Yee Lee Shing

Episodic memory across the lifespan: The contributions of associative and strategic components

The structural and functional brain circuitries supporting episodic memory undergo profound reorganization in childhood and old age. We propose a two-component framework that combines and integrates evidence from child development and aging. It posits that episodic memory builds on two interacting components: (a) the strategic component, which refers to memory control operations, and (b) the associative component, which refers to mechanisms that bind different features of a memory episode into a compound representation. We hypothesize that: (a) childrens difficulties in episodic memory primarily originate from low levels of strategic operations, and reflect the protracted development of the prefrontal cortex (PFC); (b) deficits in episodic memory performance among older adults originate from impairments in both strategic and associative components, reflecting senescent changes in the PFC and the medio-temporal lobes (MTL). Initial behavioral and neural evidence is consistent with both hypotheses. The two-component framework highlights the specificities of episodic memory in different age periods, helps to identify and dissociate its components, and contributes to understanding the interplay among maturation, learning, and senescence.

Within-person trial-to-trial variability precedes and predicts cognitive decline in old and very old age: Longitudinal data from the Berlin Aging Study

Neurocomputational modeling and empirical evidence suggest that losses in neuronal signaling fidelity cause senescent changes in behavior. We applied structural equation modeling to five-occasion 13-year longitudinal data from the Berlin Aging Study (n=447; age range at t1=70-102 years) to test whether trial-to-trial reaction time variability in perceptual speed (identical pictures) antecedes and signals longitudinal decline in levels of performance on perceptual speed (digit letter and identical pictures) and ideational fluency (category fluency). Higher trial-to-trial variability preceded and predicted greater cognitive decline in perceptual speed and ideational fluency. We conclude that trial-to-trial variability signals impending decline in cognitive performance, and that theories of neurocognitive aging need to postulate developmental cascades between senescent changes in variability and central tendency.

Memory Maintenance and Inhibitory Control Differentiate from Early Childhood to Adolescence

Existing evidence suggests that the organization of cognitive functions may differentiate during development. We investigated two key components of executive functions, memory maintenance and inhibitory control, by applying latent factor models appropriate for examining developmental differences in functional associations among aspects of cognition. Two-hundred and sixty-three children (aged 4 to 14 years) were administered tasks that required maintaining rules in mind or inhibiting a prepotent tendency to respond on the same side as the stimulus. Memory maintenance and inhibitory control were not separable in children of 4–7 or 7–9.5 years, but were differentiated in an older group (9.5–14.5 years).

Hippocampal Subfield Volumes: Age, Vascular Risk, and Correlation with Associative Memory

Aging and age-related diseases have negative impact on the hippocampus (HC), which is crucial for such age-sensitive functions as memory formation, maintenance, and retrieval. We examined age differences in hippocampal subfield volumes in 10 younger and 19 older adults, and association of those volumes with memory performance in the older participants. We manually measured volumes of HC regions CA1 and CA2 (CA1–2), sectors CA3 and CA4 plus dentate gyrus (CA3–4/DG), subiculum, and the entorhinal cortex using a contrast-optimized high-resolution PD-weighted MRI sequence. Although, as in previous reports, the volume of one region (CA1–2) was larger in the young, the difference was due to the presence of hypertensive subjects among the older adults. Among older participants, increased false alarm rate in an associative recognition memory task was linked to reduced CA3–4/DG volume. We discuss the role of the DG in pattern separation and the formation of discrete memory representations.

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.

Adult age differences in memory for name–face associations: The effects of intentional and incidental learning

Previous studies have indicated that older adults have a special deficit in the encoding and retrieval of associations. The current study assessed this deficit using ecologically valid name–face pairs. In two experiments, younger and older participants learned a series of name–face pairs under intentional and incidental learning instructions, respectively, and were then tested for their recognition of the faces, the names, and the associations between the names and faces. Under incidental encoding conditions older adults’ performance was uniformly lower than younger adults in all three tests, indicating age-related impairments in episodic memory representations. An age-related deficit specific to associations was found under intentional but not under incidental learning conditions, highlighting the importance of strategic associative processes and their decline in older adults. Separate analyses of hits and false alarms indicate that older adults’ associative deficit originated from high false alarm rates in the associative test. Older adults’ high false alarm rates potentially reflect their reduced ability to recollect the study-phase name–face pairs in the presence of intact familiarity with individual names and faces.

The influence of prior knowledge on memory: a developmental cognitive neuroscience perspective

Across ontogenetic development, individuals gather manifold experiences during which they detect regularities in their environment and thereby accumulate knowledge. This knowledge is used to guide behavior, make predictions, and acquire further new knowledge. In this review, we discuss the influence of prior knowledge on memory from both the psychology and the emerging cognitive neuroscience literature and provide a developmental perspective on this topic. Recent neuroscience findings point to a prominent role of the medial prefrontal cortex (mPFC) and of the hippocampus (HC) in the emergence of prior knowledge and in its application during the processes of successful memory encoding, consolidation, and retrieval. We take the lateral PFC into consideration as well and discuss changes in both medial and lateral PFC and HC across development and postulate how these may be related to the development of the use of prior knowledge for remembering. For future direction, we argue that, to measure age differential effects of prior knowledge on memory, it is necessary to distinguish the availability of prior knowledge from its accessibility and use.

Committing memory errors with high confidence: Older adults do but children don't

We investigated lifespan differences of confidence calibration in episodic memory, particularly the susceptibility to high-confidence errors within samples of children, teenagers, younger adults, and older adults. Using an associative recognition memory paradigm, we drew a direct link between older adults’ associative deficit and high-confidence errors. We predicted that only older adults would show high-confidence error even though their memory performance was at a similar level to that of children. Participants of all ages showed higher confidence following correct responses compared to incorrect responses, demonstrating the ability to calibrate subjective confidence in relation to memory accuracy. However, older adults were disproportionately more likely to indicate high confidence following erroneously remembered word pairs than participants of the other three age groups. Results are discussed in relation to the misrecollection account of high-confidence errors and ageing-related decline in hippocampus-dependent episodic memory functions.

EEG gamma-band synchronization in visual coding from childhood to old age: Evidence from evoked power and inter-trial phase locking

OBJECTIVE To investigate lifespan age differences in neuronal mechanisms of visual coding in the context of perceptual discrimination. METHODS We recorded EEG from 17 children (10-12 years), 16 younger adults (20-26 years), and 17 older adults (70-76 years) during a simple choice-reaction task requiring discrimination of squares and circles of different sizes. We examined age-group differences in the effect of stimulus size on early ERP components, evoked gamma-band power, and inter-trial phase-stability in the gamma band as assessed by the phase-locking index (PLI). RESULTS In the absence of age differences in discrimination accuracy, we observed reliable age differences in patterns of ERP, evoked gamma power, and PLI. P1 and N1 peak amplitudes were larger and the peak latencies longer in children than in adults. Children also showed lower levels of evoked power and PLI than adults. Older adults showed smaller increments in evoked power with increasing stimulus size than younger adults, but similar amounts of phase locking for small- and medium-sized stimuli as younger adults. CONCLUSIONS The relative importance of different coding mechanisms in early visual areas changes from childhood to old age. Due to synaptic overproduction and immature myelination, the visual system of children is less entrained by incoming information, resulting in less synchronized neuronal responses. Adults primarily rely on sparse representations formed through experience-dependent temporally synchronized neuronal interactions. In old age, senescent decline in neuronal density and neurotransmitter availability further increase the reliance on temporally synchronized processing. SIGNIFICANCE Findings from this study defy the notion that sensory aging consists in a reversal of sensory development in childhood, and point to a high degree of age specificity in mechanisms of visual coding.

Age differences in speed of processing are partially mediated by differences in axonal integrity

Advanced age is associated with declines in brain structure and in cognitive performance, but it is unclear which aspects of brain aging mediate cognitive declines. We inquired if individual differences in white matter integrity contribute to age differences in two cognitive domains with established vulnerability to aging: executive functioning and speed of processing. The participants were healthy volunteers aged 50-81, some of whom had elevated blood pressure, a known vascular risk factor. Using latent variable analyses, we examined whether age differences in regional white matter integrity mediated age-related differences in executive functions and speed of processing. Although diffusion-related latent variables showed stronger age differences than white matter volumes and white matter hyperintensity volumes, only one of them was significantly associated with cognitive performance. Smaller linear anisotropy partially mediated age-related reduction in speed of processing. The effect was significant in posterior (temporal-parietal-occipital) but not anterior (frontal) region, and appeared stronger for cognitive rather than reaction time measures of processing speed. The presence of hypertensive participants did not affect the results. We conclude that in healthy adults, deterioration of axonal integrity and ensuing breech of connectivity may underpin age-related slowing of information processing.