes include metabolic alterations, oxidative stress, DNA damage, inflammation, calcium dyshomeostasis, and several other hallmarks of age-related neural changes that do not act on their own, but are often interconnected and together may underlie age-related alterations in brain plasticity and cognitive function.

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Glucocorticoids regulate memory consolidation, facilitating long-term storage of relevant information to adequately respond to future stressors in similar conditions. This effect of glucocorticoids is well-established and is observed in multiple types of behaviour that depend on various brain regions. By and large, higher glucocorticoid levels strengthen event-related memory, while inhibition of glucocorticoid signalling impairs consolidation.

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Unlabelled: The impact of the COVID-19 pandemic on mental health, well-being, and behavior is likely influenced by individual characteristics that determine one's capacity for resilience. In this exploratory study, we examined whether individual differences in working memory (WM) capacity and habit propensity (HP), measured the outbreak, could predict variation in subsequent psychological coping efficacy (as operationalized by measures of depression, mental well-being, perceived stress, and loneliness) and behavioral adjustment (by evaluating compliance and self-reported automaticity of four COVID-19 guidelines) among Dutch older adults ( = 36) the pandemic (measured April 25 to May 6, 2020). While we found elevated levels of depression and emotional loneliness, overall mental well-being, and perceived stress were not affected by the pandemic.

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The differential impact of rural versus urban residence on mental health remains a controversial topic that requires more in-depth investigations. This calls for a valid and easy measure to assess the degree of urbanisation. The purpose of the present study was to determine the utility of a single-item self-report measure (SIDU) as a tool to classify areas along the rural-urban continuum.

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Age-related challenges and transitions can have considerable social, psychological, and physical consequences that may lead to significant changes in quality of life (QoL). As such, maintaining high levels of QoL in later life may crucially depend on the ability to demonstrate resilience (i.e.

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Background: Traumatic experiences, such as conditioned threat, are coded as enduring memories that are frequently subject to generalization, which is characterized by (re-) expression of fear in safe environments. However, the neurobiological mechanisms underlying threat generalization after a traumatic experience and the role of stress hormones in this process remain poorly understood.

Methods: We examined the influence of glucocorticoid hormones on the strength and specificity of conditioned fear memory at the level of sparsely distributed dentate gyrus (DG) engram cells in male mice.

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Emotionally arousing experiences are retained very well as seen in posttraumatic stress disorder (PTSD). Various lines of evidence indicate that reactivation of these memories renders them labile which offers a potential time-window for intervention. We tested in non-human primates whether ketamine, administered during fear memory reactivation, affected passive (inhibitory) avoidance learning.

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Stressful experiences evoke, among others, a rapid increase in brain (nor)epinephrine (NE) levels and a slower increase in glucocorticoid hormones (GCs) in the brain. Microglia are key regulators of neuronal function and contain receptors for NE and GCs. These brain cells may therefore potentially be involved in modulating stress effects on neuronal function and learning and memory.

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Recently, a petition was offered to the European Commission calling for an immediate ban on animal testing. Although a Europe-wide moratorium on the use of animals in science is not yet possible, there has been a push by the non-scientific community and politicians for a rapid transition to animal-free innovations. Although there are benefits for both animal welfare and researchers, advances on alternative methods have not progressed enough to be able to replace animal research in the foreseeable future.

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Glucocorticoid hormones are particularly potent with respect to enhancing memory formation. Notably, this occurs in close synergy with arousal (i.e.

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Exposure to stress during the early postnatal period (i.e., early life stress, ES) can impact brain physiology and modify individual variability in adult social behavior.

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Cognitive deficits and alterations in emotional behaviour are typical features of Alzheimer's disease (AD). Moreover, exposure to stress or adversity during the early life period has been associated with an acceleration of cognitive deficits and increased AD pathology in transgenic AD mouse models. Whether and how early life adversity affects fear memory in AD mice remains elusive.

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