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  • 1.
    Abulafia, Carolina
    et al.
    FLENI Foundation Department of Psychiatry, Buenos Aires, Argentina / Applied Neuroscience Laboratory, Institute for Biomedical Research, School of Medical Sciences, Universidad Católica Argentina, Buenos Aires, Argentina / Consejo Nacional de Investigaciones Científicas y Técnicas, Buenos Aires, Argentina.
    Duarte-Abritta, Bárbara
    FLENI Foundation Department of Psychiatry, Buenos Aires, Argentina.
    Villarreal, Mirta F.
    FLENI Foundation Department of Psychiatry, Buenos Aires, Argentina / Consejo Nacional de Investigaciones Científicas y Técnicas, Buenos Aires, Argentina.
    Ladrón-de-Guevara, Maria S.
    FLENI Foundation Department of Psychiatry, Buenos Aires, Argentina / Consejo Nacional de Investigaciones Científicas y Técnicas, Buenos Aires, Argentina.
    Garcia, Celeste
    FLENI Foundation Department of Psychiatry, Buenos Aires, Argentina.
    Sequeyra, Geraldine
    FLENI Foundation Department of Psychiatry, Buenos Aires, Argentina.
    Sevlever, Gustavo
    FLENI Foundation Department of Psychiatry, Buenos Aires, Argentina.
    Fiorentini, Leticia
    FLENI Foundation Department of Psychiatry, Buenos Aires, Argentina.
    Bär, Karl-Jürgen
    Department of Psychiatry and Psychotherapy, Universitätsklinikum Jena, Friedrich-Schiller-Universität, Jena, Germany.
    Gustafson, Deborah R.
    Högskolan i Skövde, Institutionen för hälsa och lärande. Högskolan i Skövde, Forskningsspecialiseringen Hälsa och Lärande. Department of Neurology, State University of New York, Downstate Medical Center, Brooklyn, NY, USA / Neuropsychiatric Epidemiology Unit, University of Gothenburg, Gothenburg, Sweden.
    Vigo, Daniel E.
    Applied Neuroscience Laboratory, Institute for Biomedical Research, School of Medical Sciences, Universidad Católica Argentina, Buenos Aires, Argentina / Consejo Nacional de Investigaciones Científicas y Técnicas, Buenos Aires, Argentina.
    Guinjoan, Salvador M.
    FLENI Foundation Department of Psychiatry, Buenos Aires, Argentina / Consejo Nacional de Investigaciones Científicas y Técnicas, Buenos Aires, Argentina / FLENI Teaching Unit, Department of Psychiatry and Mental Health, University of Buenos Aires School of Medicine, Buenos Aires, Argentina / Department of Neurophysiology, University of Buenos Aires School of Psychology, Buenos Aires, Argentina.
    Relationship between Cognitive and Sleep-wake Variables in Asymptomatic Offspring of Patients with Late-onset Alzheimer's Disease2017Ingår i: Frontiers in Aging Neuroscience, ISSN 1663-4365, E-ISSN 1663-4365, Vol. 9, artikel-id 93Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Early neuropathological changes characteristic of late-onset Alzheimer's disease (LOAD) involve brain stem and limbic structures that regulate neurovegetative functions, including sleep-wake rhythm. Indeed, sleep pattern is an emerging biomarker and a potential pathophysiological mechanism in LOAD. We hypothesized that cognitively asymptomatic, middle-aged offspring of patients with LOAD (O-LOAD) would display a series of circadian rhythm abnormalities prior to the onset of objective cognitive alterations. We tested 31 children of patients with LOAD (O-LOAD) and 19 healthy individuals without family history of Alzheimer's disease (control subjects, CS) with basic tests of cognitive function, as well as actigraphy measures of sleep-wake rhythm, cardiac autonomic function, and bodily temperature. Unexpectedly, O-LOAD displayed subtle but significant deficits in verbal episodic memory (Rey Auditory Verbal Learning Test delayed recall 10.6 +/- 0.4 vs. 8.6 +/- 0.6, t = 4.97, df = 49, p < 0.01) and language (Weschler's vocabulary 51.4 +/- 1.3 vs. 44.3 +/- 1.5, t = 2.49, df = 49, p < 0.001) compared to CS, even though all participants had results within the clinically normal range. O-LOAD showed a phase-delayed rhythm of body temperature (2.56 +/- 0.47 h vs. 3.8 +/- 0.26 h, t = 2.48, df = 40, p = 0.031). Cognitive performance in O-LOAD was associated with a series of cardiac autonomic sleep-wake variables; specifically indicators of greater sympathetic activity at night were related to poorer cognition. The present results suggest sleep pattern deserves further study as a potential neurobiological signature in LOAD, even in middle-aged, at risk individuals.

  • 2.
    Arnoldussen, Ilse A. C.
    et al.
    Department of Anatomy, Donders Institute for Brain, Cognition and Behaviour, Radboud university medical center, Nijmegen, The Netherlands.
    Sundh, Valter
    Neuropsychiatric Epidemiology Unit, Sahlgrenska Academy at University of Gothenburg, Institute for Neuroscience and Physiology, Gothenburg, Sweden.
    Bäckman, Kristoffer
    Neuropsychiatric Epidemiology Unit, Sahlgrenska Academy at University of Gothenburg, Institute for Neuroscience and Physiology, Gothenburg, Sweden.
    Kern, Silke
    Neuropsychiatric Epidemiology Unit, Sahlgrenska Academy at University of Gothenburg, Institute for Neuroscience and Physiology, Gothenburg, Sweden.
    Östling, Svante
    Neuropsychiatric Epidemiology Unit, Sahlgrenska Academy at University of Gothenburg, Institute for Neuroscience and Physiology, Gothenburg, Sweden.
    Blennow, Kaj
    Neuropsychiatric Epidemiology Unit, Sahlgrenska Academy at University of Gothenburg, Institute for Neuroscience and Physiology, Gothenburg, Sweden.
    Zetterberg, Henrik
    Neuropsychiatric Epidemiology Unit, Sahlgrenska Academy at University of Gothenburg, Institute for Neuroscience and Physiology, Gothenburg, Sweden.
    Skoog, Ingmar
    Neuropsychiatric Epidemiology Unit, Sahlgrenska Academy at University of Gothenburg, Institute for Neuroscience and Physiology, Gothenburg, Sweden.
    Kiliaan, Amanda J.
    Department of Anatomy, Donders Institute for Brain, Cognition and Behaviour, Radboud university medical center, Nijmegen, The Netherlands.
    Gustafson, Deborah R.
    Högskolan i Skövde, Institutionen för hälsa och lärande. Högskolan i Skövde, Forskningsspecialiseringen Hälsa och Lärande. Department of Neurology, State University of New York, Downstate Medical Center, Brooklyn, NY, USA / Neuropsychiatric Epidemiology Unit, Sahlgrenska Academy at University of Gothenburg, Institute for Neuroscience and Physiology, Gothenburg, Sweden.
    A 10-Year Follow-Up of Adiposity and Dementia in Swedish Adults Aged 70 Years and Older2018Ingår i: Journal of Alzheimer's Disease, ISSN 1387-2877, E-ISSN 1875-8908, Vol. 63, nr 4, s. 1325-1335Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: Adiposity measured in mid-or late-life and estimated using anthropometric measures such as body mass index (BMI) and waist-to-hip ratio (WHR), or metabolic markers such as blood leptin and adiponectin levels, is associated with late-onset dementia risk. However, during later life, this association may reverse and aging- and dementia-related processes may differentially affect adiposity measures.

    Objective: We explored associations of concurrent BMI, WHR, and blood leptin and high molecular weight adiponectin levels with dementia occurrence.

    Methods: 924 Swedish community-dwelling elderly without dementia, aged 70 years and older, systematically-sampled by birth day and birth year population-based in the Gothenburg city region of Sweden. The Gothenburg Birth Cohort Studies are designed for evaluating risk and protective factors for dementia. All dementias diagnosed after age 70 for 10 years were identified. Multivariable logistic regression models were used to predict dementia occurrence between 2000-2005, 2005-2010, and 2000-2010 after excluding prevalent baseline (year 2000) dementias. Baseline levels of BMI, WHR, leptin, and adiponectin were used.

    Results: Within 5 years of baseline, low BMI (<20 kg/m(2)) was associated with higher odds of dementia compared to those in the healthy BMI category (>= 20-24.9 kg/m(2)). Compared to the lowest quartile, leptin levels in the second quartile were associated with lower odds of dementia in women (p < 0.05).

    Conclusion: In late-life, anthropometric and metabolic adiposity measures appear to be differentially associated with dementia risk. While BMI and leptin levels are highly positively correlated, our results show that their association with dementia at age >= 70 years, is asynchronous. These data suggest that with aging, the complexity of the adiposity exposure may increase and suggests metabolic dysregulation. Additional studies are needed to better understand this complexity.

  • 3.
    Franx, Bart A. A.
    et al.
    Department of Anatomy, Donders Institute for Brain, Cognition and Behaviour, Radboud University Medical Center, Nijmegen, The Netherlands.
    Arnoldussen, Ilse A. C.
    Department of Anatomy, Donders Institute for Brain, Cognition and Behaviour, Radboud University Medical Center, Nijmegen, The Netherlands.
    Kiliaan, Amanda J.
    Department of Anatomy, Donders Institute for Brain, Cognition and Behaviour, Radboud University Medical Center, Nijmegen, The Netherlands.
    Gustafson, Deborah R.
    Högskolan i Skövde, Institutionen för hälsa och lärande. Högskolan i Skövde, Forskningsspecialiseringen Hälsa och Lärande. Department of Neurology, Section for NeuroEpidemiology, State University of New York, Downstate Medical Center, USA / Neuropsychiatric Epidemiology Unit (EPINEP), Institute for Neuroscience and Physiology, Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden.
    Weight Loss in Patients with Dementia: Considering the Potential Impact of Pharmacotherapy2017Ingår i: Drugs & Aging, ISSN 1170-229X, E-ISSN 1179-1969, Vol. 34, nr 6, s. 425-436Artikel, forskningsöversikt (Refereegranskat)
    Abstract [en]

    Unintentional body weight loss is common in patients with dementia and is linked to cognitive impairment and poorer disease outcomes. It is proposed that some dementia medications with market approval, while aiming to improve cognitive and functional outcomes of a patient with dementia, are associated with reported body weight or body mass index loss. This review presents evidence in the published literature on body weight loss in dementia, describes selected theories behind body weight loss, evaluates the potential impact of approved dementia pharmacotherapies on body weight, considers the potential role for medical foods, understands the potential influence of treatments for neuropsychiatric symptoms and signs, and finally, summarizes this important area.

  • 4.
    Gustafson, Deborah R.
    et al.
    Högskolan i Skövde, Institutionen för hälsa och lärande. Högskolan i Skövde, Forskningsspecialiseringen Hälsa och Lärande. State University of New York, NY, United States / University of Gothenburg.
    McFarlane, Samy I
    State University of New York, NY, United States.
    Epidemiology of Type 2 Diabetes and Dementia2018Ingår i: Type 2 Diabetes and Dementia / [ed] Velandai Srikanth and Zoe Arvanitakis, Elsevier, 2018, s. 5-27Kapitel i bok, del av antologi (Övrigt vetenskapligt)
    Abstract [en]

    Type 2 diabetes (T2D) has been associated with dementia in countless observational epidemiology studies. The expansion of epidemiologic research on T2D and dementia is due to scientific recognition of the roles of metabolic and vascular factors as etiologic players in dementia, as well as ominous global demographic shifts in aging, obesity, and dementia. This chapter addresses epidemiologic studies evaluating the association between T2D and late-onset dementias with foci on (1) T2D and dementia as syndromes; (2) T2D and mild cognitive impairment or cognition and cognitive decline; (3) vascular and metabolic risk factors and comorbidities; (4) genetic influences on the T2D-dementia association; (5) ethnoracial considerations; (6) T2D and brain outcomes and biological markers; and (7) clinical trials of T2D medications and cognition and dementia. © 2018 Elsevier Inc. All rights reserved.

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