ORCID Profile
0000-0002-7981-8176
Current Organisation
UNSW
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Publisher: Wiley
Date: 15-07-2019
DOI: 10.1002/GPS.5167
Abstract: Antipsychotic medications are commonly used to manage behavioural and psychological symptoms of dementia despite their side effects and harms. While the Halting Antipsychotic Use in Long-Term care (HALT) deprescribing trial was successful at reducing antipsychotic use, 19% of participants had their antipsychotics represcribed or never reached a dose of zero. The aim of this study was to investigate the reasons for represcription of antipsychotic medication and factors associated with ongoing antipsychotic use, relating to care staff requests and perceived behavioural changes. Thirty-nine of 133 HALT participants never ceased their antipsychotic medication or were represcribed a regular or pro re nata (PRN) antipsychotic after initial deprescribing. The views of nursing staff, general practitioner, and family on the circumstances leading up to these outcomes were collected via a questionnaire-based approach. This information was triangulated with observation and detailed file audit (including progress notes, medical notes, medication charts, incident reports, and hospital discharge summaries). A consensus panel reconstructed the represcribing context. Nurses were the most common drivers of represcribing (63.2%), followed by family members (39.5%), GPs (23.7%), specialists (13.2%), and hospital staff (10.5%). There were multiple drivers for antipsychotic use in 46.2% of participants. Increased agitated and aggressive behaviours were the most commonly reported reasons for represcribing even though these changes were not identified over time on objective measures. Consent and dosage practices remained poor despite education. Nursing staff are the key drivers of deprescribing particularly in response to perceived worsening agitation and aggression among male residents. The train-the-trainer model used in the HALT trial may have been insufficient on its own to improve staff competence and confidence in applying nonpharmacological approaches when responding to behaviour change.
Publisher: Elsevier BV
Date: 10-2017
DOI: 10.1016/J.JAMDA.2017.01.006
Abstract: The diagnosis of dementia and the management of its associated symptoms are aided by high-quality assessment tools. However, there is disagreement on the optimal tools among abundant alternatives and lack of consistent quality standards across the different domains of dementia-related change (ie, cognition, severity, function, behavioral and psychological symptoms, delirium, quality of life). Standardization is difficult because the relevance of a measurement tool for health professionals may depend on the clinical setting and on the dementia type and severity. To address this need, we conducted a comprehensive and clinically relevant evidence-based review of dementia-related tools and present a set of recommended tools, the Dementia Outcomes Measurement Suite. The review revealed that considerable development has occurred in terms of assessment of persons with mild cognitive impairment, executive dysfunction, cognitively mediated functional change, and apathy. More research is needed to develop and validate tools to assess health-related quality of life and specific symptoms of dementia including anxiety, wandering, and repetitive vocalizations. This extensive overview of the quality of different measures may serve as a guide for health professionals clinically and for researchers developing new or improved dementia assessment tools.
Publisher: Elsevier BV
Date: 07-2018
DOI: 10.1016/J.JAMDA.2018.05.002
Abstract: Despite limited efficacy and significant safety concerns, antipsychotic medications are frequently used to treat behavioral and psychological symptoms of dementia (BPSD) in long-term residential care. This study evaluates the sustained reduction of antipsychotic use for BPSD through a deprescribing intervention and education of health care professionals. Repeated-measures, longitudinal, single-arm study. Long-term residential care of older adults. Nursing staff from 23 nursing homes recruited 139 residents taking regular antipsychotic medication for ≥3 months, without primary psychotic illness, such as schizophrenia or bipolar disorder, or severe BPSD. An antipsychotic deprescribing protocol was established. Education of general practitioners, pharmacists, and residential care nurses focused on nonpharmacological prevention and management of BPSD. The primary outcome was antipsychotic use over 12-month follow-up secondary outcomes were BPSD (Neuropsychiatric Inventory, Cohen-Mansfield Agitation Inventory, and social withdrawal) and adverse outcomes (falls, hospitalizations, and cognitive decline). The number of older adults on regular antipsychotics over 12 months reduced by 81.7% (95% confidence interval: 72.4-89.0). Withdrawal was not accompanied by drug substitution or a significant increase in pro-re-nata antipsychotic or benzodiazepine administration. There was no change in BPSD or in adverse outcomes. In a selected s le of older adults living in long-term residential care, sustained reduction in regular antipsychotic use is feasible without an increase of BPSD.
Publisher: American Association for the Advancement of Science (AAAS)
Date: 11-04-2014
Abstract: Pathogenic mutations in the kinase PINK1 are causally related to Parkinson's disease (PD). One hypothesis proposes that PINK1 regulates mitophagy—the clearance of dysfunctional mitochondria. A second hypothesis suggests that PINK1 has a direct effect on mitochondrial complex I, affecting the maintenance of the electron transport chain (ETC) resulting in decreased mitochondrial membrane potential and dysfunctional mitochondria. In support of the second hypothesis, Morais et al. (p. 203 , published online 20 March) observed a complex I deficit in fibroblasts and neurons derived from induced pluripotent stem cells from PINK1 patients before any mitophagy was induced. The phosphoproteome of complex I in liver and brain from mice deficient for Pink1, compared to wild-type animals, revealed that Ser 250 in complex I subunit NdufA10 was differentially phosphorylated. Ser 250 is critically involved in the reduction of ubiquinone by complex I, explaining why Pink1 knockout mice, flies, and patient cell lines show decreased mitochondrial membrane potential. Synaptic defects in pink1 null mutant Drosophila could be rescued using phosphomimetic NdufA10.
Publisher: Portland Press Ltd.
Date: 04-2015
DOI: 10.1042/BST20150002
Abstract: PINK1 [phosphatase and tensin homologue (PTEN)-induced putative kinase 1] is a serine/threonine kinase targeted to mitochondria and implicated in early-onset recessive Parkinson's disease (PD). Through the phosphorylation of its downstream targets, PINK1 regulates multiple mitochondrial processes, including ATP production, stress-response and mitochondrial dynamics and quality control. The orchestration of such a wide array of functions by an in idual kinase requires a fine-tuned and versatile regulation of its activity. PINK1 proteolytic processing, trafficking and localization, as well as different post-translational modifications, affect its activity and function. Unravelling the regulatory mechanisms of PINK1 is essential for a full comprehension of its kinase function in health and disease.
Publisher: EMBO
Date: 12-09-2014
Publisher: Elsevier BV
Date: 06-2011
Publisher: Elsevier BV
Date: 2015
Publisher: Public Library of Science (PLoS)
Date: 19-01-2016
Location: United Kingdom of Great Britain and Northern Ireland
No related grants have been discovered for Liesbeth Aerts.