Participation in everyday activities among young adult relatives of parents with dementia - A qualitative study.

Previous research has shown that young adult relatives of parents with dementia experience strain through increased responsibility and changed relationships in the family with potential consequences for their emotional, mental and physical well-being. Less is known about how young adult relatives experience their participation in everyday activities typically associated with young adulthood and how their participation is affected by the parent´s dementia. This study explores young adult relatives' experiences of participation in everyday activities and how their participation was affected by having a parent with dementia. The study followed a qualitative, descriptive approach. Semi-structured individual interviews with 11 young adult relatives (aged 21 - 31) of parents with dementia were conducted. The interviews were analysed using Kirsti Malterud's iterative cross case analysis method 'Systematic text condensation'. The analysis identified three categories: Dilemmas of choosing, Not having a choice and Reversal of roles. The young adult relatives experienced dilemmas and constraints regarding participation in everyday activities usually related to young adulthood. They navigated situations where they were to choose between the parent with dementia and their own everyday activities and they often downgraded or cancelled participation in own activities related to leisure time, school, job and career. Moreover, their participation seemed affected by chores and responsibilities resulting in a lack of energy leading them to forego social activities in particular or change their choice of activities. The young adult relatives need help and support in their everyday lives. Health care professionals are encouraged to focus on relieving them from some of the responsibilities and practical tasks enabling them to live their own lives as young adults, while being part of the family and contributing towards the responsibilities and tasks with which they can cope.

Carers' experience of everyday life impacted by people with dementia who attended a cognitive stimulation therapy (CST) group intervention: a qualitative systematic review.

ObjectivesTo explore carers' experiences of everyday life impacted by people with dementia who attended a seven-week cognitive stimulation therapy (CST) group intervention.MethodsA systematic review of qualitative studies and qualitative mixed method studies was conducted. Eight databases were searched. The selected studies were screened and assessed for methodological quality using the Rayyan Qatar Computing Research Institute (QCRI) and Critical Appraisal Skills Programme Qualitative Checklist (CASP-QC). Three studies were included following an inductive content analysis.ResultsTwo themes were identified: 'Enrichment by enhanced communication' and 'Growth through positive emotional interaction'.ConclusionQualitative research on the impact of the CST group intervention on carers' everyday life with a person with dementia is scarce. Carers experienced feelings of enrichment due to improvement and equality in communication and a possible source of happiness. There was a sense of togetherness and reconnection through music and singing together as well as a sense of mutual growth, increased positive interaction, increased ability to socialize, and feelings of fondness when experiencing glimpses of the previous personality of the person with dementia. Nevertheless, knowledge about the impact of the CST group intervention on carers' personal everyday life is lacking and requires further research.

UnderstAID, an ICT Platform to Help Informal Caregivers of People with Dementia: A Pilot Randomized Controlled Study.

Information and communications technology (ICT) could support ambient assisted living (AAL) based interventions to provide support to informal caregivers of people with dementia, especially when they need to cope with their feelings of overburden or isolation. An e-learning platform (understAID application) was tested by informal caregivers from Denmark, Poland, and Spain to explore the technical and the pedagogical specifications, as well as evaluating the impact of its use on the psychological status of the participants. 61 informal caregivers completed the study taking part in the experimental (n = 30) or control (n = 31) groups. 33.3% of the caregivers were satisfied with the application and around 50% of the participants assessed it as technically and pedagogically acceptable. After using understAID the caregivers in the experimental group significantly decreased their depressive symptomatology according to the Center for Epidemiologic Studies Depression scale, but a possible benefit on their feelings of competence and satisfaction with the caring experience was also observed. The low scores obtained for satisfaction were highlighting issues that need to be modified to meet the informal caregivers' needs in national, social, and cultural context. Some possible biases are also considered and discussed to be taken into account in future improvements of understAID application.

What causes grief in dementia caregivers?

Alzheimer's disease (AD) is the most prevalent neurodegenerative disease in the world. Most AD patients become dependent on their relatives, i.e. family caregivers. Providing care to a person with AD influences caregiver's life and leads to feelings of grief, which often precede caregiver depression. The purpose of the article was to evaluate the Meuser and Marwit Caregiver Grief Inventory (MM-CGI-50) for use in Polish family caregivers and to find out determinants of grief of family caregivers of AD individuals living in Poland. A sample of 151 spouse and adult child caregivers of community-dwelling AD patients (95 females and 56 males) was interviewed to determine the influence of such factors as caregiver's age, gender, family relation to the care recipient (CR) and caregiving-related changes in caregiver's working time, leisure time and material status to find out the impact of caregiving role on intensity of caregiver grief. Caregiver grief was measured by means of MM-CGI-50. Additionally, carers were administered a questionnaire including patient's and caregiver's demographics. Also, CR's dementia assessment was informant-based and determined with investigator-administered clinical dementia rating (CDR) scale. Of all analyzed factors, only caregiver's informant dementia rating significantly influenced caregiver grief. To conclude, the effect of caregiver's age, gender, family relation to the CR and caregiving-related changes in caregiver's working time; leisure time and material status could not be found. To add, MM-CGI-50 can be effectively used to assess grief in Polish family caregivers of AD patients.

Differences in origin of reactive microglia in bone marrow chimeric mouse and rat after transient global ischemia.

Current understanding of microglial involvement in disease is influenced by the observation that recruited bone marrow (BM)-derived cells contribute to reactive microgliosis in BM-chimeric mice. In contrast, a similar phenomenon has not been reported for BM-chimeric rats. We investigated the recruitment and microglial transformation of BM-derived cells in radiation BM-chimeric mice and rats after transient global cerebral ischemia, which elicits a characteristic microglial reaction. Both species displayed microglial hyperplasia and rod cell transformation in the hippocampal CA1 region. In mice, a subpopulation of lesion-reactive microglia originated from transformed BM-derived cells. By contrast, no recruitment or microglial transformation of BM-derived cells was observed in BM-chimeric rats. These results suggest that reactive microglia in rats originate from resident microglia, whereas they have a mixed BM-derived and resident origin in mice, depending on the severity of ischemic tissue damage.

Multilocus sequence typing of Enterococcus faecalis isolates demonstrating different lesion types in broiler breeders.

A total of 69 isolates of Enterococcus faecalis from broiler breeders demonstrating different lesion types and representing eight different flocks were characterized by multilocus sequence typing. Twenty isolates obtained from healthy birds representing two additional flocks were included for comparison. A total of 12 different sequence types (STs) was obtained. Correlation between ST and lesion type was not demonstrated. However, three STs (ST82, ST174, ST177) made up 81% of the isolates associated with lesions, indicating that these STs might be particularly associated with birds. In addition, ST174, the most frequently demonstrated ST, was only obtained from affected birds. Surprisingly, ST82, previously reported to be associated with amyloid arthropathy in layers worldwide, demonstrated a high degree of diversity as to lesion types, just as healthy carriers were demonstrated among broiler breeders. STs associated with healthy birds and lesions, respectively, did not demonstrate a phylogenetic relationship.

Comparative studies on [Pasteurella] testudinis and [P.] testudinis-like bacteria and proposal of Chelonobacter oris gen. nov., sp. nov. as a new member of the family Pasteurellaceae.

A collection of 12 strains, isolated from diseased tortoises and tentatively identified as [Pasteurella] testudinis-like based on phenotypic characters, was compared with three reference strains of [P.] testudinis. All strains could be separated from the reference strains with respect to 16S rRNA gene sequences, partial sequences of the rpoB housekeeping gene and by phenotypic characters. Based upon differences in 16S rRNA and rpoB gene sequences, the new isolates are suggested to represent a novel species in a new genus of the family Pasteurellaceae Pohl 1981, for which the name Chelonobacter oris gen. nov., sp. nov. is proposed. The type strain is 1662(T) (=CCUG 55632(T)=DSM 21392(T)). beta-Haemolysis and acid production from (+)-l-arabinose, dulcitol, (-)-d-mannitol, (+)-d-mannose, trehalose and salicin separated the new strains from members of existing genera of the family Pasteurellaceae, in addition to the beta-galactosidase, urease and alpha-glucosidase reactions. Differences in indole production, phosphatase, beta-glucosidase and production of acid from dulcitol and trehalose separated C. oris from [P.] testudinis. Several phenotypic characters separated C. oris from Bisgaard's taxa 14 and 32.

Microglia protect neurons against ischemia by synthesis of tumor necrosis factor.

Microglia and infiltrating leukocytes are considered major producers of tumor necrosis factor (TNF), which is a crucial player in cerebral ischemia and brain inflammation. We have identified a neuroprotective role for microglial-derived TNF in cerebral ischemia in mice. We show that cortical infarction and behavioral deficit are significantly exacerbated in TNF-knock-out (KO) mice compared with wild-type mice. By using in situ hybridization, immunohistochemistry, and green fluorescent protein bone marrow (BM)-chimeric mice, TNF was shown to be produced by microglia and infiltrating leukocytes. Additional analysis demonstrating that BM-chimeric TNF-KO mice grafted with wild-type BM cells developed larger infarcts than BM-chimeric wild-type mice grafted with TNF-KO BM cells provided evidence that the neuroprotective effect of TNF was attributable to microglial- not leukocyte-derived TNF. In addition, observation of increased infarction in TNF-p55 receptor (TNF-p55R)-KO mice compared with TNF-p75R and wild-type mice suggested that microglial-derived TNF exerts neuroprotective effects through TNF-p55R. We finally report that TNF deficiency is associated with reduced microglial population size and Toll-like receptor 2 expression in unmanipulated brain, which might also influence the neuronal response to injury. Our results identify microglia and microglial-derived TNF as playing a key role in determining the survival of endangered neurons in cerebral ischemia.

Proliferating resident microglia express the stem cell antigen CD34 in response to acute neural injury.

Reactive microgliosis is a highly characteristic response to neural injury and disease, which may influence neurodegenerative processes and neural plasticity. We have investigated the origin and characteristics of reactive microglia in the acute phase of their activation in the dentate gyrus following transection of the entorhino-dentate perforant path projection. To investigate the possible link between microglia and hematopoietic precursors, we analyzed the expression of the stem cell marker CD34 by lesion-reactive microglia in conjunction with the proliferation marker bromodeoxyuridine (BrdU) and the use of radiation bone marrow (BM) chimeric mice. We found that CD34 is upregulated on early-activated resident microglia, rather than by infiltrating bone marrow-derived cells. The number of CD34(+) microglia peaked at day 3 when 67% of the resident CD11b/Mac-1(+) microglia co-expressed CD34, and all CD34(+) cells co-expressed Mac-1, and decreased sharply toward day 5, unlike Mac-1, which was maximally expressed at day 5. Approximately 80% of the CD34(+) cells in the denervated dentate gyrus had incorporated BrdU into their nuclei at day 3. We also showed that CD34 is upregulated on early-activated microglia in the facial motor nucleus following peripheral axotomy. The results suggest lesion-reactive microglia to consist of functionally distinct subpopulations of cells; a major population of activated resident CD34(+)Mac-1(+) microglia with a high capacity for self-renewal, and a subpopulation of CD34(-)Mac-1(+) microglia which has a mixed extrinsic and intrinsic origin and whose proliferative capacity is unknown.

A role for interferon-gamma in focal cerebral ischemia in mice.

The pro-inflammatory cytokine interferon-gamma (IFNgamma) has traditionally been associated with inflammatory CNS disease and more recently with ischemia-induced pathology. Using a murine model of focal cerebral ischemia, we found no evidence for induction of IFNgamma mRNA after permanent middle cerebral artery occlusion. In addition, we found that mice deficient in IFNgamma or IFNgamma receptors developed neocortical infarcts similar in size to those in wild type. In contrast, MBP promoter-IFNgamma-transgenic mice consistently developed significantly larger infarcts than non-transgenic mice. Because IFNgamma is a potent activator of microglia-macrophages, we investigated the involvement of microglial-macrophage-derived TNF in the larger infarcts. Numbers of TNF mRNA-expressing microglia-macrophages and levels of TNF mRNA and TNF in IFNgamma-transgenic and non-transgenic mice were similar. Furthermore, the ischemic brain damage in IFN-gamma-transgenic mice was unaffected by recombinant soluble TNF receptor I. Taken together, the data argues against a role for IFNgamma in cerebral ischemia under normal conditions. However, when present, IFNgamma significantly exacerbates ischemia-induced brain damage by mechanisms that appear to be independent of TNF or synergistic neurotoxic interactions of IFNgamma and TNF Irrespective of the mechanism(s) involved, this enhancing effect of IFNgamma on ischemia-induced neurotoxicity may need to be considered in diseases where immune IFNgamma is involved, such as multiple sclerosis.

Microglial-macrophage synthesis of tumor necrosis factor after focal cerebral ischemia in mice is strain dependent.

Commonly used inbred mouse strains display substantial differences in sensitivity to focal cerebral ischemia. Such differences can often be ascribed to differences in vascular anatomy. The authors investigated whether a contributing factor could be strain-related differences in cellular synthesis of the pleiotropic and potential neurotoxic cytokine tumor necrosis factor (TNF) in the border zone of and within the focal cerebral infarct. In all mouse strains investigated they found that TNF was synthesized by infarct and periinfarct infiltrating Mac-1 immunopositive microglia-macrophages. BALB/c mice, which developed the largest infarcts, contained significantly fewer TNF-producing microglia-macrophages compared with SJL and C57BL/6 mice at both 12 and 24 hours after permanent occlusion of the distal part of the middle cerebral artery. SJL mice developed larger infarcts than C57BL/6 mice, whereas the number of TNF-producing microglia-macrophages per infarct volume unit was comparable. Western blotting data confirmed the increased TNF levels in SJL mice compared with BALB/c and C57BL/6 mice. Furthermore, mice with 12-hour postischemic survival consistently contained two-to threefold more TNF-producing microglia-macrophages than mice with 24-hour survival. The data show that the magnitude of the cellular TNF response to cerebral ischemia is strain dependent, while the time-profile and the cellular sources of TNF are similar irrespective of genetic background. Furthermore, the lack of correlation between infarct size and cellular TNF response suggests that the functionally important TNF is produced in the very early phase (minutes to a few hours) after induction of ischemia, just as it raises the possibility that different mouse strains display different sensitivities to TNF.