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| 2. |
- Kalpouzos, Grégoria, et al.
(författare)
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Impact of negative emotion on the neural correlates of long-term recognition in younger and older adults
- 2012
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Ingår i: Frontiers in Integrative Neuroscience. - : Frontiers Media SA. - 1662-5145. ; 6:74, s. 1-25
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Tidskriftsartikel (refereegranskat)abstract
- Some studies have suggested that the memory advantage for negative emotional information over neutral information (“negativity effect”) is reduced in aging. Besides the fact that most findings are based on immediate retrieval, the neural underpinnings of long-term emotional memory in aging have so far not been investigated. To address these issues, we assessed recognition of neutral and negative scenes after 1- and 3-week retention intervals in younger and older adults using functional magnetic resonance imaging. We further used an event-related design in order to disentangle successful, false, and true recognition. This study revealed four key findings: (1) increased retention interval induced an increased rate of false recognitions for negative scenes, canceling out the negativity effect (present for hit rates only) on discrimination in both younger and older adults; (2) in younger, but not older, adults, reduced activity of the medial temporal lobe was observed over time for neutral scenes, but not for negative scenes, where stable or increased activity was seen; (3) engagement of amygdala (AMG) was observed in older adults after a 3-week delay during successful recognition of negative scenes (hits vs. misses) in comparison with neutral scenes, which may indicate engagement of automatic processes, but engagement of ventrolateral prefrontal cortex was unrelated to AMG activity and performance; and (4) after 3 weeks, but not after 1 week, true recognition of negative scenes was characterized by more activity in left hippocampus and lateral occipito-temporal regions (hits vs. false alarms). As these regions are known to be related to consolidation mechanisms, the observed pattern may indicate the presence of delayed consolidation of true memories. Nonetheless, older adults’ low performance in discrimination of negative scenes could reflect the fact that overall, after long delays of retention, they rely more on general information rather than on perceptual detail in making recognition judgments.
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| 3. |
- Laukka, Erika J., et al.
(författare)
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Preclinical Cognitive Trajectories Differ for Alzheimer's Disease and Vascular Dementia
- 2012
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Ingår i: Journal of the International Neuropsychological Society. - 1355-6177 .- 1469-7661. ; 18:2, s. 1-9
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Tidskriftsartikel (refereegranskat)abstract
- We investigated differences between Alzheimer's disease (AD) and vascular dementia (VaD) from the appearance of the first cognitive symptoms, focusing on both time of onset and rate of accelerated decline for different cognitive functions before dementia diagnosis. Data from a longitudinal population-based study were used, including 914 participants (mean age = 82.0 years, SD = 5.0) tested with a cognitive battery (word recall and recognition, Block Design, category fluency, clock reading) on up to four occasions spanning 10 years. We fit a series of linear mixed effects models with a change point to the cognitive data, contrasting each dementia group to a control group. Significant age-related decline was observed for all five cognitive tasks. Relative to time of diagnosis, the preclinical AD persons deviated from the normal aging curve earlier (up to 9 years) compared to the preclinical VaD persons (up to 6 years). However, once the preclinical VaD persons started to decline, they deteriorated at a faster rate than the preclinical AD persons. The results have important implications for identifying the two dementia disorders at an early stage and for selecting cognitive tasks to evaluate treatment effects for persons at risk of developing AD and VaD.
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| 4. |
- MacDonald, Stuart W S, et al.
(författare)
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Extrastriatal dopamine D2 receptor binding modulates intraindividual variability in episodic recognition and executive functioning.
- 2009
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Ingår i: Neuropsychologia. - : Elsevier BV. - 0028-3932 .- 1873-3514. ; 47:11, s. 2299-2304
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Tidskriftsartikel (refereegranskat)abstract
- Intraindividual variability (IIV) reflects lawful but transient within-person changes in performance. Increased IIV in cognition shares systematic associations with numerous conditions characterized by alterations in dopamine (DA) neuromodulation (e.g., old age, ADHD, schizophrenia, and Parkinson's disease). In a group of normal middle-aged adults, we examined links between PET-derived measures of D2 receptor binding in striatum, orbitofrontal cortex (OFC), anterior cingulate cortex (ACC), and hippocampus (HC) and IIV for tasks assessing recognition memory and executive functioning. An index of IIV, the intraindividual standard deviation (ISD), was computed across successful response latency trials for each cognitive outcome. Lower D2 binding in OC, ACC, and HC, but not striatum, was associated with increasing ISDs for the memory and executive measures. Consistent with neurocomputational models, the present findings suggest a role for extrastriatal DA neurotransmission in modulating variability in cognitive functioning.
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| 5. |
- MacDonald, Stuart W S, et al.
(författare)
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Intra-individual variability in behavior : links to brain structure, neurotransmission and neuronal activity.
- 2006
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Ingår i: Trends in Neurosciences. - : Elsevier BV. - 0166-2236. ; 29:8, s. 474-80
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)abstract
- Intra-individual variability reflects a transient, within-person change in behavioral performance. It is a common component of aging-related cognitive decline and the behavioral changes associated with neurodegenerative and other brain-related disorders such as traumatic brain injury and schizophrenia. Behavioral changes within an individual can reflect alterations at a systems or a cellular level in the brain, and monitoring intra-individual variability can therefore provide a warning of underlying pathology. Despite frequent reports of intra-individual variability, there is little synthesis, and no direct examination of the neural underpinnings. Here, we integrate seminal findings from cognitive research across lifespans of individuals, and also neuropsychological and neurobiological findings, to identify key questions and some potential answers, and to set challenges for fostering future research into intra-individual variability.
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| 6. |
- MacDonald, Stuart W S, et al.
(författare)
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Trajectories of cognitive decline following dementia onset : what accounts for variation in progression?
- 2011
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Ingår i: Dementia and Geriatric Cognitive Disorders. - Basel : Karger. - 1420-8008 .- 1421-9824. ; 31:3, s. 202-209
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Delineating the natural history of dementia progression has important clinical implications, including reducing caregiver burden and targeting effective drug trials. We examined whether trajectories of cognitive change differed reliably after diagnosis, and whether diverse predictors of such differences (demographic, psychological, biological, genetic, social) could be identified.METHODS: Cognitive change was examined for incident dementia cases (mild: n = 156; moderate: n = 77; severe: n = 73) and controls (n = 249) from the Kungsholmen Project, a community-based study of adults 75 years and older.RESULTS: For those with dementia, total variance attributed to between-person differences in cognitive decline was modest and linked to but a single predictor (history of cardiovascular disease). Although less variance in cognitive decline was observed for the similarly aged controls, numerous significant predictors of these differences were identified.CONCLUSION: The neurodegenerative process underlying dementia overshadows formerly significant predictors of cognitive change.
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| 7. |
- Thilers, Petra P., et al.
(författare)
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Accelerated postmenopausal cognitive decline is restricted to women with normal BMI : Longitudinal evidence from the Betula project
- 2010
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Ingår i: Psychoneuroendocrinology. - : Elsevier BV. - 0306-4530 .- 1873-3360. ; 35:4, s. 516-524
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Tidskriftsartikel (refereegranskat)abstract
- In order to determine whether cognitive performance is influenced by the menopausal transition, we tested cognitive performance at three time points, sampled women in earlier as well as later stages of the menopausal transition (40-65 years of age), and assessed the moderating influence of body mass index (BMI) on rate of change. Multilevel analyses were used to model change in cognitive performance as a function of number of years post menopause over and above chronological age. We investigated change in the menopausal transition for 10 cognitive outcomes in 193 women who were postmenopausal during the last test wave. The model, controlling for age and education, showed that postmenopausal women within the normal range of BMI (BMI 18.5-25) displayed more rapid decline than women with BMI above 25 for measures of visuospatial ability and episodic memory. In addition, there was an accelerated rate of change post menopause for all women on verbal fluency. The results support the notion that the diminished postmenopausal production of endogenous estrogen may have a slight negative influence on cognitive abilities, but mainly for women within a normal BMI range.
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| 8. |
- Wahlin, Åke, et al.
(författare)
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How health and biological age influence chronological age and sex differences in cognitive aging: Moderating, mediating, or both?
- 2006
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Ingår i: Psychology and Aging. - : American Psychological Association (APA). - 0882-7974 .- 1939-1498. ; 21:2, s. 318-332
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Tidskriftsartikel (refereegranskat)abstract
- Much research on cognitive competence in normal older adults has documented age and sex differences. We used cross-sectional data from the Victoria Longitudinal Study (n=386; age 61-95 years) to examine how health and biological age influence age and sex differences in cognitive aging. We found evidence for both moderating and mediating influences. Age differences were moderated by health status, such that the negative effects of age were most pronounced among participants of relatively better health. Sex differences were moderated by health and were pronounced among participants reporting comparatively poorer health. Although health mediated a notable amount of age-related cognitive variation, BioAge mediated considerably more variance, even after statistical control for differences in health. A complex pattern emerged for the mediation of sex differences: whereas BioAge accounted for sex-related variation in cognitive performance, health operated to suppress these differences. Overall, both health and BioAge predicted cognitive variation independently of chronological age.
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| 9. |
- Wang, Hui-Xin, et al.
(författare)
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Association of lifelong exposure to cognitive reserve-enhancing factors with dementia risk : A community-based cohort study
- 2017
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Ingår i: PLoS Medicine. - : Public Library of Science (PLoS). - 1549-1277 .- 1549-1676. ; 14:3
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Variation in the clinical manifestation of dementia has been associated with differences in cognitive reserve, although less is known about the cumulative effects of exposure to cognitive reserve factors over the life course. We examined the association of cognitive reserve-related factors over the lifespan with the risk of dementia in a community-based cohort of older adults.METHODS AND FINDINGS: Information on early-life education, socioeconomic status, work complexity at age 20, midlife occupation attainment, and late-life leisure activities was collected in a cohort of dementia-free community dwellers aged 75+ y residing in the Kungsholmen district of Stockholm, Sweden, in 1987-1989. The cohort was followed up to 9 y (until 1996) to detect incident dementia cases. To exclude preclinical phases of disease, participants who developed dementia at the first follow-up examination 3 y after the baseline were excluded (n = 602 after exclusions). Structural equation modelling was used to generate latent factors of cognitive reserve from three periods over the life course: early (before 20 y), adulthood (around 30-55 y), and late life (75 y and older). The correlation between early- and adult-life latent factors was strong (γ = 0.9), whereas early-late (γ = 0.27) and adult-late (γ = 0.16) latent factor correlations were weak. One hundred forty-eight participants developed dementia during follow-up, and 454 remained dementia-free. The relative risk (RR) of dementia was estimated using Cox models with life-course cognitive reserve-enhancing factors modelled separately and simultaneously to assess direct and indirect effects. The analysis was repeated among carriers and noncarriers of the apolipoprotein E (APOE) ε4 allele. A reduced risk of dementia was associated with early- (RR 0.57; 95% CI 0.36-0.90), adult- (RR 0.60; 95% CI 0.42-0.87), and late-life (RR 0.52; 95% CI 0.37-0.73) reserve-enhancing latent factors in separate multivariable Cox models. In a mutually adjusted model, which may have been imprecisely estimated because of strong correlation between early- and adult-life factors, the late-life factor preserved its association (RR 0.65; 95% CI 0.45-0.94), whereas the effect of midlife (RR 0.73; 95% CI 0.50-1.06) and early-life factors (RR 0.76; 95% CI 0.47-1.23) on the risk of dementia was attenuated. The risk declined progressively with cumulative exposure to reserve-enhancing latent factors, and having high scores on cognitive reserve-enhancing composite factors in all three periods over the life course was associated with the lowest risk of dementia (RR 0.40; 95% CI 0.20-0.81). Similar associations were detected among APOE ε4 allele carriers and noncarriers. Limitations include measurement error and nonresponse, with both biases likely favouring the null. Strong correlation between early- and adult-life latent factors may have led to a loss in precision when estimating mutually adjusted effects of all periods.CONCLUSIONS: In this study, cumulative exposure to reserve-enhancing factors over the lifespan was associated with reduced risk of dementia in late life, even among individuals with genetic predisposition.
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