The present review on HIV-associated neurocognitive disorders (HAND) provides a worldwide overview of studies that have investigated the rate and neuropsychological (NP) profile of HAND research since the inception of the 2007 HAND diagnostic nomenclature. In the first part, the review highlights some of the current controversies around HAND prevalence rates. In the second part, the review critically assesses some solutions to move the field forward. In the third part, we present the cross-sectional NP profile in non-Western HIV+ cohorts and in relation to Western cohorts’ findings. The adopted global perspective highlights the successful expansion of NP studies in HIV infection to culturally diverse low- to medium-income countries with high HIV burden. These studies have produced interestingly similar rates of HAND whether patients were naïve or treated and/or virally suppressed compared to the rich income countries where the NP research in NeuroHIV has originated. The perspective also demonstrates that globally, the group which is the most representative of the HIV epidemic, and thus at risk for HAND are persons with chronic HIV infection and survivors of past immunosuppression, while in relative terms, those who have been treated early with long-term viral suppression represent a minority. In the last part, we present a review of the naturalistic longitudinal NP global studies in HIV+cohorts, discuss the role of longitudinal design in solving issues around the question of asymptomatic neurocognitive impairment, and the question of biomarker discovery. Finally, we conclude by calling for greater methods and data harmonization at a global level. (JINS, 2017, 23, 860–869)

An ambition of depression biomarker research is to augment psychometric and cognitive assessment of clinically relevant phenomena with neural measures. Although such applications have been slow to arrive, we observe a steady evolution of the idea and anticipate emerging technologies with some optimism. To highlight critical themes and innovations in depression biomarker research, we take as our point of reference a specific research narrative. We begin with an early model of frontal-limbic dysfunction, which represents a conceptual shift from localized pathology to understanding symptoms as an emergent property of distributed networks. Over the decades, this model accommodates perspectives from neurology, psychiatry, clinical, and cognitive neuroscience, and preserves past insight as more complex methods become available. We also track the expanding mission of brain biomarker research: from the development of diagnostic tools to treatment selection algorithms, measures of neurocognitive functioning and novel targets for neuromodulation. To conclude, we draw from this particular research narrative future directions for biomarker research. We emphasize integration of measurement modalities to describe dynamic change in domain-general networks, and we speculate that a brain-based framework for psychiatric problems may dissolve classical diagnostic and disciplinary boundaries. (JINS, 2017, 23, 870–880)

We review the changing conceptions of schizophrenia over the past 50 years as it became understood as a disorder of brain function and structure in which neurocognitive dysfunction was identified at different illness phases. The centrality of neurocognition has been recognized, especially because neurocognitive deficits are strongly related to social and role functioning in the illness, and as a result neurocognitive measures are used routinely in clinical assessment of individuals with schizophrenia. From the original definitions of the syndrome of schizophrenia in the early 20th century, impaired cognition, especially attention, was considered to be important. Neurocognitive impairments are found in the vast majority of individuals with schizophrenia, and they vary from mild, relatively restricted deficits, to dementia-like syndromes, as early as the first psychotic episode. Neurocognitive deficits are found in the premorbid phase in a substantial minority of pre-teenage youth who later develop schizophrenia, and they apparently worsen by the prodromal, high-risk phase in a majority of those who develop the illness. While there is limited evidence for reversibility of impairments from pharmacological interventions in schizophrenia, promising results have emerged from cognitive remediation studies. Thus, we expect cognitive interventions to play a larger role in schizophrenia in the coming years. Moreover, because youth at risk for schizophrenia can be identified by an emergent high-risk syndrome, earlier interventions might be applied in a pre-emptive way to reduce disability and improve adaptation. The notion of schizophrenia as a developmental neurocognitive disorder with stages opens up a window of possibilities for earlier interventions. (JINS, 2017, 23, 881–892)

Cannabis use has been linked to impairments in neuropsychological functioning across a large and continually expanding body of research. Yet insight into underlying causal relations remains limited due to the historically cross-sectional nature of studies in this area. Recently, however, studies have begun to use more informative design strategies to delineate these associations. The aim of this article is to provide a critical evaluation and review of research that uses longitudinal designs to examine the link between cannabis use and neuropsychological functioning. In summarizing the primary findings across these studies, this review suggests that cannabis use leads to neuropsychological decline. However, across most studies, these associations were modest, were present only for the group with the heaviest cannabis use, and were often attenuated (or no longer significant) after controlling for potential confounding variables. Future studies with neuropsychological data before and after initiation of cannabis use, along with careful measurement and control of “shared risk factors” between cannabis use and poorer neuropsychological outcomes, are needed to better understand who, and under what conditions, is most vulnerable to cannabis-associated neuropsychological decline. (JINS, 2017, 23, 893–902)

Early autism research focused on behavior and cognition. In recent decades, the pace of research has accelerated, and advances in imaging and genetics have allowed the accumulation of biological data. Nevertheless, a coherent picture of the syndrome at either phenotypic or biological level has not emerged. We see two fundamental obstacles to progress in basic understanding of autism. First, the two defining features (impairment in social interactions and communication, and restricted, repetitive behaviors and interests) are historically seen as integrally related. Others hold that these two major traits are fractionable and must be studied independently, casting doubt on autism as a coherent syndrome. Second, despite much recent research on brain structure and function, environmental factors, and genetics/genomics, findings on the biological level have not generally aligned well with those on the phenotypic level. In the first two sections, we explore these challenges, and in the third section, we review approaches that may facilitate progress, such as (1) including in studies all individuals defined by social impairment without regard to repetitive behaviors, (2) forming narrowly defined subtypes by thorough characterization on specific features, both diagnostic and non-diagnostic, (3) focusing on characteristics that may be relatively robust to environmental influence, (4) studying children as early as possible, minimizing environmental influence, and including longitudinal course as an important part of the phenotype, (5) subtyping by environmental risk factors, (6) distinguishing between what participants can do and what they typically do, and (7) aggregating large data sets across sites. (JINS, 2017, 23, 903–915)

The behavior patterns of hyperactivity, impulsivity and inattention that would ultimately become recognized as Attention-Deficit Hyperactivity Disorder (ADHD) have been described for centuries. Nevertheless, in the past 35 years, advances in diagnostic methods, identification of biomarkers, and treatments have advanced at an exponential rate. ADHD is now recognized as the most common behavioral disorder of childhood, with risks extending well into adulthood for both males and females, leading to its identification as a significant public health issue. This historical neuropsychological review of ADHD emphasizes scientific highlights in the past 35 years related to ADHD, including the evolution of the diagnosis (from Hyperkinetic Reaction of Childhood to ADHD), influential theories (executive functions, cognitive-energetic, delay aversion), landmark treatment studies (Multimodal Treatment of ADHD [MTA] and Preschool ADHD Treatment Study [PATS]), and advances in brain mapping techniques (anatomic, functional, and resting state magnetic resonance imaging, diffusion tensor imaging). The review concludes by highlighting the challenges of studying and treating a heterogeneous neurodevelopmental disorder like ADHD, with emphasis on associated disorders and conditions (learning disabilities, sluggish cognitive tempo), special populations (girls, preschoolers, adults), and recommendations for scientific inquiry in the next 35 years. Neuropsychologists are well positioned to address the clinical and research challenges of the next generation of studies, especially involving advances in understanding the sexual dimor.phism, full developmental course, and dynamic risks associated with ADHD. (JINS, 2017, 23, 916–929)

Over the past 50 years, research on children and adults with learning disabilities has seen significant advances. Neuropsychological research historically focused on the administration of tests sensitive to brain dysfunction to identify putative neural mechanisms underlying learning disabilities that would serve as the basis for treatment. Led by research on classifying and identifying learning disabilities, four pivotal changes in research paradigms have produced a contemporary scientific, interdisciplinary, and international understanding of these disabilities. These changes are (1) the emergence of cognitive science, (2) the development of quantitative and molecular genetics, (3) the advent of noninvasive structural and functional neuroimaging, and (4) experimental trials of interventions focused on improving academic skills and addressing comorbid conditions. Implications for practice indicate a need to move neuropsychological assessment away from a primary focus on systematic, comprehensive assessment of cognitive skills toward more targeted performance-based assessments of academic achievement, comorbid conditions, and intervention response that lead directly to evidence-based treatment plans. Future research will continue to cross disciplinary boundaries to address questions regarding the interaction of neurobiological and contextual variables, the importance of individual differences in treatment response, and an expanded research base on (a) the most severe cases, (b) older people with LDs, and (c) domains of math problem solving, reading comprehension, and written expression. (JINS, 2017, 23, 930–940)