Neuroscience and Biobehavioral Reviews最新文献

The large number of different analytical choices used by researchers is partly responsible for the challenge of replication in neuroimaging studies. For an exhaustive robustness analysis, knowledge of the full space of analytical options is essential. We conducted a systematic literature review to identify the analytical decisions in functional neuroimaging data preprocessing and analysis in the emerging field of cognitive network neuroscience. We found 61 different steps, with 17 of them having debatable parameter choices. Scrubbing, global signal regression, and spatial smoothing are among the controversial steps. There is no standardized order in which different steps are applied, and the parameter settings within several steps vary widely across studies. By aggregating the pipelines across studies, we propose three taxonomic levels to categorize analytical choices: 1) inclusion or exclusion of specific steps, 2) parameter tuning within steps, and 3) distinct sequencing of steps. We have developed a decision support application with high educational value called METEOR to facilitate access to the data in order to design well-informed robustness (multiverse) analysis.

Lifespan developmental theories and research suggest a positive effect of adult age on prosociality. However, this effect lacks consistency, with many studies excluding the period of midlife. This study summarized cross-sectional studies on adult age and prosociality, combining 120 (independent) samples (n = 103,829) in a lifespan meta-analysis approach. Linear and quadratic age effects on prosociality were analyzed, as well as comparisons between younger, middle-aged, and older adults. Prosociality was assessed via behavioral measures and self-reports. In both these domains, results indicated small linear age effects and higher prosociality in older compared to younger adults, supporting the hypothesis of increased prosociality in older age. Additionally, leveraging open data sets (64/120 independent samples), predominantly unpublished, we found some evidence for potential quadratic age effects on behavioral prosociality: Middle-aged adults exhibited higher behavioral and self-reported prosociality than younger adults, but no differences between middle-aged and older adults were observed. This meta-analysis offers new perspectives on age trajectories of prosociality, suggesting midlife as a potentially important phase of pronounced prosociality.

A resurgence of panpsychism and dualism is a matter of ongoing debate in modern neuroscience. Although metaphysically hostile, panpsychism and dualism both persist in the science of consciousness because the former is proposed as a straightforward answer to the problem of integrating consciousness into the fabric of physical reality, whereas the latter proposes a simple solution to the problem of free will by endowing consciousness with causal power as a prerequisite for moral responsibility. I take the Integrated Information Theory (IIT) as a paradigmatic exemplar of a theory of consciousness (ToC) that makes its commitments to panpsychism and dualism within a unified framework. These features are not, however, unique for IIT. Many ToCs are implicitly prone to some degree of panpsychism whenever they strive to propose a universal definition of consciousness, associated with one or another known phenomenon. Yet, those ToCs that can be characterized as strongly emergent are at risk of being dualist. A remedy against both covert dualism and uncomfortable corollaries of panpsychism can be found in the evolutionary theory of life, called here “bioprotopsychism” and generalized in terms of autopoiesis and the free energy principle. Bioprotopsychism provides a biologically inspired basis for a minimalist approach to consciousness via the triad "chemotaxis-efference copy mechanism-counterfactual active inference" by associating the stream of weakly emergent conscious states with an amount of information (best guesses) of the brain, engaged in unconscious predictive processing.

This systematic review explored the impact of maternal immune activation (MIA) on learning and memory behavior in offspring, with a particular focus on sexual dimorphism. We analyzed 20 experimental studies involving rodent models (rats and mice) exposed to either lipopolysaccharide (LPS) or POLY I:C during gestation following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. Our findings reveal that most studies report a detrimental impact of MIA on the learning and memory performance of offspring, highlighting the significant role of prenatal environmental factors in neurodevelopment. Furthermore, this review underscores the complex effects of sex, with males often exhibiting more pronounced cognitive impairment compared to females. Notably, a small subset of studies report enhanced cognitive function following MIA, suggesting complex, context-dependent outcomes of prenatal immune challenges. This review also highlights sex differences caused by the effects of MIA in terms of cytokine responses, alterations in gene expression, and differences in microglial responses as factors that contribute to the cognitive outcomes observed.

Imbalances in dopamine activity significantly contribute to the pathophysiology of several neuropsychiatric disorders, including addiction, ADHD, schizophrenia, impulse control disorders, and Parkinson’s Disease. Neuro(active)steroids, comprising endogenous steroids that finely modulate neuronal activity, are considered crucial regulators of brain function and behavior, with implications in various physiological processes and pathological conditions. Specifically, subclasses of Neuro(active)steroids belonging to the 5α reductase pathway are prominently involved in brain disorders characterized by dopaminergic signaling imbalances. This review highlights the neuromodulatory effects of Neuro(active)steroids on the dopamine system and related aberrant behavioral phenotypes. We critically appraise the role of pregnenolone, progesterone, and allopregnanolone on dopamine signaling. Additionally, we discuss the impact of pharmacological interventions targeting 5α reductase activity in neuropsychiatric conditions characterized by excessive activation of the dopaminergic system, ranging from psychotic (endo)phenotypes and motor complications to decision-making problems and addiction.

This meta-analysis examined inhibitory control performance in the antisaccade task across mental disorders. Following PRISMA guidelines, we analyzed data from k = 146 studies (n = 13,807 participants) on antisaccade performance. Effect sizes were estimated using random-effects models and restricted maximum-likelihood estimation, with robustness tests for study heterogeneity and publication bias. Most disorders displayed elevated error rates, with schizophrenia showing the greatest impairments, followed by autism spectrum disorder, bipolar disorder and attention deficit hyperactivity disorder. Small to medium impairments were also found in eating disorders, major depressive disorder, obsessive-compulsive disorder and substance use disorder. Results were robust against corrections for publication bias and largely unaffected by confounding variables. Prolonged latencies were observed in schizophrenia, attention deficit hyperactivity disorder, bipolar disorder and obsessive compulsive disorder, with smaller and less robust effect sizes. Results indicate inhibitory control deficits in the antisaccade task across mental disorders, especially evident for error rates. While present in most disorders, results imply varying degrees of impairments, ranging from small to large in effect sizes, with largest impairments in schizophrenia.

Our intricate social brain is implicated in a range of brain disorders, where social dysfunction emerges as a common neuropsychiatric feature cutting across diagnostic boundaries. Understanding the neurocircuitry underlying social dysfunction and exploring avenues for its restoration could present a transformative and transdiagnostic approach to overcoming therapeutic challenges in these disorders. The brain's default mode network (DMN) plays a crucial role in social functioning and is implicated in various neuropsychiatric conditions. By thoroughly examining the current understanding of DMN functionality, we propose that the DMN integrates diverse social processes, and disruptions in brain communication at regional and network levels due to disease hinder the seamless integration of these social functionalities. Consequently, this leads to an altered balance between self-referential and attentional processes, alongside a compromised ability to adapt to social contexts and anticipate future social interactions. Looking ahead, we explore how adopting an integrated neurocircuitry perspective on social dysfunction could pave the way for innovative therapeutic approaches to address brain disorders.

Stimulants represent the first line pharmacological treatment for attention-deficit/hyperactivity disorder (ADHD) and are among the most prescribed psychopharmacological treatments. Their mechanism of action at synaptic level has been extensively studied. However, it is less clear how their mechanism of action determines clinically observed benefits. To help bridge this gap, we provide a comprehensive review of stimulant effects, with an emphasis on nuclear medicine and magnetic resonance imaging (MRI) findings. There is evidence that stimulant-induced modulation of dopamine and norepinephrine neurotransmission optimizes engagement of task-related brain networks, increases perceived saliency, and reduces interference from the default mode network. An acute administration of stimulants may reduce brain alterations observed in untreated individuals in fronto-striato-parieto-cerebellar networks during tasks or at rest. Potential effects of prolonged treatment remain controversial. Overall, neuroimaging has fostered understanding on stimulant mechanism of action. However, studies are often limited by small samples, short or no follow-up, and methodological heterogeneity. Future studies should address age-related and longer-term effects, potential differences among stimulants, and predictors of treatment response.

A systematic review of functional neuroimaging studies on drug (self-) administration in rodents is lacking. Here, we summarized effects of acute or chronic drug administration of various classes of drugs on brain function and determined consistency with human literature.

We performed a systematic literature search and identified 125 studies on in vivo rodent resting-state functional magnetic resonance imaging (n = 84) or positron emission tomography (n = 41) spanning depressants (n = 27), opioids (n = 23), stimulants (n = 72), and cannabis (n = 3).

Results primarily showed alterations in the striatum, consistent with the human literature. The anterior cingulate cortex and (nonspecific) prefrontal cortex were also frequently implicated. Upregulation was most often found after shorter administration and downregulation after long chronic administration, particularly in the striatum. Importantly, results were consistent across study design, administration models, imaging method, and animal states.

Results provide evidence of altered resting-state brain function in rodents upon drug administration, implicating the brain’s reward network analogous to human studies. However, alterations were more dynamic than previously known, with dynamic adaptation depending on the length of drug administration.

Elucidating the molecular mechanisms of psychopathology is crucial for optimized diagnosis and treatment. Accumulating data have underlined how mitochondrial bioenergetics affect major psychiatric disorders. However, how mitochondrial dynamics, a term addressing mitochondria quality control, including mitochondrial fission, fusion, biogenesis and mitophagy, is implicated in psychopathologies remains elusive. In this review, we summarize the existing literature on mitochondrial dynamics perturbations in psychiatric disorders/neuropsychiatric phenotypes. We include preclinical/clinical literature on mitochondrial dynamics recalibrations in anxiety, depression, post-traumatic stress disorder (PTSD), bipolar disorder and schizophrenia. We discuss alterations in mitochondrial network, morphology and shape, molecular markers of the mitochondrial dynamics machinery and mitochondrial DNA copy number (mtDNAcn) in animal models and human cohorts in brain and peripheral material. By looking for common altered mitochondrial dynamics patterns across diagnoses/phenotypes, we highlight mitophagy and biogenesis as regulators of anxiety and depression pathophysiology, respectively, as well as the fusion mediator dynamin-like 120 kDa protein (Opa1) as a molecular hub contributing to psychopathology. Finally, we comment on limitations and future directions in this novel neuropsychiatry field.