Position Statement of the American Association for Geriatric Psychiatry Regarding Principles of Care for Patients With Dementia Resulting From Alzheimer Disease

American Journal of Geriatric Psychiatry (Impact Factor: 4.24). 08/2006; 14(7):561-72. DOI: 10.1097/01.JGP.0000221334.65330.55
Source: PubMed


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    • "In contrast, when a person with dementia presents with only 'mild' effects on routine activities and cognitive function, fitness to drive should be determined on a caseby-case basis (Carmody et al. 2012). The importance of addressing fitness to drive for those with dementia has been defined in position statements published in Canada, USA, Australian and New Zealand (Lyketsos et al. 2006, Hogan et al. 2008). Hogan et al. (2008) outlined approaches to managing driving retirement in the Canadian Medical Association Journal including the family doctor's responsibility to monitor and counsel patients with progressive dementia who will eventually need to cease driving. "
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    ABSTRACT: To synthesise primary research exploring decision making practices used to determine the time to retire from driving for individuals living with a dementia. Driving requires complex cognitive and physical skills potentially compromised due to the progressive nature of dementia. Whilst on-road assessments are considered reliable indicators of driving capacity by clinicians, drivers with dementia disagree. Integrative literature review informed by Whittemore & Knafl (2005). Electronic database search of Medline, CINAHL, Web of Science, Google Scholar 1997-2012; and incremental hand search. Primary studies published in peer reviewed journals were appraised against quality assessment criteria using CASP methodological assessment tools. A total of 43 studies were retained for synthesis. Key findings were abstracted and a themes matrix was generated to identify patterns of meaning. Six themes emerged: (i) dementia may compromise the complex task of driving; (ii) defining onset and severity of dementia is problematic; (iii) symptom progression impacts on driving skills; (iv) assessment of fitness to drive remains subjective; (v) some drivers are reluctant to accept negative assessment outcomes; and (vi) the search for effective strategies to enhance acceptance of driver retirement continues. This integrative literature review identified a large body of knowledge exploring the issues of driving cessation for drivers with dementia. However a challenge remains for practitioners, drivers and their family carers regarding how best to address this highly emotive issue. Findings could inform a structured approach to address this sensitive topic in a timely manner. © 2015 John Wiley & Sons Ltd.
    Journal of Advanced Nursing 07/2015; DOI:10.1111/jan.12727 · 1.74 Impact Factor
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    • "ForAustralianmedicalpractitionersthereisnolegalobligationtoreportapatient'sdiagnosisof dementia(Carmodyetal.2013).Mandatoryreportingobligationsforimpairedphysicalorcognitive fitnesstodriveareonlylegislatedinSouthAustraliaandtheNorthernTerritory(Brownetal.2005, AustralianandNewZealandSocietyforGeriatricMedicine2009,Carmodyetal.2014).Whena clinicianassessesanindividualasdemonstratingsymptomsofdementiathatsignificantlyaffectdaily livingactivities,itisdeterminingfitnesstodrivingismorestraightforward.Incontrast,whenaperson withdementiapresentswithonly'mild'effectsonroutineactivitiesandcognitivefunction,fitnessto driveshouldbedeterminedonacase-by-casebasis(Carmodyetal.2012).Theimportanceof addressingfitnesstodriveforthosewithdementiahasbeendefinedinpositionstatementspublished inCanada,USA,AustralianandNewZealand(Hoganetal.2008,Lyketsos,etal.2006).Hoganetal. (2008)outlinedapproachestomanagingdrivingretirementinCanadianMedicalAssociationJournal includingthefamilydoctor'sresponsibilitytomonitorandcounselpatientswithprogressivedementia whowilleventuallyneedtoceasedriving.ConcurringwiththeAustralianandNewZealandSocietyfor GeriatricMedicine(2009)positionstatement,Hoganetal.alsorecommendedthat:(i)fitnesstodrive fordriverswithmilddementiacannotbesolelydeterminedusingabriefcognitivetest;and(ii) cliniciansshouldrelyonanoff-roadandonroadassessment. "

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    • "Considerable attention has been focused on the accumulation of β-amyloid peptide (Aβ) within the brain as a major etiologic factor in the pathogenesis of Alzheimer disease (AD). The commonly used drugs for AD like memantine, is a N-methyl-D-aspartic acid (NMDA) receptor antagonist, which may restore the functions of damaged neurons through reducing abnormal excitatory signals via the modulation of NMDA receptor activity [36] and cholinesterase (AChE) inhibitors suppress the enzymatic hydrolysis of neurotransmitter acetylcholine, thus maintain a higher acetylcholine concentration in the neuronal synapse [37], provide a symptomatic relief but no cure for the disease. At present, there is no curative treatment available for AD and the approved medications are used only for slowing the disease progression or providing prophylaxis. "
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    ABSTRACT: Alzheimer's disease (AD) is characterized by progressive dysfunction of memory and higher cognitive functions with abnormal accumulation of extracellular amyloid plaques and intracellular neurofibrillary tangles throughout cortical and limbic brain regions. At present no curative treatment is available, and research focuses on drugs for slowing disease progression or providing prophylaxis. Withania somnifera (WS) also known as 'ashwagandha' is used widely in Ayurvedic medicine as a nerve tonic and memory enhancer. However, there is a paucity of data on the potential neuroprotective effects of W.somnifera against β-Amyloid (1-42)-induced neuropathogenesis. In the present study, we have tested the neuroprotective effects of methanol:Chloroform (3:1) extract of ashwagandha against β-amyloid induced toxicity and HIV-1Ba-L (clade B) infection using a human neuronal SK-N-MC cell line. Our results showed that β-amyloid induced cytotoxic effects in SK-N-MC cells as shown by decreased cell growth when tested individually. Also, confocal microscopic analysis showed decreased spine density, loss of spines and decreased dendrite diameter, total dendrite and spine area in clade B infected SK-N-MC cells compared to uninfected cells. However, when ashwagandha was added to β-amyloid treated and HIV-1 infected samples, the toxic effects were neutralized. Further, the MTT cell viability assays and the peroxisome proliferator-activated receptor-γ (PPARγ) levels supported these observations indicating the neuroprotective effect of WS root extract against β-amyloid and HIV-1Ba-L (clade B) induced neuro-pathogenesis.
    PLoS ONE 10/2013; 8(10):e77624. DOI:10.1371/journal.pone.0077624 · 3.23 Impact Factor
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