Facial expression recognition across the adult life span

We report three experiments investigating the recognition of emotion from facial expressions across the adult life span. Increasing age produced a progressive reduction in the recognition of fear and, to a lesser extent, anger. In contrast, older participants showed no reduction in recognition of disgust, rather there was some evidence of an improvement. The results are discussed in terms of studies from the neuropsychological and functional imaging literature that indicate that separate brain regions may underlie the emotions fear and disgust. We suggest that the dissociable effects found for fear and disgust are consistent with the differential effects of ageing on brain regions involved in these emotions.     

Suicide across the adult life span: Replications and failures

Suicide is a multidimensional event. To understand this complexity, psychological theory is needed, which is often lacking in current research. This archival study, utilizing 60 suicide notes from across the adult life span, examines models of suicide. An attempt to replicate a previous model (1989) failed to account best for the current data and an alternative theoretical model is provided. Yet, this result should be expected, not only because psychological theory has to be open-ended to define an event, but also because empirical methods for theory construction (such as cluster analysis in this study) are not simply result seeking but are result imposing. Nevertheless, the present study strongly supported an adult life span perspective. Young adults continue to show the greatest amount of differences in their suicide; for examples, higher levels of psychopathology, lower levers of ego strength and a poorer ability to cope with life's demands, e.g., intimacy vs. isolation.     

Expected value information improves financial risk taking across the adult life span

When making decisions, individuals must often compensate for cognitive limitations, particularly in the face of advanced age. Recent findings suggest that age-related variability in striatal activity may increase financial risk-taking mistakes in older adults. In two studies, we sought to further characterize neural contributions to optimal financial risk taking and to determine whether decision aids could improve financial risk taking. In Study 1, neuroimaging analyses revealed that individuals whose mesolimbic activation correlated with the expected value estimates of a rational actor made more optimal financial decisions. In Study 2, presentation of expected value information improved decision making in both younger and older adults, but the addition of a distracting secondary task had little impact on decision quality. Remarkably, provision of expected value information improved the performance of older adults to match that of younger adults at baseline. These findings are consistent with the notion that mesolimbic circuits play a critical role in optimal choice, and imply that providing simplified information about expected value may improve financial risk taking across the adult life span.     

Brain oscillatory complexity across the life span

Objective

Considering the increasing use of complexity estimates in neuropsychiatric populations, a normative study is critical to define the ‘normal’ behaviour of brain oscillatory complexity across the life span.

Method

This study examines changes in resting-state magnetoencephalogram (MEG) complexity – quantified with the Lempel–Ziv complexity (LZC) algorithm – due to age and gender in a large sample of 222 (100 males/122 females) healthy participants with ages ranging from 7 to 84 years.

Results

A significant quadratic (curvilinear) relationship (p < 0.05) between age and complexity was found, with LZC maxima being reached by the sixth decade of life. Once that peak was crossed, complexity values slowly decreased until late senescence. Females exhibited higher LZC values than males, with significant differences in the anterior, central and posterior regions (p < 0.05).

Conclusions

These results suggest that the evolution of brain oscillatory complexity across the life span might be considered a new illustration of a ‘normal’ physiological rhythm.

Significance

Previous and forthcoming clinical studies using complexity estimates might be interpreted from a more complete and dynamical perspective. Pathologies not only cause an ‘abnormal’ increase or decrease of complexity values but they actually ‘break’ the ‘normal’ pattern of oscillatory complexity evolution as a function of age.     

Neuroanatomical correlates of intellectual ability across the life span

Attempts to correlate measures of intellectual ability with localized anatomical imaging features of the brain have yielded variable findings distributed across frontal, parietal, and temporal lobes. To better define the gray and white matter correlates of intellectual ability and the effects of sex and age, we analyzed the brains of 105 healthy individuals, ages 7-57 years, who had a Full Scale Intelligence Quotient (FSIQ) of 70 or higher. We examined associations of FSIQ with cortical thickness and with white matter volume throughout the cerebrum. Thinning of left ventromedial and right dorsolateral prefrontal cortices correlated significantly with FSIQ. Sex modified correlations of cortical thickness with FSIQ in the left inferior frontal, left cingulate, and right dorsomedial prefrontal cortices. Correlations of local white matter volumes with FSIQ varied by age, with adults showing inverse correlations of white matter volume with FSIQ in a large territory of right frontal white matter likely corresponding to fiber tracts of the superior corona radiata and superior longitudinal fasciculus. These findings corroborate the role of frontal and parietal association cortices and long association white matter fibers in higher intelligence and suggest ways in which the neuroanatomical correlates of higher intelligence may vary by sex and age.     

Catatonia in autism: implications across the life span

Background  There is increasing evidence that catatonia is an important source of impairment in adolescents and adults with autism. Aim  Review of the evaluation, diagnosis, differential diagnosis, and treatment of catatonia in autism. Method  Presentation and discussion of a case-vignette spanning early childhood to adulthood. Results  Autistic and catatonic symptoms overlap, yet catatonia is diagnosable in about one of seven adolescents and young adults with autism. Case-reports suggest that benzodiazepines and electroconvulsive therapy are effective treatments in the acute and maintenance phase for people with autism who develop catatonia. Conclusions  Catatonia should be assessed in people with autism when there is an obvious and marked deterioration in movement, vocalizations, pattern of activities, self-care, and practical skills. Benzodiazepines and electroconvulsive therapy are favored options for acute and maintenance treatment in these cases. Further studies on the possible biological-genetic overlap between autism and catatonia would be helpful.     

Evolution of white matter tract microstructure across the life span

The human brain undergoes dramatic structural change over the life span. In a large imaging cohort of 801 individuals aged 7–84 years, we applied quantitative relaxometry and diffusion microstructure imaging in combination with diffusion tractography to investigate tissue property dynamics across the human life span. Significant nonlinear aging effects were consistently observed across tracts and tissue measures. The age at which white matter (WM) fascicles attain peak maturation varies substantially across tissue measurements and tracts. These observations of heterochronicity and spatial heterogeneity of tract maturation highlight the importance of using multiple tissue measurements to investigate each region of the WM. Our data further provide additional quantitative evidence in support of the last‐in‐first‐out retrogenesis hypothesis of aging, demonstrating a strong correlational relationship between peak maturational timing and the extent of quadratic measurement differences across the life span for the most myelin sensitive measures. These findings present an important baseline from which to assess divergence from normative aging trends in developmental and degenerative disorders, and to further investigate the mechanisms connecting WM microstructure to cognition.     

Dynamic functional connectivity profile of the salience network across the life span

The insular cortex and anterior cingulate cortex together comprise the salience or midcingulo‐insular network, involved in detecting salient events and initiating control signals to mediate brain network dynamics. The extent to which functional coupling between the salience network and the rest of the brain undergoes changes due to development and aging is at present largely unexplored. Here, we examine dynamic functional connectivity (dFC) of the salience network in a large life span sample (n = 601; 6–85 years old). A sliding‐window analysis and k‐means clustering revealed five states of dFC formed with the salience network, characterized by either widespread asynchrony or different patterns of synchrony between the salience network and other brain regions. We determined the frequency, dwell time, total transitions, and specific state‐to‐state transitions for each state and subject, regressing the metrics with subjects'' age to identify life span trends. A dynamic state characterized by low connectivity between the salience network and the rest of the brain had a strong positive quadratic relationship between age and both frequency and dwell time. Additional frequency, dwell time, total transitions, and state‐to‐state transition trends were observed with other salience network states. Our results highlight the metastable dynamics of the salience network and its role in the maturation of brain regions critical for cognition.     

Variability of familial risk of Alzheimer disease across the late life span

CONTEXT: The role of genetic factors in Alzheimer disease (AD) varies across the late life span, complicating efforts to quantify the risk of AD for relatives of probands with AD. OBJECTIVES: To visualize the changing levels of familial risk according to proband onset age and the age of the at-risk relative and to determine the familiality of age at onset in AD. DESIGN: A retrospective, informant-based family study. SETTING, PATIENTS, AND OTHER PARTICIPANTS: Siblings and parents of probands with AD (relatives = 4687; probands = 904), ascertained at geriatric clinic and nursing home settings, and of elderly probands without dementia (relatives = 7649; probands = 1525) who were spouses of probands, participants at senior centers, or nursing home residents without dementia. MAIN OUTCOME MEASURES: Informant-based assessments of AD in the relatives were used to generate 3-dimensional surfaces representing the patterns of risk of AD across the late life span depending on the specific onset age of the proband with AD (or assessment age of the elderly proband without dementia). We then constructed a 3-dimensional, age-specific, 10-year hazard rate ratio (HRR) surface representing the relative risk of AD in relatives of probands with AD with smoothly shifting levels of onset age compared with relatives of elderly probands without dementia. RESULTS: The HRR surface peaked (HRR, 13.0) for younger sexagenarian relatives related to probands with AD with onset age in their early 60s. The HRRs dropped sharply both as the proband age at onset and the age of the relative increased. For relatives aged in their late 80s, the HRR fell lower than 2.0 regardless of proband onset age and their lower-limit 95% confidence intervals were less than 1.0. CONCLUSIONS: The role of genetic risk factors decreases with increasing onset age of the proband with AD regardless of the age of the relatives themselves. The familiality of onset age is greatly reduced at later ages. The role of environmental risk factors in AD likely increases with onset age.     

Social support and resilience to stress across the life span: A neurobiologic framework

This review discusses selected neurobiologic and genetic factors—including noradrenergic and hypothalamic-pituitary-adrenal axis markers, oxytocin pathways, and serotonin transporter and brain-derived neurotrophic factor gene polymorphisms—in the context of resilience to stress, with an emphasis on social support. Social support’s impact on medical and psychiatric health outcomes is reviewed, and putative mediators are discussed. The reviewed literature indicates that social support is exceptionally important to maintaining good physical and psychological health in the presence of genetic, developmental, and other environmental risks. Future studies should continue to explore the neurobiologic factors associated with social support’s contribution to stress resilience.     

Attention and memory evaluation across the life span: heterogeneous effects of age and education

The developmental sequences of attention and memory were studied by utilizing normative data derived from the neuropsychological battery named NEUROPSI ATTENTION AND MEMORY. A sample of 521 Spanish-speaking individuals, aged 6 to 85 years, participated in this study. In the adult sample, educational level ranged from 0 to 22 years of education. Data from subtests measuring orientation, attention and concentration, executive functions, working memory, immediate and delayed verbal memory, and immediate and delayed visual memory were included. The factor structure of the analyzed battery is presented. The effects of age and education on this structure were analyzed. Results suggested that although attention and memory are related, their developmental sequences are separated from one another. During childhood, the development of selective and sustained attention, attentional-working memory, and executive functions showed a fast improvement in performance. Development of verbal memory and place and person orientation showed a slower increment in scores. In the adult sample it was found that factors related to memory are sensitive to age, whereas those related to attention and executive functions are sensitive to education. The consideration of both the developmental sequence, as well as differential effects of education, can improve the sensitivity and specificity of neuropsychological measures, allowing early diagnosis of cognitive dysfunction and implementation of adequate rehabilitation programs.     

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.     

Human brain changes across the life span: a review of 56 longitudinal magnetic resonance imaging studies

There is consistent evidence that brain volume changes in early and late life. Most longitudinal studies usually only span a few years and include a limited number of participants. In this review, we integrate findings from 56 longitudinal magnetic resonance imaging (MRI) studies on whole brain volume change in healthy individuals. The individual longitudinal MRI studies describe only the development in a limited age range. In total, 2,211 participants were included. Age at first measurement varied between 4 and 88 years of age. The studies included in this review were performed using a large range of methods (e.g., different scanner protocols and different acquisition parameters). We applied a weighted regression analysis to estimate the age dependency of the rate of relative annual brain volume change across studies. The results indicate that whole brain volume changes throughout the life span. A wave of growth occurs during childhood/adolescence, where around 9 years of age a 1% annual brain growth is found which levels off until at age 13 a gradual volume decrease sets in. During young adulthood, between ～18 and 35 years of age, possibly another wave of growth occurs or at least a period of no brain tissue loss. After age 35 years, a steady volume loss is found of 0.2% per year, which accelerates gradually to an annual brain volume loss of 0.5% at age 60. The brains of people over 60 years of age show a steady volume loss of more than 0.5%. Understanding the mechanisms underlying these plastic brain changes may contribute to distinguishing progressive brain changes in psychiatric and neurological diseases from healthy aging processes. Hum Brain Mapp, 2012. © 2011 Wiley Periodicals, Inc     

Lexical emotional expression across the life span: quantitative and qualitative analyses of word list generation tasks

The current study examined the effects of age and gender on emotional and nonemotional expression using an experimental word list generation (WLG) task (also referred to in the literature as verbal fluency) from the New York Emotion Battery (Borod, Welkowitz, & Obler, 1992). Subjects were 28 young ( M = 29.6 years), 28 middle-aged (M = 49.8 years), and 28 older (M = 69.9 years) healthy adults. The WLG task consists of 8 emotional (E; 3 positive and 5 negative) and 8 nonemotional (NE) categories. We developed and present here a detailed word error-type analysis that was used to evaluate the lexical output. In this study, both quantitative (amount of output and error-types) and qualitative (accuracy and intensity) analyses were used. While subjects produced more nonemotional than emotional words and more positive than negative words, the amount of error-free output and the number of errors did not change with age. An age group by error-type interaction indicated that older adults, especially men, produced more repetition errors than younger adults. The error-free output was subsequently rated for accuracy and emotional intensity. The rating data revealed that older women's overall lexical output was less accurate than that produced by younger women. Also, negative emotional words were more accurate and intense than positive emotional words. The procedures described here have implications for research assessing word list generation and emotional expression in clinical populations.     

Behavioral phenotyping of mouse models of neurodevelopmental disorders: relevant social behavior patterns across the life span

Social responses are a key element for behavioral phenotyping of mouse models of neurodevelopmental disorders associated with social deficits. Here we describe selected behavioral responses that can be measured in developing and adult mice, with special emphasis on ultrasonic vocalizations, a behavioral response not yet systematically characterized in most of the genetic mouse models of social abnormalities. A recently developed task to measure social approach relevant to the first core symptom of autism is highlighted. We also focus on those developmental factors, including litter size, litter composition, and early social milieu, that are often underestimated when measuring adult social behavior in mouse models of neurodevelopmental disorders. We present a summary of available data concerning social behavioral responses in mice with targeted gene mutations. We conclude by suggesting that assessment of early behavioral traits, and corresponding relationships with adult behavioral profiles, could be a useful strategy to investigate mouse models of neurodevelopmental disorders associated with social deficits.