Ye In (Jane) Hwang, Kitty-Rose Foley, Samuel Arnold, and Julian Trollor
Autism spectrum disorder (ASD), or autism, is a neurodevelopmental disorder that is typically recognized and diagnosed in childhood. There is no established biological marker for autism; rather, the diagnosis is made based on observation of behavioral traits, including (a) persistent deficits in social interaction and communication, and (b) restricted, repetitive patterns of behavior, interests, or activities. Because autism is a spectrum disorder, autistic individuals are a highly heterogeneous group and differ widely in the presentation and severity of their symptoms. The established prevalence of ASD is approximately 1% of the population.
Information about autism in adulthood is limited; most of the literature examines childhood and adolescence. While the term “later life” has traditionally been associated with those over the age of 65, a dire lack of understanding exists for those on the autism spectrum beyond early adulthood.
Individuals remain on the spectrum into later life, though some mild improvements in symptoms are observed over time. Autistic adults experience high levels of physical and mental health comorbidities. Rates of participation in employment and education are also lower than that of the general population. Quality of life is reportedly poorer for autistic adults than for nonautistic peers, though this is not affected by age. More robust studies of the health, well-being, and needs of autistic adults are needed, especially qualitative investigations of adulthood and aging and longitudinal studies of development over the lifespan.
Shellie-Anne T. Levy and Glenn E. Smith
Dementia, also now known as major neurocognitive disorder, is a syndrome involving decline in two or more areas of cognitive function sufficient to disrupt a person’s daily function. Mild cognitive impairment (MCI), also known as minor neurocognitive disorder, represents a syndrome on the continuum of cognitive decline that is a stage prior to development of functional deficits. It involves decline in one or more areas of cognitive function with independence in instrumental activities of daily living, even though they may require greater effort or compensation on the part of the individual. Neuropsychological assessment of cognition and behavior provides the most powerful biomarkers for MCI and dementia syndromes associated with neurodegenerative diseases. Discrete cognitive and behavioral patterns that occur early in the course of cognitive decline aids in differential clinical diagnosis. Additionally, all diagnostic schemes for dementia syndromes include criteria that require the appraisal of functional status, which tests an individual’s capacity to engage in decision making and carry out activities of daily living independently. Methods for assessing functional status have historically had poor reliability and validity. Nevertheless, in a clinical setting, neuropsychologists rely on a combination of self-report, collateral informants, caregiver questionnaires, and objective performance-based measures to better assess functional status. Revisions to clinical criteria for dementia reflect the adoption of new research diagnostic criteria for neurodegenerative diseases, largely driven by the National Institutes of Aging (NIA) and the Alzheimer’s Association 2011 research criteria for Alzheimer’s disease (AD). The new approach differentiates the syndromic presentations common to most neurodegenerative diseases from the etiologies (AD, LBD, VaD, etc.) based on biomarkers. In the preclinical stage, biomarker abnormalities are present years before clinical symptom manifestation. In mild cognitive impairment stage, there is a report/concern for cognitive change by the patient, informant, or clinician. There is objective cognitive decline from estimated premorbid functioning and preserved independence in functional abilities. In the dementia stage, in the context of impaired functional status, there may be prominent cognitive and behavioral symptoms that may involve impairment in memory, executive function, visuospatial functioning, and language, as well as changes in personality and behavior. The most common dementias are AD, dementia with Lewy bodies (DLB), frontotemporal dementia (FTD), and vascular dementia (VaD). All can follow a trajectory of cognitive decline similar to the aforementioned stages and are associated with neuropathogenic mechanisms that may or may not be distinctive for a particular syndrome. Briefly, Alzheimer’s dementia is associated with accumulation of amyloid plaques and tau neurofibrillary tangles. Lewy body dementias (i.e., Parkinson’s disease dementia and DLB) are characterized by Lewy bodies (alpha-synuclein aggregates) and Lewy neurites in the brainstem, limbic system, and cortical regions; DLB is also associated with diffuse amyloid plaques. Frontotemporal dementia is a conglomerate of syndromes that may overlap and include behavioral variant FTD, semantic dementia, and primary progressive aphasia (PPA). FTD dementia syndromes are marked by frontotemporal lobar degeneration (FTLD) caused by pathophysiological processes involving FTLD-tau, FTLD-TDP, FTLD-FUS, or their combination, as well as beta amyloid. Lastly, vascular dementia is associated with cerebrovascular disease that can include large artery occlusions, microinfarcts, brain hemorrhages, and silent brain infarcts; comorbid AD pathology may lower the threshold for dementia conversion. There is an emerging shift in the field toward exploring prevention strategies for dementia. Given the lack of precision in our language regarding the distinction between dementia syndromes and etiologies, we can reallocate some of our efforts to preventing dementia more broadly rather than intervening on a certain pathology. Research already supports that many individuals have biomarker evidence of brain pathology without showing cognitive impairment or even sufficient levels of pathology in the brain to warrant a diagnosis without ever displaying the clinical syndrome of dementia. That said, building cognitive reserve or resilience through lifestyle and behavioral factors may slow the rate of cognitive decline and prevent the risk of a future dementia epidemic.
Philip Sayegh, David J. Moore, and Pariya Fazeli Wheeler
Since the first cluster of people with HIV was identified in 1981, significant biomedical advances, most notably the development of antiretroviral therapy (ART), have led to considerably increased life expectancy as well as a reduction in the morbidity and mortality associated with HIV/AIDS. As a result, HIV/AIDS is no longer considered a terminal illness, but rather a chronic illness, and many persons living with HIV/AIDS are beginning to enter or have already reached later life. In fact, Americans ages 50 years and older comprise approximately half of all individuals with HIV/AIDS and represent the most rapidly growing subpopulation of persons living with HIV/AIDS in the United States.
Despite significant advances in HIV/AIDS treatment and prognosis, older adults living with HIV (OALH) face a number of unique challenges and circumstances that can lead to exacerbated symptoms and poorer outcomes, despite demonstrating generally better ART adherence than their younger counterparts. These detrimental outcomes are due to both chronological aging and cohort effects as well as social and behavioral factors and long-term ART use. For instance, neurocognitive deficits and neuropsychiatric symptoms, including depression, anxiety, apathy, and fatigue, are often observed among OALH, which can result in feelings of loneliness, social isolation, and reduced social support. Taken together, these factors can lead to elevated levels of problems with everyday functioning (e.g., activities of daily living) among OALH. In addition, sociocultural factors such as race/ethnicity, ageism, sexism, homophobia, transphobia, geographic region, socioeconomic status and financial well-being, systemic barriers and disparities, and cultural values and beliefs play an influential role in determining outcomes.
Notwithstanding the challenges associated with living with HIV/AIDS in later life, many persons living with HIV/AIDS are aging successfully. HIV/AIDS survivor and community mobilization efforts, as well as integrated care models, have resulted in some significant improvements in overall HIV/AIDS patient care. In addition, interventions aimed at improving successful aging outcomes among OALH are being developed in an attempt to effectively reduce the psychological and physical morbidity associated with HIV disease.
Life is filled with goals or intentions that people hope to realize. Some of these are rather mundane (e.g., remembering to purchase a key ingredient for a recipe when stopping at the market), while others are more significant (e.g., remembering to pick up one’s child from school at the end of the day). Prospective memory represents the ability to form and then realize intentions at an appropriate time. A fundamental aspect of prospective memory is that one is engaged in one or more tasks (i.e., ongoing activities) between the formation of an intention and the opportunity to realize the goal. For instance, in the shopping example, one might form the intention at home and then travel to the market and collect several other items before walking past the desired ingredient. Considerable research has demonstrated that the efficiency of prospective memory declines with age, although age-related differences are not universal.
The neurocognitive processes underpinning age-related differences in the formation and realization of delayed intentions have been investigated in studies using event-related brain potentials. This research reveals that age-related differences in prospective memory arise from the disruption of neural systems supporting the successful encoding of intentions, the detection of prospective memory cues, and possibly processes supporting the retrieval of intentions from memory when a cue is encountered or efficiently shifting from the ongoing activity to the prospective element of the task. Therefore, strategies designed to ameliorate age-related declines in prospective memory should target a variety of processes engaged during the encoding, retrieval, and enactment of delayed intentions.
David J. Madden and Zachary A. Monge
Age-related decline occurs in several aspects of fluid, speed-dependent cognition, particularly those related to attention. Empirical research on visual attention has determined that attention-related effects occur across a range of information processing components, including the sensory registration of features, selection of information from working memory, controlling motor responses, and coordinating multiple perceptual and cognitive tasks. Thus, attention is a multifaceted construct that is relevant at virtually all stages of object identification. A fundamental theme of attentional functioning is the interaction between the bottom-up salience of visual features and top-down allocation of processing based on the observer’s goals. An underlying age-related slowing is prominent throughout visual processing stages, which in turn contributes to age-related decline in some aspects of attention, such as the inhibition of irrelevant information and the coordination of multiple tasks. However, some age-related preservation of attentional functioning is also evident, particularly the top-down allocation of attention. Neuroimaging research has identified networks of frontal and parietal brain regions relevant for top-down and bottom-up attentional processing. Disconnection among these networks contributes to an age-related decline in attention, but preservation and perhaps even increased patterns of functional brain activation and connectivity also contribute to preserved attentional functioning.