51 research outputs found

    A two decade dementia incidence comparison from the Cognitive Function and Ageing Studies I and II.

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    Dramatic global increases in future numbers of people with dementia have been predicted. No multicentre population-based study powered to detect changes over time has reported dementia incidence. MRC Cognitive Function and Ageing Study (CFAS) undertook baseline interviews in populations aged 65+ years in England and Wales (1989-1994). Three areas (CFAS I) were selected for new sampling two decades later (2008-2011) with same geographical boundaries, sampling and approach methods (CFAS II). At 2 years CFAS I interviewed 5,156 (76% response) with 5,288 interviewed in CFAS II (74% response). Here we report a 20% drop in incidence (95% CI: 0-40%), driven by a reduction in men across all ages above 65. In the UK we estimate 209,600 new dementia cases per year. This study was uniquely designed to test for differences across geography and time. A reduction of age-specific incidence means that the numbers of people estimated to develop dementia in any year has remained relatively stable.CFAS II has been supported by the UK Medical Research Council (Research Grant: G06010220) and received additional support from the National Institute for Health Research (NIHR), comprehensive clinical research networks in West Anglia, Nottingham City and Nottinghamshire County NHS Primary Care trusts and the dementias and neurodegenerative disease research Network (DeNDRoN) in Newcastle. MRC CFAS I was funded by the MRC (Research Grant: G9901400) and the National Health Service (NHS). F.E.M. is supported by the MRC (Research Grant: U105292687). This research was done within the UK National Institute of Health Research collaboration for leadership in applied health research and care for Cambridgeshire and Peterborough (CLAHRC EoE), the Biomedical Research Centre infrastructures at Cambridge and Newcastle upon Tyne. We thank the participants, their families, the general practitioners and their staff, the primary care trusts and CCGs for their cooperation and support. We thank the CFAS II fieldwork interviewers at Cambridge, Nottingham and Newcastle for their valuable contribution. Funding was given by UK Medical Research Council.This is the final version of the article. It first appeared from Nature Publishing Group via http://dx.doi.org/10.1038/ncomms1139

    The clinical diagnosis of Lewy body dementia

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    SIGLEAvailable from British Library Document Supply Centre- DSC:DX175778 / BLDSC - British Library Document Supply CentreGBUnited Kingdo

    DIAGNOSIS AND TREATMENT OF PSYCHOSIS IN DEMENTIA WITH LEWY BODIES

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    Gerontopsychiatrie

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    Nicotinic I-123-5IA-85380 single photon emission computed tomography as a predictor of cognitive progression in alzheimer's disease and dementia with Lewy bodies

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    Objective: To investigate normalized 123I-5-Iodo-3-[2(S)-2-azetidinylmethoxy] pyridine (5IA-85380) single photon emission computed tomography (SPECT) imaging, a marker for the α4β2 nicotinic receptor, as a predictor of cognitive progression in Alzheimer's disease (AD) and dementia with Lewy bodies (DLB). Methods: Thirty-one patients with dementia (16 patients with AD and 15 patients with DLB) underwent 123I-5IA-85380 SPECT scanning. Image analysis was performed using statistical parametric mapping (SPM2), which involved spatial preprocessing of scans to standard Montreal Neurological Institute space and intensity normalization of each image to its mean global brain activity. Results: Regression analysis revealed that reduced normalized 123I-5IA-85380 uptake in left superior, middle, and inferior frontal gyri and prepost central and anterior cingulate regions significantly correlated with decline in executive function in a pooled group comprising AD and DLB. Conclusion: The findings, although preliminary, suggest that the cholinergic system may be more involved in neurodegenerative processes affecting some cognitive processes more than others, as such, this procedure may be useful for increased understanding of the pathophysiological mechanisms responsible for neurodegeneration
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