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[PMID]: 29524680
[Au] Autor:van den Brink AMA; Gerritsen DL; de Valk MMH; Mulder AT; Oude Voshaar RC; Koopmans RTCM
[Ad] Address:De Waalboog, 'Joachim en Anna', Center for Specialized Geriatric Care, Postbus 31071, 6503 CB, Nijmegen, The Netherlands; Radboud University Medical Center, Radboud Institute for Health Sciences, Department of Primary and Community Care, Postbus 9101, 6500 HB, Nijmegen, The Netherlands. Electronic a
[Ti] Title:What do nursing home residents with mental-physical multimorbidity need and who actually knows this? A cross-sectional cohort study.
[So] Source:Int J Nurs Stud;81:89-97, 2018 Feb 26.
[Is] ISSN:1873-491X
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:OBJECTIVE: Aging societies will bring an increase in the number of long-term care residents with mental-physical multimorbidity. To optimize care for these residents, it is important to study their care needs, since unmet needs lower quality of life. To date, knowledge about care needs of residents with mental-physical multimorbidity is limited. The aim of this study was to explore (un)met care needs of residents with mental-physical multimorbidity and determinants of unmet needs. METHODS: Cross-sectional cohort study among 141 residents with mental-physical multimorbidity without dementia living in 17 geronto-psychiatric nursing home units across the Netherlands. Data collection consisted of chart review, semi-structured interviews, (brief) neuropsychological testing, and self-report questionnaires. The Camberwell Assessment of Need for the Elderly (CANE) was used to rate (un)met care needs from residents' and nursing staff's perceptions. Descriptive and multivariate regression analyses were conducted. RESULTS: Residents reported a mean number of 11.89 needs (SD 2.88) of which 24.2% (n = 2.88, SD 2.48) were unmet. Nursing staff indicated a mean number of 14.73 needs (SD 2.32) of which 10.8% (n = 1.59, SD 1.61) were unmet. According to the residents, most unmet needs were found in the social domain as opposed to the psychological domain as reported by the nursing staff. Different opinions between resident and nursing staff about unmet needs was most common in the areas accommodation, company, and daytime activities. Further, nearly half of the residents indicated 'no need' regarding behavior while the nursing staff supposed that the resident did require some kind of support. Depression, anxiety and less care dependency were the most important determinants of unmet needs. CONCLUSIONS: Systematic assessment of care needs showed differences between the perspectives of resident and nursing staff. These should be the starting point of a dialogue between them about needs, wishes and expectations regarding care. This dialogue can subsequently lead to the most optimal individually tailored care plan. To achieve this, nurses with effective communication and negotiation skills, are indispensable.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  2 / 271796 MEDLINE  
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[PMID]: 29524634
[Au] Autor:Robson E; Tweedy C; Manzanza N; Taylor JP; Atkinson P; Randall F; Reeve A; Clowry GJ; LeBeau FEN
[Ad] Address:Institute of Neuroscience, Newcastle University, Medical School, Framlington Place, Newcastle-upon-Tyne NE2 4HH, UK.
[Ti] Title:Impaired fast network oscillations and mitochondrial dysfunction in a mouse model of alpha-synucleinopathy (A30P).
[So] Source:Neuroscience;, 2018 Mar 07.
[Is] ISSN:1873-7544
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Intracellular accumulation of alpha-synuclein (α-syn) is a key pathological process evident in Lewy body dementias (LBD), including Parkinson's disease dementia (PDD) and dementia with Lewy bodies (DLB). LBD results in marked cognitive impairments and changes in cortical networks. To assess the impact of abnormal α-syn expression on cortical network oscillations relevant to cognitive function, we studied changes in fast beta/gamma network oscillations in the hippocampus in a mouse line that over-expresses human mutant α-syn (A30P). We found an age-dependent reduction in the power of the gamma (20-80 Hz) frequency oscillations in slices taken from mice aged 9-16 months (9+), that was not present in either young 2-6 months old (2+) A30P mice, or in control mice at either age. The mitochondrial blockers potassium cyanide and rotenone both reduced network oscillations in a concentration-dependent manner in aged A30P mice and aged control mice but slices from A30P mice showed a greater reduction in the oscillations. Histochemical analysis showed an age-dependent reduction in cytochrome c oxidase (COX) activity, suggesting a mitochondrial dysfunction in the 9+A30P group. A deficit in COX IV expression was confirmed by immunohistochemistry. Overall, our data demonstrate an age-dependent impairment in mitochondrial function and gamma frequency activity associated with the abnormal expression of α-syn. These findings provide mechanistic insights into the consequences of over-expression of α-syn which might contribute to cognitive decline.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  3 / 271796 MEDLINE  
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[PMID]: 29524426
[Au] Autor:Chiba-Falek O; Gottschalk WK; Lutz MW
[Ad] Address:Department of Neurology, Duke University Medical Center, Durham, NC, USA; Center for Genomic and Computational Biology, Duke University Medical Center, Durham, NC, USA. Electronic address: o.chibafalek@duke.edu.
[Ti] Title:The effects of the TOMM40 poly-T alleles on Alzheimer's disease phenotypes.
[So] Source:Alzheimers Dement;, 2018 Mar 07.
[Is] ISSN:1552-5279
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The TOMM40 poly-T is a polymorphism in intron 6 of the TOMM40 gene, which is adjacent to and in linkage disequilibrium with APOE. Roses etal identified the association between the length of TOMM40 poly-T with the risk and age of onset of late-onset Alzheimer's disease (LOAD). Following the original discovery, additional studies found associations between the TOMM40 poly-T and LOAD-related phenotypes independent of APOE genotypes, while others did not replicate these associations. Furthermore, the identity of the TOMM40 poly-T risk allele has been controversial between different LOAD-related phenotypes. Here, we propose a framework to address the conflicting findings with respect to the TOMM40 poly-T allele associations with LOAD phenotypes and their functional effects. The framework is used to interpret previous studies as means to gain insights regarding the nature of the risk allele, very long versus short. We suggest that the identity of the TOMM40 poly-T risk allele depends on the phenotype being evaluated, the ages of the study subjects at the time of assessment, and the context of the APOE genotypes. In concluding remarks, we outline future studies that will inform the mechanistic interpretation of the genetic data.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  4 / 271796 MEDLINE  
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[PMID]: 29508455
[Au] Autor:Palma JA; Kaufmann H
[Ad] Address:Department of Neurology, Dysautonomia Center, New York University School of Medicine, New York, New York, USA.
[Ti] Title:Treatment of autonomic dysfunction in Parkinson disease and other synucleinopathies.
[So] Source:Mov Disord;33(3):372-390, 2018 Mar.
[Is] ISSN:1531-8257
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Dysfunction of the autonomic nervous system afflicts most patients with Parkinson disease and other synucleinopathies such as dementia with Lewy bodies, multiple system atrophy, and pure autonomic failure, reducing quality of life and increasing mortality. For example, gastrointestinal dysfunction can lead to impaired drug pharmacodynamics causing a worsening in motor symptoms, and neurogenic orthostatic hypotension can cause syncope, falls, and fractures. When recognized, autonomic problems can be treated, sometimes successfully. Discontinuation of potentially causative/aggravating drugs, patient education, and nonpharmacological approaches are useful and should be tried first. Pathophysiology-based pharmacological treatments that have shown efficacy in controlled trials of patients with synucleinopathies have been approved in many countries and are key to an effective management. Here, we review the treatment of autonomic dysfunction in patients with Parkinson disease and other synucleinopathies, summarize the nonpharmacological and current pharmacological therapeutic strategies including recently approved drugs, and provide practical advice and management algorithms for clinicians, with focus on neurogenic orthostatic hypotension, supine hypertension, dysphagia, sialorrhea, gastroparesis, constipation, neurogenic overactive bladder, underactive bladder, and sexual dysfunction. 2018 International Parkinson and Movement Disorder Society.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Data-Review
[do] DOI:10.1002/mds.27344

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[PMID]: 29494806
[Au] Autor:Ovsepian SV; O'Leary VB; Zaborszky L; Ntziachristos V; Dolly JO
[Ad] Address:Institute for Biological and Medical Imaging, Helmholtz Zentrum Munich, German Research Center for Environmental Health, Neuherberg, Germany; Munich School of Bioengineering, Technical University Munich, Munich, Germany; International Centre for Neurotherapeutics, Dublin City University, Dublin, Ire
[Ti] Title:Synaptic vesicle cycle and amyloid : Biting the hand that feeds.
[So] Source:Alzheimers Dement;, 2018 Mar 01.
[Is] ISSN:1552-5279
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The synaptic vesicle cycle (SVC) holds center stage in the biology of presynaptic terminals. Through recurrent exocytosis and endocytosis, it facilitates a sequence of events enabling chemical neurotransmission between functionally related neurons. As a fundamental process that links the interior of nerve cells with their environment, the SVC is also critical for signaling and provides an entry route for a range of pathogens and toxins, enabling detrimental effects. In Alzheimer's disease, the SVC is both the prime site of amyloid production and toxicity. In this study, we discuss the emerging evidence for physiological and pathological effects of A on various stages of the SVC, from postfusion membrane recovery to trafficking, docking, and priming of vesicles for fusion and transmitter release. Understanding of the mechanisms of A interaction with the SVC within the unifying calcium hypothesis of aging and Alzheimer's disease should further elucidate the fundamental biology of the presynaptic terminal and reveal novel therapeutic targets for Alzheimer's disease and other age-related dementias.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  6 / 271796 MEDLINE  
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[PMID]: 29466734
[Au] Autor:Iannielli A; Bido S; Folladori L; Segnali A; Cancellieri C; Maresca A; Massimino L; Rubio A; Morabito G; Caporali L; Tagliavini F; Musumeci O; Gregato G; Bezard E; Carelli V; Tiranti V; Broccoli V
[Ad] Address:Division of Neuroscience, San Raffaele Scientific Institute, 20132 Milan, Italy.
[Ti] Title:Pharmacological Inhibition of Necroptosis Protects from Dopaminergic Neuronal Cell Death in Parkinson's Disease Models.
[So] Source:Cell Rep;22(8):2066-2079, 2018 Feb 20.
[Is] ISSN:2211-1247
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Dysfunctions in mitochondrial dynamics and metabolism are common pathological processes associated with Parkinson's disease (PD). It was recently shown that an inherited form of PD and dementia is caused by mutations in the OPA1 gene, which encodes for a key player in mitochondrial fusion and structure. iPSC-derived neural cells from these patients exhibited severe mitochondrial fragmentation, respiration impairment, ATP deficits, and heightened oxidative stress. Reconstitution of normal levels of OPA1 in PD-derived neural cells normalized mitochondria morphology and function. OPA1-mutated neuronal cultures showed reduced survival invitro. Intriguingly, selective inhibition of necroptosis effectively rescued this survival deficit. Additionally, dampening necroptosis in MPTP-treated mice protected from DA neuronal cell loss. This human iPSC-based model captures both early pathological events in OPA1 mutant neural cells and the beneficial effects of blocking necroptosis, highlighting this celldeath process as a potential therapeutic target for PD.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Data-Review

  7 / 271796 MEDLINE  
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[PMID]: 29462608
[Au] Autor:Khalil B; Morderer D; Price PL; Liu F; Rossoll W
[Ad] Address:Department of Neuroscience, Mayo Clinic, Jacksonville, FL 32224 USA.
[Ti] Title:mRNP assembly, axonal transport, and local translation in neurodegenerative diseases.
[So] Source:Brain Res;, 2018 Feb 17.
[Is] ISSN:1872-6240
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:The development, maturation, and maintenance of the mammalian nervous system rely on complex spatiotemporal patterns of gene expression. In neurons, this is achieved by the expression of differentially localized isoforms and specific sets of mRNA-binding proteins (mRBPs) that regulate RNA processing, mRNA trafficking, and local protein synthesis at remote sites within dendrites and axons. There is growing evidence that axons contain a specialized transcriptome and are endowed with the machinery that allows them to rapidly alter their local proteome via local translation and protein degradation. This enables axons to quickly respond to changes in their environment during development, and to facilitate axon regeneration and maintenance in adult organisms. Aside from providing autonomy to neuronal processes, local translation allows axons to send retrograde injury signals to the cell soma. In this review, we discuss evidence that disturbances in mRNP transport, granule assembly, axonal localization, and local translation contribute to pathology in various neurodegenerative diseases, including spinal muscular atrophy (SMA), amyotrophic lateral sclerosis (ALS), frontotemporal dementia (FTD), and Alzheimer's disease (AD).
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:Publisher

  8 / 271796 MEDLINE  
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[PMID]: 29454102
[Au] Autor:Oliveira BCL; Bellozi PMQ; Reis HJ; de Oliveira ACP
[Ad] Address:Department of Pharmacology, Universidade Federal de Minas Gerais, Belo Horizonte, 31270-901, Brazil. Electronic address: bcabraloliveira@yahoo.com.br.
[Ti] Title:Inflammation as a Possible Link Between Dyslipidemia and Alzheimer's Disease.
[So] Source:Neuroscience;376:127-141, 2018 Feb 14.
[Is] ISSN:1873-7544
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Alzheimer's disease (AD) is the leading cause of dementia worldwide. This pathological condition is characterized not only by A and tau accumulation in the central nervous system (CNS), but also by inflammation, processes that can lead to neurodegeneration. Besides that, other factors may contribute to the development of AD, such as dyslipidemias. Changes in lipid levels can either influence the activity of enzymes related to the protein deposition that occurs in this pathological condition, or enhance the peripheral and CNS immune responses. Furthermore, cholesterol-associated genes are frequently associated with AD. Here, we extensively reviewed the literature and, based on the existing evidences, we suggest inflammation as an important link between dyslipidemias and AD.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1802
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  9 / 271796 MEDLINE  
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[PMID]: 29409009
[Au] Autor:Torok J; Maia PD; Powell F; Pandya S; Raj A; Alzheimer's Disease Neuroimaging Initiative
[Ad] Address:Department of Radiology, Weill Cornell Medical College of Cornell University, 407 E. 61 Street, RR106, New York, NY 10065, USA.
[Ti] Title:A method for inferring regional origins of neurodegeneration.
[So] Source:Brain;, 2018 02 02.
[Is] ISSN:1460-2156
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Alzheimer's disease, the most common form of dementia, is characterized by the emergence and spread of senile plaques and neurofibrillary tangles, causing widespread neurodegeneration. Though the progression of Alzheimer's disease is considered to be stereotyped, the significant variability within clinical populations obscures this interpretation on the individual level. Of particular clinical importance is understanding where exactly pathology, e.g. tau, emerges in each patient and how the incipient atrophy pattern relates to future spread of disease. Here we demonstrate a newly developed graph theoretical method of inferring prior disease states in patients with Alzheimer's disease and mild cognitive impairment using an established network diffusion model and an L1-penalized optimization algorithm. Although the 'seeds' of origin using our inference method successfully reproduce known trends in Alzheimer's disease staging on a population level, we observed that the high degree of heterogeneity between patients at baseline is also reflected in their seeds. Additionally, the individualized seeds are significantly more predictive of future atrophy than a single seed placed at the hippocampus. Our findings illustrate that understanding where disease originates in individuals is critical to determining how it progresses and that our method allows us to infer early stages of disease from atrophy patterns observed at diagnosis.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:Publisher
[do] DOI:10.1093/brain/awx371

  10 / 271796 MEDLINE  
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[PMID]: 29400714
[Au] Autor:Shi Y; Lin S; Staats KA; Li Y; Chang WH; Hung ST; Hendricks E; Linares GR; Wang Y; Son EY; Wen X; Kisler K; Wilkinson B; Menendez L; Sugawara T; Woolwine P; Huang M; Cowan MJ; Ge B; Koutsodendris N; Sandor KP; Komberg J; Vangoor VR; Senthilkumar K; Hennes V; Seah C; Nelson AR; Cheng TY; Lee SJ; August PR; Chen JA; Wisniewski N; Hanson-Smith V; Belgard TG; Zhang A; Coba M; Grunseich C; Ward ME; van den Berg LH; Pasterkamp RJ; Trotti D; Zlokovic BV; Ichida JK
[Ad] Address:Department of Stem Cell Biology and Regenerative Medicine, Keck School of Medicine, University of Southern California, Los Angeles, California, USA.
[Ti] Title:Haploinsufficiency leads to neurodegeneration in C9ORF72 ALS/FTD human induced motor neurons.
[So] Source:Nat Med;24(3):313-325, 2018 Mar.
[Is] ISSN:1546-170X
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:An intronic GGGGCC repeat expansion in C9ORF72 is the most common cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD), but the pathogenic mechanism of this repeat remains unclear. Using human induced motor neurons (iMNs), we found that repeat-expanded C9ORF72 was haploinsufficient in ALS. We found that C9ORF72 interacted with endosomes and was required for normal vesicle trafficking and lysosomal biogenesis in motor neurons. Repeat expansion reduced C9ORF72 expression, triggering neurodegeneration through two mechanisms: accumulation of glutamate receptors, leading to excitotoxicity, and impaired clearance of neurotoxic dipeptide repeat proteins derived from the repeat expansion. Thus, cooperativity between gain- and loss-of-function mechanisms led to neurodegeneration. Restoring C9ORF72 levels or augmenting its function with constitutively active RAB5 or chemical modulators of RAB5 effectors rescued patient neuron survival and ameliorated neurodegenerative processes in both gain- and loss-of-function C9ORF72 mouse models. Thus, modulating vesicle trafficking was able to rescue neurodegeneration caused by the C9ORF72 repeat expansion. Coupled with rare mutations in ALS2, FIG4, CHMP2B, OPTN and SQSTM1, our results reveal mechanistic convergence on vesicle trafficking in ALS and FTD.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Data-Review
[do] DOI:10.1038/nm.4490


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