Prevention of Older Adult Infantilization by Nursing Home Professionals: An Intervention Program.

This study analyzes the efficacy of a brief psychoeducational program aimed at preventing older adult infantilization by nursing home professionals. We examined whether an experimental group of professionals reported less infantilization than those of a control group. Changes in stereotypes and humanization were regarded as sub-targets. The sample comprised 154 staff members. Infantilization, humanization, and negative stereotypes toward older adults were assessed before and after the intervention, and repeated measures of ANOVA and one-way ANCOVAs were conducted. Infantilization and negative stereotypes decreased in the experimental group. Significant post-intervention differences were found between the experimental and control groups both in infantilization and negative stereotypes but not in humanization. Results reflect the relevance of developing specific interventions focused on preventing infantilization as well as the need for professionals' training and education to generate a culture of change.

Silver and copper as pollution tracers in Neogene to Holocene estuarine sediments from southwestern Spain.

Estuaries are very sensitive ecosystems to human activities and the natural evolution of their drainage basins located upstream. Pollution derived from human activities, such as historical mining or recent industrial wastes, can significantly affect their environmental quality. This paper analyzes the silver and copper contents of four cores extracted in two estuaries of SW Spain. Its chronology and vertical evolution allow to differentiate the effects of several pollution episodes (natural, Roman, 19th-20th centuries) on its different sedimentary environments in the last 6 million years. Possible future applications are included in the fields of environmental management or even education.

Central vascular disease and exacerbated pathology in a mixed model of type 2 diabetes and Alzheimer's disease.

Aging remains the main risk factor to suffer Alzheimer's disease (AD), though epidemiological studies also support that type 2 diabetes (T2D) is a major contributor. In order to explore the close relationship between both pathologies we have developed an animal model presenting both AD and T2D, by crossing APP/PS1 mice (AD model) with db/db mice (T2D model). We traced metabolic and cognitive evolution before T2D or AD pathology is present (4 weeks of age), when T2D has debuted but no senile plaques are present (14 weeks of age) and when both pathologies are well established (26 weeks of age). APP/PS1xdb/db mice showed an age-dependent synergistic effect between T2D and AD. Significant brain atrophy and tau pathology were detected in the cortex by 14 weeks, that spread to the hippocampus by 26 weeks of age. Severe cognitive impairment was also detected as soon as at 14 weeks of age. Interestingly, in APP/PS1xdb/db mice we observed a shift in Aß soluble/insoluble levels, and whereas more toxic soluble species were favoured, senile plaques (SP) were reduced. An overall increase of microglia activation was observed in APP/PS1xdb/db mice. We also found exacerbated hemorrhagic burden in APP/PS1xdbd/db mice, suggesting that blood brain barrier alterations may be responsible for the early pathological features observed. Moreover, metabolic parameters can predict many of these alterations, supporting a role for T2D in AD pathology. This new model provides a relevant tool to further explore the relationship between T2D, AD and vascular implications, offering the possibility to assess therapeutic approaches, that by improving T2D metabolic control could delay or prevent AD pathology.

Rapid ß-amyloid deposition and cognitive impairment after cholinergic denervation in APP/PS1 mice.

Although extensive evidence supports the role of ß-amyloid (Aß) in Alzheimer disease (AD), the neurotoxic mechanisms underlying AD pathogenesis are not understood. On the other hand, neuronal loss is the pathologic feature that best correlates with cognitive impairment. We hypothesized that cholinergic neurodegeneration may lead to Aß deposition and tested this by inducing selective cholinergic lesions in APPswe/PS1dE9 mice with murine p75 saporin (mu p75-SAP). Intracerebroventricular lesions that removed approximately 50% of cholinergic innervation to the cortex and hippocampus were induced in animals with incipient (∼3 months) and marked (∼7 months of age) Aß deposition. Cranial windows were implanted, and Aß deposition was monitored in vivo using multiphoton microscopy. Deposition of Aß was increased as soon as 7 days after the lesion, and this effect was maintained up to 3 months later. Postmortem studies using immunohistochemistry with an anti-Aß antibody corroborated these findings in both cerebral cortex and hippocampus. Tau phosphorylation was also significantly increased after the lesions. Cholinergic denervation resulted in early memory impairment at 3 months of age that worsened with age (∼7 months); there was a synergistic effect between cholinergic denervation and the presence of APP/PS1 transgenes. Altogether, our data suggest that cholinergic denervation may trigger Aß deposition and synergistically contribute to cognitive impairment in AD patients.

Differential central pathology and cognitive impairment in pre-diabetic and diabetic mice.

Although age remains the main risk factor to suffer Alzheimer's disease (AD) and vascular dementia (VD), type 2 diabetes (T2D) has turned up as a relevant risk factor for dementia. However, the ultimate underlying mechanisms for this association remain unclear. In the present study we analyzed central nervous system (CNS) morphological and functional consequences of long-term insulin resistance and T2D in db/db mice (leptin receptor KO mice). We also included C57Bl6 mice fed with high fat diet (HFD) and a third group of C57Bl6 streptozotocin (STZ) treated mice. Db/db mice exhibited pathological characteristics that mimic both AD and VD, including age dependent cognitive deterioration, brain atrophy, increased spontaneous hemorrhages and tau phosphorylation, affecting the cortex preferentially. A similar profile was observed in STZ-induced diabetic mice. Moreover metabolic parameters, such as body weight, glucose and insulin levels are good predictors of many of these alterations in db/db mice. In addition, in HFD-induced hyperinsulinemia in C57Bl6 mice, we only observed mild CNS alterations, suggesting that central nervous system dysfunction is associated with well established T2D. Altogether our results suggest that T2D may promote many of the pathological and behavioral alterations observed in dementia, supporting that interventions devoted to control glucose homeostasis could improve dementia progress and prognosis.