Dementia In People Research Articles

An exploration of the impact of younger-onset dementia on employment.

This study explored the emergence of dementia in people who were still working. A qualitative life course approach was used to describe the experience from the onset of dementia-related symptoms to the time when the person left the workforce. The emergence of dementia at work for the participants in this study took the form of a slow transition that initially was not noticed by co-workers. It brought about subtle changes as the person became forgetful, disorganised, made mistakes and was slower. Over time the person's job performance continued to deteriorate and others at the workplace started to realise that there was a problem. Some were seen to be poor workers and so experienced difficulties with supervisors and co-workers. Others encountered difficulties managing changing relationships at work and negotiating the complex world of the workplace. Few were able to continue working beyond their diagnosis, and several raised concerns about the lack of opportunities for people who develop dementia while still employed. Given the greater participation of older people in the workforce, findings highlight the importance of identifying and supporting workers with declining cognitive function.

Computerised cognition-based interventions for preventing dementia in people with mild cognitive impairment

Computerised cognition-based interventions for preventing dementia in people with mild cognitive impairment

Portuguese version of Wechsler Memory Scale–3rd edition’s utility with demented elderly adults

ABSTRACTThe purpose of this study is to analyze the utility of the Portuguese version of the Wechsler Memory Scale-3rd edition (WMS-III) with demented elderly people, namely its capacity to detect and discriminate between subcortical vascular dementia (SVD) and Alzheimer's disease (AD). We assessed early demented patients (SVD = 16; AD = 36) aged 65 or older who were compared to a control group (n = 40). Both clinical groups were adequately matched in terms of disease severity, overall cognitive functioning, depressive symptomatology, and pre-morbid intelligence. Between-group's differences were evaluated using the Quade's rank analysis of covariance. We also computed indexes and subtests optimal cut-off scores, and the corresponding sensitivity, specificity, and positive and negative predictive values, which were able to successfully discriminate between patients and healthy subjects. The SVD patients had a better overall memory performance than AD patients on the majority of the indexes and the delayed condition subtests of the WMS-III. The AD patients only showed a better performance on digit span subtest. Several measures discriminated patients from healthy subjects. This study suggests some recommendations for the diagnostic accuracy of the Portuguese version of WMS-III in dementia and about differential diagnosis between SVD and AD.

Benzodiazepines Not Causally Related to Increased Dementia Risk

mentia and co Benzodiazepine use by elderly adults did not seem to be causally related to an increased risk for degnitive decline, according to results from a prospective study. The study included 3,434 individuals 65 or older without dementia. For at least 10 years prior to enrollment in the study, all participants had been members of Group Health, an integrated health delivery system in the Northwest United States that maintains computerized pharmacy data, including names, strengths, dates dispensed, and amounts dispensed of drugs used by its members. Thirty percent of participants had filled at least one prescription for a benzodiazepine in the 10 years before entering the study, with 3% of participants having used the drug within 6 months of study entry. The researchers categorized patients based on their level of use, with patients falling into the highest-use category having taken at least 121 total standardized daily doses (TSDDs). The median level of use within that group was 375 TSDDs, equivalent to slightly over a year of daily use. The researchers found no association between the use of benzodiazepines at the TSDD level defined as highest use in this study and dementia (HR, 1.07) or Alzheimer’s disease (HR, 0.95), compared with nonuse. “When we split the highest category of benzodiazepine use into two groups, the hazard ratio for dementia was 1.11 (0.78–1.58) for 121–364 TSDDs and 1.03 (0.73–1.44) for greater than or equal to 365 TSDDs. Findings for Alzheimer’s disease were similar,” said Shelly L. Gray, PharmD, professor of pharmacy at the University of Washington School of Pharmacy, Seattle, and her colleagues [BMJ 2016;352:i90 doi: http://dx.doi. org/10.1136/bmj.i90]. A slightl y increased risk for dementia benzodiazepine use but no increased of dementia and that these drugs are for study participants classified as low risk in those with the highest level of associated with many adverse events, users (taking 1–30 TSDDs) or moderate exposure. ... Overall, our pattern of health care providers are still advised to users (taking 31–120 TSDDs) of benzofindings does not support the theory avoid benzodiazepines in older adults to diazepine was found, when compared that cumulative benzodiazepine use at prevent important adverse health outwith nonusers. Low users of benzodithe levels observed in our population comes, withdrawal, and dependence,” azepine were also at increased risk for is causally related to an increased risk according to the researchers. CfA Alzheimer’s disease (HR, 1.27). for dementia or cognitive decline. ... “W e found a slightly higher risk of Nonetheless, given the mixed evidence Katie Wagner Lennon is a web content dementia in people with the lowest regarding benzodiazepines and risk editor with Frontline Medical News. Benzodiazepines Not Causally Related to Increased Dementia Risk

The development of Attitudes of People from Ethnic Minorities to Help-Seeking for Dementia (APEND): a questionnaire to measure attitudes to help-seeking for dementia in people from South Asian backgrounds in the UK.

People from South Asian backgrounds present to dementia services relatively late, often responding to crises. We aimed to devise and validate a theory of planned behaviour questionnaire to measure attitudes that predict medical help-seeking for UK-based South Asian people, to assess the effectiveness of future interventions promoting earlier help-seeking. We used focus groups to establish the content validity of culturally relevant questionnaire items, then asked participants to complete the questionnaire. We analysed reliability and validity and established the concurrent validity of questionnaire attitudes through correlation with willingness to seek help from a doctor for memory problems. We also correlated the scale with knowledge of dementia. The strongest predictor of willingness to seek help was perceived social pressure from significant others around help-seeking; these attitudes were associated with beliefs about the views of family members and embarrassment around help-seeking. Willingness to seek help was also strongly associated with attitudes about the benefits of seeing a doctor for memory problems, attitudes that were related to specific beliefs about what doctors can do to help. Attitudes in the questionnaire predicted 77% of variance in willingness to seek help, but no relationship was found with dementia knowledge. We present the Attitudes of People from Ethnic Minorities to Help-Seeking for Dementia (APEND) questionnaire, a valid and reliable measure of attitudes that influence help-seeking for dementia in people from South Asian backgrounds, which could assess the impact of intervention studies. We suggest that interventions target attitudes specified here, rather than dementia knowledge. Copyright © 2016 John Wiley & Sons, Ltd.

Assessments for dementia in people with learning disabilities

Assessments for dementia in people with learning disabilities

Statins for the prevention of dementia.

This is an update of a Cochrane review first published in 2001 and then updated in 2009. Vascular risk factors including high cholesterol levels increase the risk of dementia due to Alzheimer's disease and of vascular dementia. Some observational studies have suggested an association between statin use and lowered incidence of dementia. To evaluate the efficacy and safety of statins for the prevention of dementia in people at risk of dementia due to their age and to determine whether the efficacy and safety of statins for this purpose depends on cholesterol level, apolipoprotein E (ApoE) genotype or cognitive level. We searched ALOIS (the Specialized Register of the Cochrane Dementia and Cognitive Improvement Group), The Cochrane Library, MEDLINE, EMBASE, PsycINFO, CINAHL, LILACS, ClinicalTrials.gov and the World Health Organization (WHO) Portal on 11 November 2015. We included double-blind, randomised, placebo-controlled trials in which statins were administered for at least 12 months to people at risk of dementia. We used standard methodological procedures expected by Cochrane. We included two trials with 26,340 participants aged 40 to 82 years of whom 11,610 were aged 70 or older. All participants had a history of, or risk factors for, vascular disease. The studies used different statins (simvastatin and pravastatin). Mean follow-up was 3.2 years in one study and five years in one study. The risk of bias was low. Only one study reported on the incidence of dementia (20,536 participants, 31 cases in each group; odds ratio (OR) 1.00, 95% confidence interval (CI) 0.61 to 1.65, moderate quality evidence, downgraded due to imprecision). Both studies assessed cognitive function, but at different times using different scales, so we judged the results unsuitable for a meta-analysis. There were no differences between statin and placebo groups on five different cognitive tests (high quality evidence). Rates of treatment discontinuation due to non-fatal adverse events were less than 5% in both studies and there was no difference between statin and placebo groups in the risk of withdrawal due to adverse events (26,340 participants, 2 studies, OR 0.94, 95% CI 0.83 to 1.05). There is good evidence that statins given in late life to people at risk of vascular disease do not prevent cognitive decline or dementia. Biologically, it seems feasible that statins could prevent dementia due to their role in cholesterol reduction and initial evidence from observational studies was very promising. However, indication bias may have been a factor in these studies and the evidence from subsequent RCTs has been negative. There were limitations in the included studies involving the cognitive assessments used and the inclusion of participants at moderate to high vascular risk only.

Primary and secondary prevention interventions for cognitive decline and dementia - An overview

Dementia is a syndrome characterised by deterioration in memory, thinking, behaviour, and the ability to perform everyday activities, which ultimately may lead to total dependence and death. Since the world’s population is steadily growing older, the number of people with dementia is also increasing. It is therefore of utmost importance to identify effective strategies to prevent or delay its onset.The key findings of this overview of reviews are based on evidence from eight systematic reviews. The results for the single interventions targeting cognitively healthy people suggest that compared to controls: Antihypertensive drugs may lead to a slight decrease in incidence of dementia in people with hypertension (low certainty of evidence). Statin therapy probably leads to little or no difference on incidence of dementia in people with, or at risk of, cardiovascular disease (moderate certainty). Omega-3 Fatty Acids (FAs) probably lead to little or no effect on cognitive test scores (moderate to high certainty). Computerised cognitive training probably leads to a slight improvement in cognitive test scores directly after the training (moderate certainty). Aerobic exercise may lead to little or no effect on cognitive test scores (low certainty). The results for the interventions targeting people with mild cognitive impairment suggest that compared to control: Cholinesterase inhibitors probably lead to a slight decrease in dementia incidence, but to significantly more adverse events (moderate certainty). Vitamin E probably leads to little or no difference in incidence of Alzheimer’s dementia (moderate certainty). Omega-3 FAs probably lead to little or no difference in cognitive test scores (moderate to high certainty). We did not find any reviews that evaluated the effects of interventions targeting more than one risk factor, and we can therefore not say anything about the combined effects of these interventions.

Down Syndrome and Dementia: Relationship and Clinical features

Down syndrome (DS) is the most common genetic cause for Mental Retardation (MR). Many individuals with DS now are living into middle and older adulthood and experiencing age related health problems including dementia. People with Down syndrome have an increased risk of developing Dementia of Alzheimer Type (DAT) from middle age on. The comorbid picture of Down syndrome and Dementia of Alzheimer Type presents a unique challenge to the clinician in both diagnosis and management. The purpose of this article is to describe the relationship between DS and DAT and to present a framework for clinical assessment and management of dementia in people with DS.

Cognitive function, depressive symptoms, function level, and quality of life in mild dementia and amnestic-mild cognitive impairment

The present study aimed to investigate the relationship among neurocognitive variables, depressive symptoms, functional activities, and the quality of life (QoL) in patients with mild dementia and single-domain amnestic mild cognitive impairment (a-MCI). Materials and Methods: Thirty-seven mild dementia patients and thirty a-MCI participants were recruited. All subjects participated in a series of neuropsychological measures (Cognitive Abilities Screening Instrument, family pictures, and digit span), geriatric depression scale‑15 (GDS-15), activities of daily living (ADL), The Lawton instrumental ADL scale (IADL) and QoL‑Alzheimer’s disease. Results: Multiple regression analysis revealed that only depressive symptoms was a predictor for the QoL in mild dementia (β= -0.56, P ＜ 0.001). In contrast, all variables were not associated with the QoL in a‑MCI. Mildly demented people scored significantly lower on most aspects of cognitive functioning and reported poorer performances on IADL than a-MCI. There were no significant differences on GDS, ADL, and QoL between the two groups. Conclusion: Findings indicated that depressive symptoms contributed to the QoL in mild dementia. Interventions targeting depressive symptoms in mild dementia may improve their QoL during their early stages of dementia.

Role of Trisomy 21 Mosaicism in Sporadic and Familial Alzheimer's Disease.

Trisomy 21 and the consequent extra copy of the amyloid precursor protein (APP) gene and increased beta-amyloid (Aβ) peptide production underlie the universal development of Alzheimer's disease (AD) pathology and high risk of AD dementia in people with Down syndrome (DS). Trisomy 21 and other forms of aneuploidy also arise among neurons and peripheral cells in both sporadic and familial AD and in mouse and cell models thereof, reinforcing the conclusion that AD and DS are two sides of the same coin. The demonstration that 90% of the neurodegeneration in AD can be attributed to the selective loss of aneuploid neurons generated over the course of the disease indicates that aneuploidy is an essential feature of the pathogenic pathway leading to the depletion of neuronal cell populations. Trisomy 21 mosaicism also occurs in neurons and other cells from patients with Niemann-Pick C1 disease and from patients with familial or sporadic frontotemporal lobar degeneration (FTLD), as well as in their corresponding mouse and cell models. Biochemical studies have shown that Aβ induces mitotic spindle defects, chromosome mis-segregation, and aneuploidy in cultured cells by inhibiting specific microtubule motors required for mitosis. These data indicate that neuronal trisomy 21 and other types of aneuploidy characterize and likely contribute to multiple neurodegenerative diseases and are a valid target for therapeutic intervention. For example, reducing extracellular calcium or treating cells with lithium chloride (LiCl) blocks the induction of trisomy 21 by Aβ. The latter finding is relevant in light of recent reports of a lowered risk of dementia in bipolar patients treated with LiCl and in the stabilization of cognition in AD patients treated with LiCl.

TMEM106B, a frontotemporal lobar dementia (FTLD) modifier, associates with FTD-3-linked CHMP2B, a complex of ESCRT-III.

BackgroundTransmembrane protein 106B (TMEM106B) has been identified as a risk factor for frontotemporal lobar degeneration, which is the second most common form of progressive dementia in people under 65 years of age. Mutations in charged multivesicular body protein 2B (CHMP2B), which is involved in endosomal protein trafficking, have been found in chromosome 3-linked frontotemporal dementia. Despite the number of studies on both CHMP2B and TMEM106B in the endolysosomal pathway, little is known about the relationship between CHMP2B and TMEM106B in the endosomal/autophagy pathway.ResultsThis study found that endogenous TMEM106B was partially sequestered in CHMP2B-positive structures, suggesting its possible involvement in endosomal sorting complexes required for transport (ESCRT)-associated pathways. The role of single nucleotide polymorphisms of TMEM106B (T185, S185, or S134N) in the ESCRT-associated pathways were characterized. The T185 and S185 variants were more localized to Rab5-/Rab7-positive endosomes compared with S134N, while all of the variants were more localized to Rab7-positive endosomes compared to Rab5-positive endosomes. T185 was more associated with CHMP2B compared to S185. Autophagic flux was slightly reduced in the T185-expressing cells compared to the control or S185-expressing cells. Moreover, T185 slightly enhanced the accumulation of EGFR, impairments in autophagic flux, and neurotoxicity that were caused by CHMP2BIntron5 compared to S185-expressing cells.ConclusionsThese findings suggest that the T185 variant functions as a risk factor in neurodegeneration with endolysosomal defects. This study provides a better understanding of pathogenic functions of TMEM106B, which is a risk factor for the progression of neurodegenerative diseases that are associated with endosomal defects in the aged brain.Electronic supplementary materialThe online version of this article (doi:10.1186/s13041-015-0177-z) contains supplementary material, which is available to authorized users.

Dietary interventions for prevention of dementia in people with mild cognitive impairment

This is the protocol for a review and there is no abstract. The objectives are as follows: In this review we set out to evaluate the effects of dietary interventions for prevention of dementia in people with mild cognitive impairment (MCI).

The Soul in Dementia: Falling in Love in a Dementia Clinic

In spiritual care, demented people also present symptoms reminiscent of those often encountered during an analytical cure in certain psychoses and in neuroses involving narcissism or melancholia: that is, some psychic indifference toward the processes of credere and transfer, and love as such. Clinics devoted to the spiritual care of people with dementia question the role of the credere and love in their most crucial aspects for psychic health. How and why do these patients fall in love? A study of the clinical implications of these questions in relation with observations gathered among people suffering from severe dementia should allow us a better understanding of the meaning of soul, consciousness, and cognition.

Cognitive impairments may mimic delusions

Delusions are often recognized as key to the concept of psychosis. What is delusion is one of the basic questions of psychopathology. The common denominator of definitions of delusions is the divergence between the strong conviction in the delusional belief and superior evidences to the contrary which are continually ignored. An implicit, sustainably unspoken assumption is that the person with delusional belief has cognitive capacities to process the (counter-)arguments relevant to their delusion. However, individual’s cognitive capacities are not being emphasized when delusions are evaluated. Moreover, the impact of cognitive decline on formation of delusions is neglected, both in theory and practice. We elaborate that cognitive deficits may facilitate, oppose, or mimic delusions. We focus on the last, which can lead to diagnosing as delusion what could be explained by cognitive decline and better called pseudo-delusion. The risk is significant when cognition is impaired, as in demented people; an issue which has not yet been debated. True delusions are incompatible with person’s cognitive capacities, i.e., if we take into account person’s cognitive status, we still cannot understand how the person holds the strange belief with an extraordinary conviction. Pseudo-delusions would be beliefs, thoughts or judgments that at first seem delusional (they are false, subculturally atypical beliefs that are strongly maintained in the face of counterargument), but lose the essence of delusions after we take cognitive impairment into account. Pseudo-delusions could actually be explained or understood by person’s cognitive impairments, they “fit into” them. The reported reality-based contents of delusions in the elderly, poor response to antipsychotics and lack of association with early or family history of psychiatric disorders could in part be accounted for by the bias of misdiagnosing the cognitive impairment as the delusion. Not recognizing that the cognitive impairment underlies formation of pseudo-delusions and misdiagnosing it as delusions may lead to focusing on antipsychotic treatment, instead on treatment of the underlying cognitive deficit.

Care considerations for dementia in people with Down's syndrome: a management perspective.

Dementia is common in people with Down's syndrome as they age. Having dementia raises huge care considerations for carers and staff. Excellence in care requires attention to a wide variety of interrelated issues. Carers and staff need to have a good understanding of what it means to have dementia to deliver person-centered care. In addition, they need to be clear at all stages of the disease about the outcomes they want to achieve for the person. This will necessitate taking into account both health and social care issues, as well as looking at the physical environment. Staffing and staff training are crucial in providing the right support at the right time. Finally, a vignette of excellence in care is presented.

Effect of an interactive therapeutic robotic animal on engagement, mood states, agitation and psychotropic drug use in people with dementia: a cluster-randomised controlled trial protocol

IntroductionApathy, agitated behaviours, loneliness and depression are common consequences of dementia. This trial aims to evaluate the effect of a robotic animal on behavioural and psychological symptoms of dementia in...

Qualifications for nurses for the care of patients with dementia and support to their caregivers: A pilot evaluation of the dementia care management curriculum

A substantial increase of people with dementia (PwD) is predicted for the future. Nurses are taking over important tasks to support PwD, which requires a specialized qualification. The aim was to identify points for revision and to further improve the Dementia Care Manager (DCM) curriculum as a basis for probable qualification of nurses caring for PwD. We conducted a summative evaluation study to revise the first version of the DCM curriculum. The study was conducted in the primary health care setting. Nurses and lecturers of the first theoretical and practical implementation were involved. Questionnaire-based interviews with nurses and lecturers after every module during the theoretical qualification. Besides, nurses rated the curriculum after the end of the theoretical part and evaluated the DCM tasks and the usefulness of the curriculum contents after the practical phase in questionnaire-based interviews. Descriptive statistics were used for analysis. A total of five nurses and 33 lecturers participated in the first theoretical and practical implementation of the DCM qualification. Generally, nurses and lecturers assessed the curriculum contents as "very important" or "important." In particular, the job-related issues, the variety of course topics and the close combination of theory and practice were highly valued. The practical implementation of the DCM was rated predominantly as "important" by nurses for the delivery of care for PwD. To optimize the theoretical DCM curriculum, participants suggested increasing the number of lessons for two of the modules (gerontopsychiatry, interdisciplinary case reviews). Furthermore, nurses preferred a longer practical phase, whereas some lecturers called for larger group sizes of participants. The DCM qualification enhances nurses' competencies to care for PwD. The curriculum regards an interprofessional, cooperative team approach as the potential to improve health care supply for demented people and to better support their caregivers.

Psychotherapy for depression in older veterans via telemedicine: a randomised, open-label, non-inferiority trial

Many older adults with major depression, particularly veterans, do not have access to evidence-based psychotherapy. Telemedicine could increase access to best-practice care for older adults facing barriers of mobility, stigma, and geographical isolation. We aimed to establish non-inferiority of behavioural activation therapy for major depression delivered via telemedicine to same-room care in largely male, older adult veterans. In this randomised, controlled, open-label, non-inferiority trial, we recruited veterans (aged ≥58 years) meeting DSM-IV criteria for major depressive disorder from the Ralph H Johnson Veterans Affairs Medical Center and four associated community outpatient-based clinics in the USA. We excluded actively psychotic or demented people, those with both suicidal ideation and clear intent, and those with substance dependence. The study coordinator randomly assigned participants (1:1; block size 2-6; stratified by race; computer-generated randomisation sequence by RGK) to eight sessions of behavioural activation for depression either via telemedicine or in the same room. The primary outcome was treatment response according to the Geriatric Depression Scale (GDS) and Beck Depression Inventory (BDI; defined as a 50% reduction in symptoms from baseline at 12 months), and Structured Clinical Interview for DSM-IV, clinician version (defined as no longer being diagnosed with major depressive disorder at 12 months follow-up), in the per-protocol population (those who completed at least four treatment sessions and for whom all outcome measurements were done). Those assessing outcomes were masked. The non-inferiority margin was 15%. This trial is registered with ClinicalTrials.gov, number NCT00324701. Between April 1, 2007, and July 31, 2011, we screened 780 patients, and the study coordinator randomly assigned participants to either telemedicine (120 [50%]) or same-room treatment (121 [50%]). We included 100 (83%) patients in the per-protocol analysis in the telemedicine group and 104 (86%) in the same-room group. Treatment response according to GDS did not differ significantly between the telemedicine (22 [22·45%, 90% CI 15·52-29·38] patients) and same-room (21 [20·39%, 90% CI 13·86-26·92]) groups, with an absolute difference of 2·06% (90% CI -7·46 to 11·58). Response according to BDI also did not differ significantly (telemedicine 19 [24·05%, 90% CI 16·14-31·96] patients; same room 19 [23·17%, 90% CI 15·51-30·83]), with an absolute difference of 0·88% (90% CI -10·13 to 11·89). Response on the Structured Clinical Interview for DSM-IV, clinician version, also did not differ significantly (39 [43·33%, 90% CI 34·74-51·93] patients in the telemedicine group and 46 [48·42%, 90% CI 39·99-56·85] in the same-room group), with a difference of -5·09% (-17·13 to 6·95; p=0·487). Results from the intention-to-treat population were similar. MEM analyses showed that no significant differences existed between treatment trajectories over time for BDI and GDS. The criteria for non-inferiority were met. We did not note any adverse events. Telemedicine-delivered psychotherapy for older adults with major depression is not inferior to same-room treatment. This finding shows that evidence-based psychotherapy can be delivered, without modification, via home-based telemedicine, and that this method can be used to overcome barriers to care associated with distance from and difficulty with attendance at in-person sessions in older adults. US Department of Veterans Affairs.

Reelin protects against amyloid β toxicity in vivo.

Alzheimer's disease (AD) is a currently incurable neurodegenerative disorder and is the most common form of dementia in people over the age of 65 years. The predominant genetic risk factor for AD is the ε4 allele encoding apolipoprotein E (ApoE4). The secreted glycoprotein Reelin enhances synaptic plasticity by binding to the multifunctional ApoE receptors apolipoprotein E receptor 2 (Apoer2) and very low density lipoprotein receptor (Vldlr). We have previously shown that the presence of ApoE4 renders neurons unresponsive to Reelin by impairing the recycling of the receptors, thereby decreasing its protective effects against amyloid β (Aβ) oligomer-induced synaptic toxicity in vitro. We showed that when Reelin was knocked out in adult mice, these mice behaved normally without overt learning or memory deficits. However, they were strikingly sensitive to amyloid-induced synaptic suppression and had profound memory and learning disabilities with very low amounts of amyloid deposition. Our findings highlight the physiological importance of Reelin in protecting the brain against Aβ-induced synaptic dysfunction and memory impairment.