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Biomedical subjects

Ulman Lindenberger

Publications and source records attributed to Ulman Lindenberger.

At least 19 recordsLinked to original sources
PubMed2006

Neuromodulation of associative and organizational plasticity across the life span: empirical evidence and neurocomputational modeling.

Developmental plasticity is the key mechanism that allows humans and other organisms to modify and adapt to contextual and experiential influences. Thus, reciprocal co-constructive interactions between behavioral and neuronal plasticity play important roles in regulating neurobehavioral development across the life span. This review focuses on behavioral and neuronal evidence of lifespan differences in associative memory plasticity and plasticity of the functional organization of cognitive and cortical processes, as well as the role of the dopaminergic system in modulating such plasticity. Special attention is given to neurocomputational models that help exploring lifespan differences in neuromodulation of neuronal and behavioral plasticity. Simulation results from these models suggest that lifespan changes in the efficacy of neuromodulatory mechanisms may shape associative memory plasticity and the functional organization of neurocognitive processes by affecting the fidelity of neuronal signal transmission, which has consequences for the distinctiveness of neurocognitive representations and the efficacy of distributed neural coding.

Animals↗
PubMed2006

Cortical EEG correlates of successful memory encoding: implications for lifespan comparisons.

In the course of their lives, individuals experience a myriad of events. Some of them leave stable traces, and others fade away quickly. Recent advances in functional imaging methods allow researchers to contrast neuronal patterns of remembered against not remembered events at initial encoding. Research on young adults using functional magnetic resonance imaging (fMRI), intracranial, and standard electroencephalographic (EEG) recordings has identified differences between remembered and not remembered items in patterns of medio-temporal and prefrontal brain activity. However, little is known about the ways in which such neuronal patterns of successful encoding evolve across the lifespan as a function of maturation, senescence, and the accumulation of experience. Here, we first review empirical evidence on neuronal correlates of successful memory from middle childhood to old age. Based on the observation that associative and strategic components of episodic memory seem to follow different age gradients, we propose a conceptual framework for predicting age changes in neuronal patterns of successful encoding.

Age Factors↗
PubMed2006

The correlative triad among aging, dopamine, and cognition: current status and future prospects.

The brain neuronal systems defined by the neurotransmitter dopamine (DA) have since long a recognized role in the regulation of motor functions. More recently, converging evidence from patient studies, animal research, pharmacological intervention, and molecular genetics indicates that DA is critically implicated also in higher-order cognitive functioning. Many cognitive functions and multiple markers of striatal and extrastriatal DA systems decline across adulthood and aging. Research examining the correlative triad among adult age, DA, and cognition has found strong support for the view that age-related DA losses are associated with age-related cognitive deficits. Future research strategies for examining the DA-cognitive aging link include assessing (a) the generality/specificity of the effects; (b) the relationship between neuromodulation and functional brain activation; and (c) the release of DA during actual task performance.

Aging↗
PubMed2006

Genetic influences on dynamic complexity of brain oscillations.

Human electroencephalogram (EEG) consists of complex aperiodic oscillations that are assumed to indicate underlying neural dynamics such as the number and degree of independence of oscillating neuronal networks. EEG complexity can be estimated using measures derived from nonlinear dynamic systems theory. Variations in such measures have been shown to be associated with normal individual differences in cognition and some neuropsychiatric disorders. Despite the increasing use of EEG complexity measures for the study of normal and abnormal brain functioning, little is known about genetic and environmental influences on these measures. Using the pointwise dimension (PD2) algorithm, this study assessed heritability of EEG complexity at rest in a sample of 214 young female twins consisting of 51 monozygotic (MZ) and 56 dizygotic (DZ) pairs. In MZ twins, intrapair correlations were high and statistically significant; in DZ twins, correlations were substantially smaller. Genetic analyses using linear structural equation modeling revealed high and significant heritability of EEG complexity: 62-68% in the eyes-closed condition, and 46-60% in the eyes-open condition. Results suggest that individual differences in the complexity of resting electrocortical dynamics are largely determined by genetic factors. Neurophysiological mechanisms mediating genetic variation in EEG complexity may include the degree of structural connectivity and functional differentiation among cortical neuronal assemblies.

Adolescent↗
PubMed2006

Dual-tasking postural control: aging and the effects of cognitive demand in conjunction with focus of attention.

Postural control in everyday life is generally accompanied by posture-unrelated cognitive activity. Thus, mild forms of dual-tasking postural control are the norm rather than the exception. Based on this consideration and available evidence, we propose and empirically examined, in young and old adults, a non-monotonic, U-shaped relation between the efficacy of postural control and concurrent cognitive demands that reflect opposing trends of the effects of attention focus and attentional resource competition. When instructed to perform an easy cognitive task that presumably shifted the focus of attention away from posture control, the center of body pressure (COP) excursions decreased both in young and older adults relative to a single-task baseline where the focus of attention was explicitly directed towards the postural control task itself. However, when performing more demanding cognitive tasks, older adults showed increased COP displacements, in line with the predicted U-shape function, whereas young adults did not. We outline mechanisms linking postural control to cognitive demand and suggest routes for future investigation.

Adult↗
PubMed2006

On the power of multivariate latent growth curve models to detect correlated change.

We evaluated the statistical power of single-indicator latent growth curve models (LGCMs) to detect correlated change between two variables (covariance of slopes) as a function of sample size, number of longitudinal measurement occasions, and reliability (measurement error variance). Power approximations following the method of Satorra and Saris (1985) were used to evaluate the power to detect slope covariances. Even with large samples (N = 500) and several longitudinal occasions (4 or 5), statistical power to detect covariance of slopes was moderate to low unless growth curve reliability at study onset was above .90. Studies using LGCMs may fail to detect slope correlations because of low power rather than a lack of relationship of change between variables. The present findings allow researchers to make more informed design decisions when planning a longitudinal study and aid in interpreting LGCM results regarding correlated interindividual differences in rates of development.

Aging↗
PubMed2005

Regional brain changes in aging healthy adults: general trends, individual differences and modifiers.

Brain aging research relies mostly on cross-sectional studies, which infer true changes from age differences. We present longitudinal measures of five-year change in the regional brain volumes in healthy adults. Average and individual differences in volume changes and the effects of age, sex and hypertension were assessed with latent difference score modeling. The caudate, the cerebellum, the hippocampus and the association cortices shrunk substantially. There was minimal change in the entorhinal and none in the primary visual cortex. Longitudinal measures of shrinkage exceeded cross-sectional estimates. All regions except the inferior parietal lobule showed individual differences in change. Shrinkage of the cerebellum decreased from young to middle adulthood, and increased from middle adulthood to old age. Shrinkage of the hippocampus, the entorhinal cortices, the inferior temporal cortex and the prefrontal white matter increased with age. Moreover, shrinkage in the hippocampus and the cerebellum accelerated with age. In the hippocampus, both linear and quadratic trends in incremental age-related shrinkage were limited to the hypertensive participants. Individual differences in shrinkage correlated across some regions, suggesting common causes. No sex differences in age trends except for the caudate were observed. We found no evidence of neuroprotective effects of larger brain size or educational attainment.

Adult↗
PubMed2005

Studying individual aging in an interindividual context: typical paths of age-related, dementia-related, and mortality-related cognitive development in old age.

This study has 2 objectives: (a) to explore typical paths of cognitive development associated with aging, terminal decline, and dementia and (b) to promote and illustrate an individual-oriented approach to the study of cognitive aging based on longitudinal panel data from a population-based sample (N = 500; age range-sub(T1)= 60-80, where T refers to time) tested at 3 occasions 5 years apart. Results document interindividual differences in multivariate patterns of change. Although cognitive changes generally covary, the present study indicates that subgroups of individuals develop along different paths characterized by selective changes in subsets of cognitive functions. Typical progression of dementia followed a developmental cascade from low declarative memory, via low functioning across all observed cognitive measures, to dementia diagnosis, and finally, death.

Aged↗
PubMed2005

Social participation attenuates decline in perceptual speed in old and very old age.

Does an engaged and active lifestyle in old age alleviate cognitive decline, does high cognitive functioning in old age increase the possibility of maintaining an engaged and active lifestyle, or both? The authors approach this conundrum by applying a structural equation model for testing dynamic hypotheses, the dual change score model (J. J. McArdle & F. Hamagami, 2001), to 3-occasion longitudinal data from the Berlin Aging Study (Time 1: n=516, age range=70-103 years). Results reveal that within a bivariate system of perceptual speed and social participation, with age and sociobiographical status as covariates, prior scores of social participation influence subsequent changes in perceptual speed, while the opposite does not hold. Results support the hypothesis that an engaged and active lifestyle in old and very old age may alleviate decline in perceptual speed.

Aged↗
PubMed2005

Environmental topography and postural control demands shape aging-associated decrements in spatial navigation performance.

This study tests the hypothesis that aging-induced cognitive permeation of sensorimotor functions contributes to adult age differences in spatial navigation performance. Virtual maze-like museums were projected in front of a treadmill. Sixteen 20-30-year-old men and sixteen 60-70-year-old men performed a way-finding task in city-block or variable topographies while walking with or without support. Walking support attenuated age-related decrements in navigational learning. Navigation load increased trunk-angle variability for older adults only. Age differences in spatial knowledge persisted despite perfect place-finding performance. City-block topography was easier than variable topography for younger adults only, indicating age-related differences in reliance on spatial relational learning. Attempts at supporting older adults' navigation performance should consider sensorimotor/cognitive interactions and qualitative differences in navigational activity.

Adult↗
PubMed2005

Aging neuromodulation impairs associative binding: a neurocomputational account.

Relative to young adults, older adults are particularly impaired in episodic memory tasks requiring associative binding of separate components into compound episodes, such as tasks requiring item-context and item-item binding. This associative-binding deficit has been attributed to senescent changes in frontal-hippocampal circuitry but has not been formally linked to impaired neuromodulation involving this circuitry. Previous neurocomputational work showed that impaired neuromodulation could result in less distinct neurocognitive representations. Here we extend this computational principle to simulate aging-related deficits in associative binding. As expected, networks with simulated deficiency in neuromodulation resulted in less distinct internal representations than did networks simulating the processing and performance of young adults, and were also more impaired under task conditions that required associative binding. The findings suggest that senescent changes in neuromodulatory mechanisms may play a basic role in aging-related impairment in associative binding by reducing the efficacy of distributed conjunctive coding.

Aged↗
PubMed2004

Transformations in the couplings among intellectual abilities and constituent cognitive processes across the life span.

Two-component theories of intellectual development over the life span postulate that fluid abilities develop earlier during child development and decline earlier during aging than crystallized abilities do, and that fluid abilities support or constrain the acquisition and expression of crystallized abilities. Thus, maturation and senescence compress the structure of intelligence by imposing age-specific constraints upon its constituent processes. Hence, the couplings among different intellectual abilities and cognitive processes are expected to be strong in childhood and old age. Findings from a population-based study of 291 individuals aged 6 to 89 years support these predictions. Furthermore, processing robustness, a frequently overlooked aspect of processing, predicted fluid intelligence beyond processing speed in old age but not in childhood, suggesting that the causes of more compressed functional organization of intelligence differ between maturation and senescence. Research on developmental changes in functional brain circuitry may profit from explicitly recognizing transformations in the organization of intellectual abilities and their underlying cognitive processes across the life span.

Adolescent↗
PubMed2003

Plasticity of memory for new learning in very old age: a story of major loss?

Longitudinal survivors of the Berlin Aging Study (N = 96, mean age = 84 years, range 75-101 years) were instructed and trained in a mnemonic skill to examine plasticity of episodic memory performance in very old age. Performance gains after mnemonic instruction were modest, and most individuals were unable to further enhance their performance during 4 sessions of mnemonic practice. Whereas the proportion of variance explained by measures from the broad fluid-ability domain (e.g., perceptual speed) increased with training, the proportion of variance explained by crystallized-ability domain (e.g., word knowledge) and sociobiographical variables decreased. Furthermore, prior 6-year longitudinal changes (loss) in perceptual speed predicted individual differences in plasticity. Results suggest that aging-induced biological factors are a prominent source of individual differences in cognitive plasticity in very old age.

Age Factors↗
PubMed2003

The fate of cognition in very old age: six-year longitudinal findings in the Berlin Aging Study (BASE).

The authors report full-information longitudinal age gradients in 4 intellectual abilities on the basis of 6-year longitudinal changes in 132 individuals (mean age at T1 = 78.27, age range = 70-100) from the Berlin Aging Study. Relative to the cross-sectional parent sample (N = 516, mean age at T1 = 84.92 years), this sample was positively selected because of differential mortality and experimental attrition. Perceptual speed, memory, and fluency declined with age. In contrast, knowledge remained stable up to age 90, with evidence for decline thereafter. Age gradients were more negative in old old (n = 66, mean age at T1 = 83.04) than in old (n = 66, mean age at T1 = 73.77) participants. Rates of decline did not differ reliably between men and women or between participants with high versus low life-history status. They conclude that intellectual development after age 70 varies by distance to death, age, and intellectual ability domain.

Age Factors↗
PubMed2003

Age-based structural dynamics between perceptual speed and knowledge in the Berlin Aging Study: direct evidence for ability dedifferentiation in old age.

According to 2-component theories of intelligence, negative cross-sectional age gradients in mechanic (broad Gf) and pragmatic (broad Gc) cognitive components reflect the increasing constraining of the former in the expression and integrity of the latter component. The authors examined this widely held but untested assumption by applying a recently proposed dynamic structural modeling technique, the bivariate dual change score model, to longitudinal data from the Berlin Aging Study (N = 516, age range = 70-103 years). Mechanics and pragmatics were indexed by perceptual speed and knowledge, respectively. As hypothesized, results indicated that changes in knowledge are dominated by perceptual speed and offered strong support for the notion of "mechanization" of pragmatic abilities in old and very old age.

Aged↗
PubMed2002

Age-related changes in task-switching components: the role of task uncertainty.

The present study examined age differences in executive functioning, using an externally cued task-switching paradigm. Two components of task switching were assessed: the ability to maintain and select among task sets (general switch costs) and the ability to switch between task sets (specific switch costs). In contrast to previous findings, we found large age-related differences in specific switch costs, especially when the number of potentially relevant task sets is increased from two to four. Age-related differences in general switch costs were absent when external task cues subserved executive processing in task switching. Generally, the findings suggest that age-related impairments in task-switching components vary as a function of task uncertainty, such as the presence of environmental prompts to behavior.

Adult↗
PubMed2002

Relations between aging sensory/sensorimotor and cognitive functions.

Recent evidence is reviewed to examine relations among sensory, sensorimotor, and cognitive aging. Age-heterogeneous cross-sectional data sets show substantial covariation among sensory, sensorimotor and intellectual abilities, and an increase in covariation from adulthood to old and very old age. Recent longitudinal analyses suggest that changes in sensory and intellectual functioning are interrelated. Experimental studies investigate the interdependence between cognitive and sensory/sensorimotor aging by examining the effects of simulated sensory loss on cognitive performance, or the effects of cognitive load manipulations on sensory or motor performance. Generally, both types of manipulations hinder older adults' performance more than that of younger adults. Theoretically, the age-associated intensification of the links among sensory, sensorimotor and cognitive functions observed both correlationally and experimentally may point to (a). common causes influencing all three functions; (b). an increase in resource overlap, cross-domain resource competition, and compensatory tradeoffs; and (c). a combination of the two. Future research aiming at discerning the relative import of these possibilities would profit from an integration of experimental and correlational research strategies.

Aging↗