Journal articles on the topic 'Senile dementia Treatment New Zealand'
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Keim, Kevin L., and B�la Kiss. "New drug strategies in the treatment of senile dementia of different origin." Drug Development Research 14, no. 3-4 (1988): 181. http://dx.doi.org/10.1002/ddr.430140302.
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Schmidt, Joachim, Hans-Dieter Fischer, and Christian Wustmann. "Strategies and new aspects in the pharmacology of drugs for the treatment of senile dementia." Drug Development Research 14, no. 3-4 (1988): 251–62. http://dx.doi.org/10.1002/ddr.430140317.
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Fekete, Gy�rgy. "New drug strategies in the treatment of senile dementia of different origins: Satellite symposium of 2nd world congress of neuroscience." Drug Development Research 14, no. 3-4 (1988): 183–84. http://dx.doi.org/10.1002/ddr.430140303.
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Maiese, Kenneth, Zhao Zhong Chong, Jinling Hou, and Yan Chen Shang. "New Strategies for Alzheimer Disease and Cognitive Impairment." Oxidative Medicine and Cellular Longevity 2, no. 5 (2009): 279–89. http://dx.doi.org/10.4161/oxim.2.5.9990.
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Approximately five million people suffer with Alzheimer disease (AD) and more than twenty-four million people are diagnosed with AD, pre-senile dementia, and other disorders of cognitive loss worldwide. Furthermore, the annual cost per patient with AD can approach $200,000 with an annual population aggregate cost of $100 billion. Yet, complete therapeutic prevention or reversal of neurovascular injury during AD and cognitive loss is not achievable despite the current understanding of the cellular pathways that modulate nervous system injury during these disorders. As a result, identification of novel therapeutic targets for the treatment of neurovascular injury would be extremely beneficial to reduce or eliminate disability from diseases that lead to cognitive loss or impairment. Here we describe the capacity of intrinsic cellular mechanisms for the novel pathways of erythropoietin and forkhead transcription factors that may offer not only new strategies for disorders such as AD and cognitive loss, but also function as biomarkers for disease onset and progression.
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Shevtsova, E. F., D. V. Vinogradova, M. E. Neganova, P. N. Shevtsov, B. V. Lednev, and S. O. Bachurin. "Mitochondria are an Important Target in the Search for new Drugs for the Treatment of Alzheimer′s Disease and Senile Dementia." Biomedical Chemistry: Research and Methods 1, no. 3 (2018): e00058. http://dx.doi.org/10.18097/bmcrm00058.
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The review and summarizes own and literature data about the role of mitochondria as the important target in the search for drugs for the treatment of neurodegenerative diseases. Aging is a major risk factor for sporadic forms of various neurodegenerative diseases, including Alzheimer′s disease. One of the most argued and currently accepted theories is the Mitochondrial Free Radical Theory of Aging. Mitochondrial hypotheses of the development of sporadic forms of neurodegenerative diseases particularly Alzheimer′s disease, are closely connected with it. Impairments of mitochondrial functions lead to a decrease in their ability to regulate calcium homeostasis in the cell and to a decrease in the threshold for the induction of mitochondrial permeability transition (MPT) pores. MPT inhibitors can be considered as a promising approach to the treatment of neurodegenerative diseases, since these drugs can not only exhibit the properties of neuroprotectors, but also can provide normalization of synaptic activity due to increased calcium capacity of mitochondria. The review presents data on the number of MPT inhibitors, including endogenous compounds melatonin and N-acetylserotonin, their bioisosteric analogue Dimebon and a number of other compounds. The use of mitochondria as a basis for the formation of screening strategy for the search for compounds for the treatment of neurodegenerative diseases is of particular interest – both as a test of their potential toxicity, and as a basis for the creation of metabolic stimulants and drugs with neuroprotective and cognitive-stimulating effect.
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Pardo-Moreno, Teresa, Anabel González-Acedo, Antonio Rivas-Domínguez, Victoria García-Morales, Francisco Jose García-Cozar, Juan Jose Ramos-Rodríguez, and Lucía Melguizo-Rodríguez. "Therapeutic Approach to Alzheimer’s Disease: Current Treatments and New Perspectives." Pharmaceutics 14, no. 6 (May 24, 2022): 1117. http://dx.doi.org/10.3390/pharmaceutics14061117.
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Alzheimer’s disease (AD) is the most common cause of dementia. The pathophysiology of this disease is characterized by the accumulation of amyloid-β, leading to the formation of senile plaques, and by the intracellular presence of neurofibrillary tangles based on hyperphosphorylated tau protein. In the therapeutic approach to AD, we can identify three important fronts: the approved drugs currently available for the treatment of the disease, which include aducanumab, donepezil, galantamine, rivastigmine, memantine, and a combination of memantine and donepezil; therapies under investigation that work mainly on Aβ pathology and tau pathology, and which include γ-secretase inhibitors, β-secretase inhibitors, α-secretase modulators, aggregation inhibitors, metal interfering drugs, drugs that enhance Aβ clearance, inhibitors of tau protein hyperphosphorylation, tau protein aggregation inhibitors, and drugs that promote the clearance of tau, and finally, other alternative therapies designed to improve lifestyle, thus contributing to the prevention of the disease. Therefore, the aim of this review was to analyze and describe current treatments and possible future alternatives in the therapeutic approach to AD.
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Swakowska, Katarzyna, and Anna Staniszewska. "Alzheimer's disease: classification and diagnosis criteria." Journal of Education, Health and Sport 11, no. 7 (July 5, 2021): 22–29. http://dx.doi.org/10.12775/jehs.2021.11.07.002.
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In recent years, the intensity of population aging has increased and the incidence of senile diseases, including dementia, has significantly increased. With the aging of populations in Europe, knowledge about the detection and diagnosis of dementia has increased in the last decade. Due to the increase in the number of patients, new therapies and precise diagnostic criteria have been introduced, contributing to faster diagnosis of the disease. Alzheimer's disease (AD) is the biggest cause of dementia in old age. It is characterized by progressive cognitive deficits, especially memory, and disorders such as: apathy, agitation and psychotic symptoms. Alzhaimer's disease is a degenerative brain disease caused by the deposition of pathological B-amyloid protein tau and alpha-synuclein in the brain, causing atrophy of neurons and their connections. The basis for diagnosis of dementia in the course of Alzheimer's disease are ICD-10 or DSM-IV criteria. The clinical course and symptoms in the course of AD are defined by the Global Deterioration Scale (GDS), the scale also determines the stage of the disease. Acetylcholinesterase inhibitor drugs and memantine are used to treat the symptoms of Alzheimer's disease. Prompt diagnosis and treatment significantly delays the progression of the disease and helps to prolong normal functioning of the patient.
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Greve, Melissa, and Daniel O'Connor. "A survey of Australian and New Zealand old age psychiatrists' preferred medications to treat behavioral and psychological symptoms of dementia (BPSD)." International Psychogeriatrics 17, no. 2 (June 2005): 195–205. http://dx.doi.org/10.1017/s1041610205001481.
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Background: People with behavioral and psychological symptoms of dementia (BPSD) are often prescribed psychotropic medications. There is little evidence that one class of medication is more effective and safer than another and so expert opinion plays an important role in shaping local practice. In an earlier U.S. survey of psychiatrists and neurologists, limited consensus emerged regarding the pharmacological management of BPSD. We repeated this study to check consensus levels in Australia and New Zealand, following the introduction of newer atypical neuroleptics, antidepressants and cholinesterase inhibitors, and to identify areas where drug trials will be of greatest benefit.Methods: A brief structured survey, similar to one used in the U.S.A., was posted to a random sample of members of the Australian and New Zealand Faculty of Psychiatry of Old Age.Results: We received 106 replies (71% response). Respondents, who had 14 years' experience on average, rated atypical neuroleptics as their treatment of choice for dementia complicated by psychosis, verbal aggression, physical aggression, sundowning and persistent yelling. Opinions varied widely regarding the management of other symptoms and the role of second-line treatments.Conclusion: Atypical neuroleptics were preferred by most respondents for treatment of most BPSD. These views, while based on considerable clinical experience, have only limited backing from published reports, and head-to-head studies of available treatments are required to ensure that clinical practice has scientific support.
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Weiner, Michael, Susan Wells, and Ngaire Kerse. "Perspectives of general practitioners towards evaluation and treatment of cardiovascular diseases among older people." Journal of Primary Health Care 1, no. 3 (2009): 198. http://dx.doi.org/10.1071/hc09198.
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INTRODUCTION: Risk of cardiovascular disease (CVD) events increases with age. With treatment, individuals with highest risk accrue greater absolute risk reduction. New Zealands CVD guidelines provide no upper age limit for risk assessment. Guidance for treating those over 75 years is limited. Little is known about GPs attitudes regarding assessing and managing cardiovascular risk among older people. METHODS: A 39-item questionnaire including three cases representing various risk was developed and administered to 500 GPs randomly selected from a registry. RESULTS: Of the GPs, 379 were eligible; 86 (22%) responded to the questionnaire. Most were male (57%), between 40 and 59 years of age (74%), of European ethnicity (57%), had a medical degree from NZ (60%), and had been practising for at least 10 years (98%). Respondents were less likely to assess risk with increasing patient age and more likely to manage risk according to individual risk factors, rather than absolute risk. Marked variation occurred in intent to assess risk for a patient aged 78 years, according to living environment, co-morbidity, and functional status. In general, respondents indicated that they would usually assess risk for a 78-year-old community-dwelling patient without dementia but not for such a patient living in residential care or with dementia. DISCUSSION: This is New Zealands first report of GPs perspectives about assessing and managing CVD risk for older patients. Findings are consistent with international studies. More support and training in lifestyle assessment is needed, as well as clearer guidance for assessing and managing risk among older patients. KEYWORDS: Cardiovascular diseases; risk assessment; preventive medicine; geriatrics; public health
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Frenchman, I. Barton, and Theodore Prince. "Clinical Experience With Risperidone, Haloperidol, and Thioridazine for Dementia-Associated Behavioral Disturbances." International Psychogeriatrics 9, no. 4 (December 1997): 431–35. http://dx.doi.org/10.1017/s1041610297004560.
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The efficacy and safety of risperidone, haloperidol, and thioridazine for treating dementia-associated behavioral disturbances were evaluated in a retrospective study of 186 patients aged 65 years or older with DSM-III-R or DSM-IV diagnoses of Alzheimer's dementia, senile dementia NOS, or organic brain syndrome. Study patients were selected from the charts of 12,000 residents of 60 long-term-care facilities in New Jersey if they were treated with one of the three agents for behaviours dangerous to themselves or others. The 186 selected patients included 60 treatedwith risperidone (mean, 1 mg/day), 83 with haloperidol (mean, 2 mg/day), and 43 with thioridazine (mean, 33 mg/day). Target behaviors were violence (74 patients), shouting (31), delusions (26), paranoia (19), pacing (3), and mixed behaviors (33). Target behaviors improved in 94% of patients given risperidone, 65% given haloperidol, and 67% given thioridazine (p < .001). Treatment failures (treatment discontinued in patients because of side effects or no improvement) were more frequent in patients started on haloperidol (28) or thioridazine (15) than on risperidone (3). Extrapyramidal symptoms were reported in 7% of patients taking risperidone, 22% taking haloperidol, and 18% taking thioridazine. Safe, effective doses are readily achieved with risperidone but difficult to achieve with haloperidol or thioridazine because their effective doses often cause unacceptable side effects. These data are only suggestive because no guidelines exist for defining or measuring behavioral disturbances or for how they are affected by social, psychological, or environmental factors.
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Allsop, David, and Jennifer Mayes. "Amyloid β-peptide and Alzheimer's disease." Essays in Biochemistry 56 (August 18, 2014): 99–110. http://dx.doi.org/10.1042/bse0560099.
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One of the hallmarks of AD (Alzheimer's disease) is the formation of senile plaques in the brain, which contain fibrils composed of Aβ (amyloid β-peptide). According to the ‘amyloid cascade’ hypothesis, the aggregation of Aβ initiates a sequence of events leading to the formation of neurofibrillary tangles, neurodegeneration, and on to the main symptom of dementia. However, emphasis has now shifted away from fibrillar forms of Aβ and towards smaller and more soluble ‘oligomers’ as the main culprit in AD. The present chapter commences with a brief introduction to the disease and its current treatment, and then focuses on the formation of Aβ from the APP (amyloid precursor protein), the genetics of early-onset AD, which has provided strong support for the amyloid cascade hypothesis, and then on the development of new drugs aimed at reducing the load of cerebral Aβ, which is still the main hope for providing a more effective treatment for AD in the future.
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Demianov, S. V., A. G. Syrkina, E. V. Vyshlov, I. V. Maximov, A. E. Baev, V. A. Markov, R. S. Karpov, and V. V. Ryabov. "QUALITY OF CARE FOR PATIENTS WITH MYOCARDIAL INFARCTION WITH ST SEGMENT ELEVATION. REAL CLINICAL PRACTICE OF THE SIBERIAN INVASIVE CENTER." Siberian Medical Journal 33, no. 4 (February 13, 2019): 54–61. http://dx.doi.org/10.29001/2073-8552-2018-33-4-54-61.
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Background. There are many quality indicators for evaluation of quality of care in patients with myocardial infarction in the USA and Europe, but no such indicators exist in Russia.Material and Methods. This retrospective study included 475 STEMI patients, admitted within the first 12 hours during 2016. The baseline characteristics and treatment of our STEMI patients were compared with the OPERA register (France). The quality of care in STEMI patients was assessed using the quality criteria of the Association of Acute Cardiovascular Care of the European Society of Cardiology. Thrombolytic therapy, primary PCI, cardiogenic shock, pulmonary edema, acute LV aneurysm, and acute psychotic disorders were endpoints for a comparative assessment of quality of care in different age groups.Results. The following was more frequent among patients of our center: female, history of MI, hypertension, dyslipidemia and smoker. Our patients were less likely to receive primary PCI and GP IIb/IIIa inhibitor, but more often thrombolytic therapy, LMWH, aspirin, inhibitor P2Y12, beta-blocker, ACEI/ARBs and statins. All eligible STEMI patients received reperfusion and recommended medication, but hospital mortality was higher than in the OPERA register (7.4% versus 4.6%; p<0.05). Senile STEMI patients are less likely to undergo invasive reperfusion due to severe comorbidity, dementia and acute psychotic disorders, which leads to a manifold increase in hospital mortality.Conclusion. It is necessary to develop new devices for PCI of calcinated lesions, and methods for neuroprotection to overcome the existing barriers to ensure high-tech care in senile STEMI patients.
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Parnell, Miles, Li Guo, Mohamed Abdi, and M. Francesca Cordeiro. "Ocular Manifestations of Alzheimer’s Disease in Animal Models." International Journal of Alzheimer's Disease 2012 (2012): 1–13. http://dx.doi.org/10.1155/2012/786494.
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Alzheimer’s disease (AD) is the most common form of dementia, and the pathological changes of senile plaques (SPs) and neurofibrillary tangles (NFTs) in AD brains are well described. Clinically, a diagnosis remains a postmortem one, hampering both accurate and early diagnosis as well as research into potential new treatments. Visual deficits have long been noted in AD patients, and it is becoming increasingly apparent that histopathological changes already noted in the brain also occur in an extension of the brain; the retina. Due to the optically transparent nature of the eye, it is possible to image the retina at a cellular level noninvasively and thus potentially allow an earlier diagnosis as well as a way of monitoring progression and treatment effects. Transgenic animal models expressing amyloid precursor protein (APP) presenilin (PS) and tau mutations have been used successfully to recapitulate the pathological findings of AD in the brain. This paper will cover the ocular abnormalities that have been detected in these transgenic AD animal models.
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Mitchell, Terry, Michael Woodward, and Yuichi Hirose. "A survey of attitudes of clinicians towards the diagnosis and treatment of mild cognitive impairment in Australia and New Zealand." International Psychogeriatrics 20, no. 1 (February 2008): 77–85. http://dx.doi.org/10.1017/s1041610207005583.
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ABSTRACTObjectives: The aim of the study was to assess the attitudes of clinicians to the diagnostic construct of mild cognitive impairment (MCI), their approach to relaying the diagnosis to patients and families, and recommended treatment and follow-up.Method: An anonymous questionnaire was sent out to 503 members of the Australian Society for Geriatric Medicine (ASGM) and New Zealand Geriatrics Society (NZGS), of whom 163 replied.Results: Most responders (83%) had diagnosed MCI. About 70% rated the importance of separating MCI from dementia, or MCI from normal cognition, as 4 or 5 on a scale from 1 (not very important) to 5 (very important). Most responders reported that they would inform their patients and families of a diagnosis of MCI, and used that term. A minority used the term “early Alzheimer's disease,” but 44% of NZGS members used other terms to relay the diagnosis compared to 13% of ASGM members. Follow-up was most often recommended at 6–12 months. Non-pharmacological treatment (such as mental stimulation strategies) was recommended most often, followed by no treatment.Conclusions: The diagnostic entity of MCI appears to have a general acceptance among those who responded to the survey, and the term has gained use in clinical practice. Most clinicians are recommending follow-up, recognizing the high risk for progression. Treatment recommendations do not favor pharmaceuticals, reflecting the current evidence for lack of effect.
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Ranjan*, Navi, and Manorma Kumari. "Acetylcholinesterase inhibition by medicinal plants: A Review." Annals of Plant Sciences 6, no. 06 (June 2, 2017): 1640. http://dx.doi.org/10.21746/aps.2017.06.003.
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Acetylcholinesterase (AChE), the predominant cholinesterase in the brain, hydrolyzes ACh to choline and acetate, thereby terminating the effect of this neurotransmitter at cholinergic synapses. Therefore, AChE is the target of cholinesterase inhibitors used for addressing the cholinergic deficit in Alzheimer’s disease (AD) patients. Despite decades of research and advances in our understanding of its aetiology and pathogenesis, current pharmacotherapeutic options for AD are still very limited and represent an area of need that is currently unmet. The leading AD therapeutics involves AChE inhibitors, resulting in increased acetylcholine concentrations in the synaptic cleft and enhanced cholinergic transmission. Compounds showing an AChE inhibitory effect are also used for the treatment of senile dementia, myastenia gravis, Parkinson’s disease and ataxia. Taking into account that the inhibition of AChE has been one of the most used strategies for treating AD and that existing drugs are effective only against mild to moderate type of disease while presenting considerable side effects, the search for new sources of effective and selective anti acetylcholinesterase agents with fewer side effects is imperative. Various plants and phytochemical substances have demonstrated AChE inhibitory activity and thus could be beneficial in the treatment of neurodegenerative disorders such as AD.
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Shikh, E. V., N. N. Shindryaeva, E. V. Rebrova, N. I. Lapidus, O. V. Zhukova, I. V. Stuk, and I. G. Koroleva. "A personalised approach to the choice of oral anticoagulants in elderly and senile patients with atrial fibrillation." Meditsinskiy sovet = Medical Council, no. 14 (August 13, 2022): 228–34. http://dx.doi.org/10.21518/2079-701x-2022-16-14-228-234.
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Introduction. In recent years, data have been accumulated regarding possible associations between cognitive impairment and atrial fibrillation. The results of retrospective and prospective studies confirm that anticoagulant therapy in patients with AF can reduce the risk of cognitive impairment and dementia.Objective. To study the individual characteristics of elderly and senile patients with atrial fibrillation, influencing the choice of anticoagulant therapy, with a view to its subsequent optimization.Materials and methods. The study included 159 patients with atrial fibrillation of non-valvular genesis aged over 60 years. 4 groups of patients were formed. The largest number of patients received rivaroxaban and warfarin (36.4% and 34.6%, respectively). 26 (16.3%) patients were treated with dabigatran, 20 (12.6%) patients with apixaban. The risk of thromboembolic complications was assessed on the CHA2DS2-VASc scale. The HAS-BLED scale was used to assess the risk of bleeding. A pharmacogenetic study (carriage of polymorphic alleles of the CYP2C9 and VCORC1 genes) was conducted in 138 patients. Cognitive impairment was assessed by a Mini-Cog test and a battery of frontal tests.Results. Taking oral anticoagulants reduces the risk of stroke and dementia in patients; the presence of cognitive impairment, in turn, significantly reduces the patient’s adherence to therapy and reduces the effectiveness of therapy. Patients’ adherence to therapy was significantly lower by 10–20% in patients with cognitive impairment according to the Mini-Cog test and a battery of frontal tests. In the absence of pronounced cognitive impairment (higher adherence to treatment) and availability and willingness to control INR, warfarin remains the drug of choice in patients with renal insufficiency.Conclusions. A number of problems with the use of oral anticoagulants in elderly patients with atrial fibrillation have been identified. The ease of use of new oral anticoagulants, the absence of the need to select doses and monitor therapy is an important factor when choosing a drug.
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Wostyn, Peter, Debby Van Dam, Kurt Audenaert, and Peter Paul De Deyn. "Increased Cerebrospinal Fluid Production as a Possible Mechanism Underlying Caffeine's Protective Effect against Alzheimer's Disease." International Journal of Alzheimer's Disease 2011 (2011): 1–6. http://dx.doi.org/10.4061/2011/617420.
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Alzheimer's disease (AD), the most common type of dementia among older people, is characterized by the accumulation of β-amyloid (Aβ) senile plaques and neurofibrillary tangles composed of hyperphosphorylated tau in the brain. Despite major advances in understanding the molecular etiology of the disease, progress in the clinical treatment of AD patients has been extremely limited. Therefore, new and more effective therapeutic approaches are needed. Accumulating evidence from human and animal studies suggests that the long-term consumption of caffeine, the most commonly used psychoactive drug in the world, may be protective against AD. The mechanisms underlying the suggested beneficial effect of caffeine against AD remain to be elucidated. In recent studies, several potential neuroprotective effects of caffeine have been proposed. Interestingly, a recent study in rats showed that the long-term consumption of caffeine increased cerebrospinal fluid (CSF) production, associated with the increased expression of Na+-K+ATPase and increased cerebral blood flow. Compromised function of the choroid plexus and defective CSF production and turnover, with diminished clearance of Aβ, may be one mechanism implicated in the pathogenesis of late-onset AD. If reduced CSF turnover is a risk factor for AD, then therapeutic strategies to improve CSF flow are reasonable. In this paper, we hypothesize that long-term caffeine consumption could exert protective effects against AD at least in part by facilitating CSF production, turnover, and clearance. Further, we propose a preclinical experimental design allowing evaluation of this hypothesis.
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Peri, Kathryn, Ngaire Kerse, Simon Moyes, Shane Scahill, Charlotte Chen, Jae Beom Hong, and Carmel M. Hughes. "Is psychotropic medication use related to organisational and treatment culture in residential care." Journal of Health Organization and Management 29, no. 7 (November 16, 2015): 1065–79. http://dx.doi.org/10.1108/jhom-10-2013-0236.
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Purpose – The purpose of this paper is to establish the relationship between organisational culture and psychotropic medication use in residential care. Design/methodology/approach – Cross-sectional analyses of staff and resident’s record survey in residential aged care facilities in Auckland, New Zealand (NZ). The competing values framework categorised organisational culture as clan, hierarchical, market driven or adhocracy and was completed by all staff. The treatment culture tool categorised facilities as having resident centred or traditional culture and was completed by registered nursing staff and general practitioners (GP). Functional and behavioural characteristics of residents were established by staff report and health characteristics and medications used were ascertained from the health record. Multiple regression was used to test for associations between measures of culture with psychotropic medication use (anxiolytics, sedatives, major tranquillisers). Findings – In total 199 staff, 27 GP and 527 residents participated from 14 facilities. On average 8.5 medications per resident were prescribed and 42 per cent of residents received psychotropic medication. Having a diagnosis of anxiety or depression (odds ratio (OR) 3.18, 95 per cent confidence interval (CI) 1.71, 5.91), followed by persistent wandering (OR 2.53, 95 per cent CI 1.59, 4.01) and being in a dementia unit (OR 2.45, 95 per cent CI 1.17, 5.12) were most strongly associated with psychotropic use. Controlling for resident- and facility-level factors, health care assistants’ assignation of hierarchical organisational culture type was independently associated with psychotropic medication use, (OR 1.29, CI 1.08, 1.53) and a higher treatment culture score from the GP was associated with lower use of psychotropic medication (OR 0.95, CI 0.92, 0.98). Originality/value – Psychotropic medication use remains prevalent in residential care facilities in NZ. Interventions aimed at changing organisational culture towards a less hierarchical and more resident-centred culture may be another avenue to improve prescribing in residential aged care.
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van der Ploeg, Eva S., Barbara Eppingstall, Cameron J. Camp, Susannah J. Runci, John Taffe, and Daniel W. O'Connor. "A randomized crossover trial to study the effect of personalized, one-to-one interaction using Montessori-based activities on agitation, affect, and engagement in nursing home residents with Dementia." International Psychogeriatrics 25, no. 4 (December 14, 2012): 565–75. http://dx.doi.org/10.1017/s1041610212002128.
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ABSTRACTBackground: Increasingly more attention has been paid to non-pharmacological interventions as treatment of agitated behaviors that accompany dementia. The aim of the current study is to test if personalized one-to-one interaction activities based on Montessori principles will improve agitation, affect, and engagement more than a relevant control condition.Methods: We conducted a randomized crossover trial in nine residential facilities in metropolitan Melbourne, Australia (n = 44). Personalized one-to-one activities that were delivered using Montessori principles were compared with a non-personalized activity to control for the non-specific benefits of one-to-one interaction. Participants were observed 30 minutes before, during, and after the sessions. The presence or absence of a selected physically non-aggressive behavior was noted in every minute, together with the predominant type of affect and engagement.Results: Behavior counts fell considerably during both the Montessori and control sessions relative to beforehand. During Montessori activities, the amount of time spend actively engaged was double compared to during the control condition and participants displayed more positive affect and interest as well. Participants with no fluency in English (all from non-English speaking backgrounds) showed a significantly larger reduction in agitation during the Montessori than control sessions.Conclusion: Our results show that even non-personalized social contact can assist in settling agitated residents. Tailoring activities to residents’ needs and capabilities elicit more positive interactions and are especially suitable for people who have lost fluency in the language spoken predominantly in their residential facility. Future studies could explore implementation by family members and volunteers to avoid demands on facilities’ resources.Trial Registration: Australian New Zealand Clinical Trials Registry – ACTRN12609000564257.
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Ren, Q. W., T. S. E. Yi-Kei, L. I. Hang-Long, Y. U. Si-Yeung, W. O. N. G. Pui-Fai, W. U. Mei-Zhen, T. S. E. Hung-Fat, and Y. I. U. Kai-Hang. "Statin use is associated with lower risk of new onset dementia in patients with heart failure." European Heart Journal 42, Supplement_1 (October 1, 2021). http://dx.doi.org/10.1093/eurheartj/ehab724.0850.
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Abstract Background Increasing number of heart failure (HF) patients diagnosed with dementia due to improved treatment and aging population. Data relating to the association of statin use on the risk of dementia incidence among patients with HF are sparse. Methods Using a previously validated territory-wide clinical information registry, statin use was ascertained among all eligible patients with HF (N=241,995) from 1996 to 2019. Propensity score matching was used to balance baseline covariates between statin nonusers (167,738 patients) with statin users (74,257 patients). Competing risk regression with Cox proportional-hazard models was performed to estimate the risk of incident dementia associated with statin use. Results Of all eligible subjects, the mean age was 76.5±13.0 years, 115,371 (47.7%) was male. Over a median follow-up of 2.7 years (interquartile range [IQR]: 0.6 to 6.7), 13,482 (5.6%) patients were diagnosed with dementia including Alzheimer's disease (N=5,253), senile dementia uncomplicated (N=4,273), arteriosclerotic dementia (N=3,262), and others (N=694). Statin use (vs. none) was associated with a 58% lower risk of dementia incidence (multivariable-adjusted sub-distribution hazard ratio [SHR]=0.42; 95% Confidence Interval [CI], 0.38 to 0.46) after accounting for death as a competing risk. Moreover, the male gender was associated with a 51% lower risk of dementia incidence (multivariable-adjusted SHR=0.59; 95% CI (0.54–0.65) compared with females. Conclusion Our study suggests that there is substantial sex difference in the incidence of dementia among HF patients. Moreover, statin use is associated with a significantly lower risk of incident dementia in HF. Funding Acknowledgement Type of funding sources: None.
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Beaglehole, Ben, Giles Newton-Howes, Richard Porter, and Chris Frampton. "Impact of diagnosis on outcomes for compulsory treatment orders in New Zealand." BJPsych Open 8, no. 5 (August 1, 2022). http://dx.doi.org/10.1192/bjo.2022.547.
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Background Compulsory community treatment orders (CTOs) are controversial because they enforce psychiatric treatment of patients in the community. It is important to know which patients benefit from compulsory treatment to better inform CTO use. Aims To examine the effect of a range of diagnoses on outcomes associated with CTOs to determine whether there are specific outcome signatures for CTOs according to diagnosis. Method New Zealand's Ministry of Health databases provided demographic, service use and medication-dispensing data for all individuals placed on a CTO between 2009 and 2018. We used a hierarchical approach to categorise individuals according to diagnosis. Admission rates, admission days per year, community care and medication dispensing were analysed according to diagnosis and CTO status. Results In total, 14 726 patients were placed on a CTO over the 10-year period between 1 January 2009 and 31 December 2018. For psychotic disorders, CTOs were associated with reduced admission frequency and duration. However, the opposite occurred for dementia disorders, bipolar disorders, major depressive disorder and personality disorders. Higher rates of medications, including depot antipsychotic medications, were dispensed on CTOs for all diagnostic groups. Conclusions CTOs were associated with reduced admission frequency and admission days per year for patients with psychotic disorders, whereas the opposite occurred for other diagnostic groups. Rather than seeking to establish whether CTOs are effective, we suggest that there are specific outcome signatures associated with CTOs for different disorders and knowledge of these can improve understanding and clinical practice in this area.
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Zhang, Yuan, Man Wang, and Wenguang Chang. "Iron dyshomeostasis and ferroptosis in Alzheimer’s disease: Molecular mechanisms of cell death and novel therapeutic drugs and targets for AD." Frontiers in Pharmacology 13 (September 16, 2022). http://dx.doi.org/10.3389/fphar.2022.983623.
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Alzheimer’s disease (AD) is a degenerative disease of the central nervous system that is the most common type of senile dementia. Ferroptosis is a new type of iron-dependent programmed cell death identified in recent years that is different from other cell death forms. Ferroptosis is induced by excessive accumulation of lipid peroxides and reactive oxygen species (ROS) in cells. In recent years, it has been found that ferroptosis plays an important role in the pathological process of AD. Iron dyshomeostasis contribute to senile plaques (SP) deposition and neurofibrillary tangles (NFTs). Iron metabolism imbalance in brain and the dysfunction of endogenous antioxidant systems including system Xc- and glutathione peroxidase (GPX) are closely related to the etiopathogenesis of AD. Dysfunction of nuclear receptor coactivator 4 (NCOA4)-mediated ferritinophagy induced ferroptosis can accelerates the pathological process of AD. In addition, NRF2, through regulating the expression of a considerable number of genes related to ferroptosis, including genes related to iron and glutathione metabolism, plays an important role in the development of AD. Here, we review the potential interaction between AD and ferroptosis and the major pathways regulating ferroptosis in AD. We also review the active natural and synthetic compounds such as iron chelators, lipid peroxidation inhibitors and antioxidants available to treat AD by alleviating iron dyshomeostasis and preventing ferroptosis in mice and cell models to provide valuable information for the future treatment and prevention of AD.
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Levinger, Pazit, Anita M. Y. Goh, Jeremy Dunn, Josephine Katite, Ritu Paudel, Adrian Onofrio, Frances Batchelor, Maya G. Panisset, and Keith D. Hill. "Exercise interveNtion outdoor proJect in the cOmmunitY—ENJOY program for independence in dementia: a feasibility pilot randomised controlled trial study protocol." Pilot and Feasibility Studies 8, no. 1 (March 22, 2022). http://dx.doi.org/10.1186/s40814-022-01027-x.
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Abstract Background While the underlying neuropathology of dementia is not curable, interventions and treatment, such as physical activity, can offer physical and functional gains leading to better mobility, independence and quality of life. The Seniors Exercise Park program is an evidence-based physical and social activity program using an innovative design in outdoor exercise equipment specifically designed for older people. This unique program has never been tested with older people living with dementia. This study will evaluate the feasibility of delivering the Seniors Exercise Park program for people living with mild to moderate dementia in residential aged-care. This study will identify the optimal physical activity program, evaluate the safety of equipment usage and determine optimal supervision needs. The potential physical, social, quality of life and cognitive benefits of participation in the Seniors Exercise Park program will also be examined. Methods This is a feasibility pilot randomised controlled design with pre-post evaluation. Adults aged ≥ 60 years who have symptoms of dementia and/or who have been diagnosed with dementia will be recruited from an aged-care facility in Melbourne. Participants allocated to the intervention group will undergo a 12-week structured supervised physical activity program using the outdoor Seniors Exercise Park equipment followed by a 12-week maintenance phase (unstructured physical activity). Participants will be assessed at baseline, 3 and 6 months. Participants allocated to the control group will attend activities provided by the aged-care facility. A sample of 12 participants per group is the targeted sample size. Feasibility will be evaluated in terms of recruitment rate, retention, attendance, overall adherence, dropout rate, adverse events, modifications to the exercise program delivery and supervision needs. A comprehensive suite of cognitive and health-related questionnaires and physical function measures will also be collected. Discussion The ENJOY program for independence in dementia will determine the suitability of the Seniors Exercise Park program for people diagnosed with mild to moderate dementia. Outcomes could inform future design of dementia-friendly built environments to increase physical activity participation for residential aged-care facilities. Trial registration This trial is registered with the Australian New Zealand Clinical Trials Registry—Registry Number ACTRN12620000733976. Registered on the 13th of July 2020.
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Gibson, Rosemary, Anthony Dowell, Linda Jones, and Philippa Gander. "Non-pharmacological interventions a feasible option for addressing dementia-related sleep problems in the context of family care." Pilot and Feasibility Studies 7, no. 1 (May 26, 2021). http://dx.doi.org/10.1186/s40814-021-00851-x.
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Abstract Background Sleep disturbances are challenging symptoms associated with mild cognitive impairment or dementia (MCIoD). This study assessed the feasibility of sleep monitoring and non-pharmacological interventions to improve the sleep of New Zealanders with MCIoD and their family carers. Methods A 5-week multi-modal intervention consisting of timed bright light therapy, physical activity, and sleep education was piloted. Sleep was monitored for a week at baseline and conclusion of the trial using actigraphy, diaries, and questionnaires alongside additional health and wellbeing information concerning both care recipients and carers. Results Fifteen pairs participated, 9 completed the trial. Patterns of attrition and participant feedback are discussed. Case studies showed that six of the care recipients had minor improvements to sleep efficiency. Some also had improved subjective sleep ratings and quality of life. Changes did not clearly translate to family carers. However, five of them also showed some improvements in sleep status and mental health. Health deterioration of care recipients may mask the effects of the intervention. Conclusions It is feasible to use non-pharmacological sleep interventions for people with MCIoD and their family carers. Given the limited treatment options, further consideration of such interventions in future research and clinical practice is warranted. Trial registration As this study was to assess the feasibility of proposed methods, it was an observational study without case-control groups nor a medical-based intervention, clinical registration was not required. A future full version of the trial would be registered with the Australian New Zealand Clinical Trails Registry.
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Jayakody, Dona M. P., Osvaldo P. Almeida, Andrew H. Ford, Marcus D. Atlas, Nicola T. Lautenschlager, Peter L. Friedland, Suzanne Robinson, et al. "Hearing aids to support cognitive functions of older adults at risk of dementia: the HearCog trial- clinical protocols." BMC Geriatrics 20, no. 1 (November 26, 2020). http://dx.doi.org/10.1186/s12877-020-01912-1.
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Abstract Background Globally, about 50 million people were living with dementia in 2015, with this number projected to triple by 2050. With no cure or effective treatment currently insight, it is vital that factors are identified which will help prevent or delay both age-related and pathological cognitive decline and dementia. Observational data have suggested that hearing loss is a potentially modifiable risk factor for dementia, but no conclusive evidence from randomised controlled trials is currently available. Methods The HearCog trial is a 24-month, randomised, controlled clinical trial aimed at determining whether a hearing loss intervention can delay or arrest the cognitive decline. We will randomise 180 older adults with hearing loss and mild cognitive impairment to a hearing aid or control group to determine if the fitting of hearing aids decreases the 12-month rate of cognitive decline compared with the control group. In addition, we will also determine if the expected clinical gains achieved after 12 months can be sustained over an additional 12 months and if losses experienced through the non-correction of hearing loss can be reversed with the fitting of hearing aids after 12 months. Discussion The trial will also explore the cost-effectiveness of the intervention compared to the control arm and the impact of hearing aids on anxiety, depression, physical health and quality of life. The results of this trial will clarify whether the systematic correction of hearing loss benefits cognition in older adults at risk of cognitive decline. We anticipate that our findings will have implications for clinical practice and health policy development. Trial registration Australian and New Zealand Clinical Trials Registry (ANZCTR: 12618001278224), registered on 30.07.2018.
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Ashford, J. Wesson, Frederick A. Schmitt, Michael F. Bergeron, Peter J. Bayley, James O. Clifford, Qun Xu, Xiaolei Liu, et al. "Now is the Time to Improve Cognitive Screening and Assessment for Clinical and Research Advancement." Journal of Alzheimer's Disease, April 11, 2022, 1–11. http://dx.doi.org/10.3233/jad-220211.
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Alzheimer’s disease (AD) is the only cause of death ranked in the top ten globally without precise early diagnosis or effective means of prevention or treatment. Further, AD was identified as a pandemic [1] well before COVID-19 was dubbed a 21st century pandemic [2]. And now, with the realization of the prominent secondary impacts of pandemics, there is a growing, widespread recognition of the tremendous magnitude of the impending burden from AD in an aging world population in the coming decades [3]. This appreciation has amplified the growing and pressing need for a new, efficacious, and practical platform to detect and track cognitive decline, beginning in the preliminary (prodromal) phases of the disease, sensitively, accurately, effectively, reliably, efficiently, and remotely [4–7]. Moreover, the parallel necessity of clarifying and understanding risk factors, developing successful prevention strategies [8–17], and discovering and monitoring viable and effective treatments could all benefit from accurate and efficient screening and assessment platforms. Modern recognition of AD [18] as a common affliction of the elderly began in 1968 with a paper by Blessed, Tomlinson, & Roth [19] in which two tests, one a brief assessment of cognitive function and the other a measure of daily function, demonstrated impairment which was associated with the postmortem counts of neurofibrillary tangles, composed mainly of microtubule-associated protein-tau (tau), in the brain, though not to senile plaques, composed mainly of amyloid-β (Aβ). Even in more recent analyses, the tangles correspond with the severity of dementia more than the plaques [20, 21]. Since 1960, a plethora of cognitive tests, paper and pencil [22, 23], simple screening models [24], and computerized [25–27], have been developed to assess the dysfunction associated with AD. However, there has been limited application of Modern Test Theory, which includes Item Characteristic Curve Analysis, used in the technological development of such tools [28–31], along with widespread failure to understand the underlying AD pathological process to guide test development [32, 33]. The lack of such development has likely been a major contributor to the failure of the field to develop timely screening approaches for AD [34, 35], inaccurate assessment of the progression of AD [36], and even now, failure to find an effective approach to stopping AD.
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Mengdai, Xu, Mo Xiaoxing, Huang Hao, Liu Liegang, and Yang Wei. "Yeast beta-Glucan effects on gut microbiota for regulating insulin signaling system on alzheimer's disease." Proceedings of the Nutrition Society 79, OCE2 (2020). http://dx.doi.org/10.1017/s0029665120002116.
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AbstractIntroduction:Alzheimer's disease (AD) is a progressive neurodegenerative disease for dementia in adults. The main pathological alterations are extracellular senile plaque deposits, intracellular neurofibrillary tangles and neuronal apoptosis. Recent researches indicated that T2D is closely with AD by insulin resistance in central nerves system progression. Nevertheless, the pathological mechanism remains unclear and treatment is limited. β-glucan extracted from yeast, as a dietary fiber with high bioactivity, edible, good taste and easy-obtainable, have been showed abilities such as anti-diabetic, anti-inflammatory and prebiotic. Based on this, β-glucan can reduce insulin resistance and maintain gut microbiota thereby alleviating lesions of early AD.Materials and Methods:In this study, we used 36 male wild-type C57BL/6J mice were divided to 3 groups (control (C) mice injected i.c.v. with 0.9% saline as a vehicle, mice injected i.c.v. with Aβ1–42 (Aβ1–42 group), mice injected with Aβ1–42 and soluble yeast β-glucan 100 mg/kg body weight by oral gavage daily (o.g.) for 5 wks (Aβ1–42 + Glu)). H&E method was detected for structure of hippocampus. Morris water maze test was performed to assess the cognitive performance of Aβ-infusion mice. The microbiota composition was analyzed by 16sRNA sequencing. The levels of inflammatory were measured in hippocampal and plasma by Meso-scale Discovery (MSD). Western blot was performed to detect the level of protein in insulin signaling pathway. One-way ANNOVA with Student-Newman-Keuls was applied for the data analysis through SPSS software version 22.0.Results:As demonstrated by H&E sections, β-glucan reduced neuron damage in AD mice hippocampus. Decreased the levels of Aβ and phosphorylation of Tau protein expression in hippocampus (P < 0.05) and ameliorated insulin resistance (p-IRS-1) in hippocampus (P < 0.05). According by results from MSD and Western-blot that showed TNF-α (P < 0.05), phosphorylated JNK (P < 0.01) and Tau were up-regulated in AD but β-glucan group decreased. In addition, the abundance of beneficial bacteria in β-glucan mice is increased (g_Alistipes, g_Rikeenella and g_Saccharibecteria genera incerae sedies).Discussion:Summary, this study illustrated that β-glucan regulated insulin signaling for ameliorating learning and memory deficit in AD. Due to β-glucan can not pass Blood-Brain-Barrier, we hypothesized that β-glucan could regulates gut microbiota by metabolites for ameliorating neuron damage. Our study provides new ideas for the prevention of AD.
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Reuben, Aaron, Terrie E. Moffitt, Wickliffe C. Abraham, Antony Ambler, Maxwell L. Elliott, Ahmad R. Hariri, Honalee Harrington, et al. "Improving risk indexes for Alzheimer’s disease and related dementias for use in midlife." Brain Communications 4, no. 5 (September 1, 2022). http://dx.doi.org/10.1093/braincomms/fcac223.
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Abstract Knowledge of a person’s risk for Alzheimer’s disease and related dementias (ADRDs) is required to triage candidates for preventive interventions, surveillance, and treatment trials. ADRD risk indexes exist for this purpose, but each includes only a subset of known risk factors. Information missing from published indexes could improve risk prediction. In the Dunedin Study of a population-representative New Zealand-based birth cohort followed to midlife (N = 938, 49.5% female), we compared associations of four leading risk indexes with midlife antecedents of ADRD against a novel benchmark index comprised of nearly all known ADRD risk factors, the Dunedin ADRD Risk Benchmark (DunedinARB). Existing indexes included the Cardiovascular Risk Factors, Aging, and Dementia index (CAIDE), LIfestyle for BRAin health index (LIBRA), Australian National University Alzheimer’s Disease Risk Index (ANU-ADRI), and risks selected by the Lancet Commission on Dementia. The Dunedin benchmark was comprised of 48 separate indicators of risk organized into 10 conceptually distinct risk domains. Midlife antecedents of ADRD treated as outcome measures included age-45 measures of brain structural integrity [magnetic resonance imaging-assessed: (i) machine-learning-algorithm-estimated brain age, (ii) log-transformed volume of white matter hyperintensities, and (iii) mean grey matter volume of the hippocampus] and measures of brain functional integrity [(i) objective cognitive function assessed via the Wechsler Adult Intelligence Scale-IV, (ii) subjective problems in everyday cognitive function, and (iii) objective cognitive decline measured as residualized change in cognitive scores from childhood to midlife on matched Weschler Intelligence scales]. All indexes were quantitatively distributed and proved informative about midlife antecedents of ADRD, including algorithm-estimated brain age (β's from 0.16 to 0.22), white matter hyperintensities volume (β's from 0.16 to 0.19), hippocampal volume (β's from −0.08 to −0.11), tested cognitive deficits (β's from −0.36 to −0.49), everyday cognitive problems (β's from 0.14 to 0.38), and longitudinal cognitive decline (β's from −0.18 to −0.26). Existing indexes compared favourably to the comprehensive benchmark in their association with the brain structural integrity measures but were outperformed in their association with the functional integrity measures, particularly subjective cognitive problems and tested cognitive decline. Results indicated that existing indexes could be improved with targeted additions, particularly of measures assessing socioeconomic status, physical and sensory function, epigenetic aging, and subjective overall health. Existing premorbid ADRD risk indexes perform well in identifying linear gradients of risk among members of the general population at midlife, even when they include only a small subset of potential risk factors. They could be improved, however, with targeted additions to more holistically capture the different facets of risk for this multiply determined, age-related disease.
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Phillips, Matthew C. L., Laura M. Deprez, Grace M. N. Mortimer, Deborah K. J. Murtagh, Stacey McCoy, Ruth Mylchreest, Linda J. Gilbertson, et al. "Randomized crossover trial of a modified ketogenic diet in Alzheimer’s disease." Alzheimer's Research & Therapy 13, no. 1 (February 23, 2021). http://dx.doi.org/10.1186/s13195-021-00783-x.
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Abstract Background Brain energy metabolism is impaired in Alzheimer’s disease (AD), which may be mitigated by a ketogenic diet. We conducted a randomized crossover trial to determine whether a 12-week modified ketogenic diet improved cognition, daily function, or quality of life in a hospital clinic of AD patients. Methods We randomly assigned patients with clinically confirmed diagnoses of AD to a modified ketogenic diet or usual diet supplemented with low-fat healthy-eating guidelines and enrolled them in a single-phase, assessor-blinded, two-period crossover trial (two 12-week treatment periods, separated by a 10-week washout period). Primary outcomes were mean within-individual changes in the Addenbrookes Cognitive Examination - III (ACE-III) scale, AD Cooperative Study - Activities of Daily Living (ADCS-ADL) inventory, and Quality of Life in AD (QOL-AD) questionnaire over 12 weeks. Secondary outcomes considered changes in cardiovascular risk factors and adverse effects. Results We randomized 26 patients, of whom 21 (81%) completed the ketogenic diet; only one withdrawal was attributed to the ketogenic diet. While on the ketogenic diet, patients achieved sustained physiological ketosis (12-week mean beta-hydroxybutyrate level: 0.95 ± 0.34 mmol/L). Compared with usual diet, patients on the ketogenic diet increased their mean within-individual ADCS-ADL (+ 3.13 ± 5.01 points, P = 0.0067) and QOL-AD (+ 3.37 ± 6.86 points, P = 0.023) scores; the ACE-III also increased, but not significantly (+ 2.12 ± 8.70 points, P = 0.24). Changes in cardiovascular risk factors were mostly favourable, and adverse effects were mild. Conclusions This is the first randomized trial to investigate the impact of a ketogenic diet in patients with uniform diagnoses of AD. High rates of retention, adherence, and safety appear to be achievable in applying a 12-week modified ketogenic diet to AD patients. Compared with a usual diet supplemented with low-fat healthy-eating guidelines, patients on the ketogenic diet improved in daily function and quality of life, two factors of great importance to people living with dementia. Trial registration This trial is registered on the Australia New Zealand Clinical Trials Registry, number ACTRN12618001450202. The trial was registered on August 28, 2018.