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In this article, we, for the first time, provide a comprehensive overview and unified framework of the impact of poverty and low socioeconomic status (SES) on the brain and behaviour. While there are many studies on the impact of low SES on the brain (including cortex, hippocampus, amygdala, and even neurotransmitters) and behaviours (including educational attainment, language development, development of psychopathological disorders), prior studies did not integrate behavioural, educational, and neural findings in one framework. Here, we argue that the impact of poverty and low SES on the brain and behaviour are interrelated. Specifically, based on prior studies, due to a lack of resources, poverty and low SES are associated with poor nutrition, high levels of stress in caregivers and their children, and exposure to socio-environmental hazards. These psychological and physical injuries impact the normal development of several brain areas and neurotransmitters. Impaired functioning of the amygdala can lead to the development of psychopathological disorders, while impaired hippocampus and cortex functions are associated with a delay in learning and language development as well as poor academic performance. This in turn perpetuates poverty in children, leading to a vicious cycle of poverty and psychological/physical impairments. In addition to providing economic aid to economically disadvantaged families, interventions should aim to tackle neural abnormalities caused by poverty and low SES in early childhood. Importantly, acknowledging brain abnormalities due to poverty in early childhood can help increase economic equity. In the current study, we provide a comprehensive list of future studies to help understand the impact of poverty on the brain., (© 2024 Walter de Gruyter GmbH, Berlin/Boston.)

Major depressive disorder (MDD) symptoms commonly occur after trauma-exposure, both alone and in combination with post-traumatic stress disorder (PTSD). This article reviews recent research on comorbidity between these disorders, including its implications for symptom severity and response to treatment. Despite considerable symptom overlap, the two disorders represent distinct constructs and depend, at least in part, on separate biological mechanisms. Both, however, are also clearly related to stress psychopathology. We recommend that more research focus specifically on the study of individual differences in symptom expression in order to identify distinct subgroups of individuals and develop targeted treatments. However, a barrier to this line of inquiry is the trend of excluding particular patients from clinical trials of new interventions based on symptom severity or comorbidity. Another obstacle is the overreliance on self-report measures in human research. We argue that developing computer-based behavioral measures in order to supplement self-report can help address this challenge. Furthermore, we propose that these measures can help tie findings from human and non-human animal research. A number of paradigms have been used to model MDD-and PTSD-like behavior in animals. These models remain valuable for understanding the biological basis of these disorders in humans and for identifying potential interventions, but they have been underused for the study of comorbidity. Although the interpretation of animal behavior remains a concern, we propose that this can also be overcome through the development of close human analogs to animal paradigms.

Many students suffer from anxiety when performing numerical calculations. Mathematics anxiety is a condition that has a negative effect on educational outcomes and future employment prospects. While there are a multitude of behavioral studies on mathematics anxiety, its underlying cognitive and neural mechanism remain unclear. This article provides a systematic review of cognitive studies that investigated mathematics anxiety. As there are no prior neural network models of mathematics anxiety, this article discusses how previous neural network models of mathematical cognition could be adapted to simulate the neural and behavioral studies of mathematics anxiety. In other words, here we provide a novel integrative network theory on the links between mathematics anxiety, cognition, and brain substrates. This theoretical framework may explain the impact of mathematics anxiety on a range of cognitive and neuropsychological tests. Therefore, it could improve our understanding of the cognitive and neurological mechanisms underlying mathematics anxiety and also has important applications. Indeed, a better understanding of mathematics anxiety could inform more effective therapeutic techniques that in turn could lead to significant improvements in educational outcomes.

High homocysteine levels in Alzheimer's disease (AD) result from low activity of the trans-sulfuration pathway. Glutathione levels are also low in AD. L-cysteine is required for the synthesis of glutathione. The synthesis of coenzyme A (CoA) requires L-cysteine, which is synthesized via the trans-sulfuration pathway. CoA is required for the synthesis of acetylcholine and appropriate cholinergic neurotransmission. L-cysteine is required for the synthesis of molybdenum-containing proteins. Sulfite oxidase (SUOX), which is a molybdenum-containing protein, could be dysregulated in AD. SUOX detoxifies the sulfites. Glutaminergic neurotransmission could be dysregulated in AD due to low levels of SUOX and high levels of sulfites. L-cysteine provides sulfur for iron-sulfur clusters. Oxidative phosphorylation (OXPHOS) is heavily dependent on iron-sulfur proteins. The decrease in OXPHOS seen in AD could be due to dysregulations of the trans-sulfuration pathway. There is a decrease in aconitase 1 (ACO1) in AD. ACO1 is an iron-sulfur enzyme in the citric acid cycle that upon loss of an iron-sulfur cluster converts to iron regulatory protein 1 (IRP1). With the dysregulation of iron-sulfur cluster formation ACO1 will convert to IRP1 which will decrease the 2-oxglutarate synthesis dysregulating the citric acid cycle and also dysregulating iron metabolism. Selenomethionine is also metabolized by the trans-sulfuration pathway. With the low activity of the trans-sulfuration pathway in AD selenoproteins will be dysregulated in AD. Dysregulation of selenoproteins could lead to oxidant stress in AD. In this article, we propose a novel treatment for AD that addresses dysregulations resulting from low activity of the trans-sulfuration pathway and low L-cysteine.

Treatment-resistant schizophrenia (TRS) is a severe form of schizophrenia. The severity of illness is positively related to homocysteine levels, with high homocysteine levels due to the low activity of the transsulfuration pathway, which metabolizes homocysteine in synthesizing L-cysteine. Glutathione levels are low in schizophrenia, which indicates shortages of L-cysteine and low activity of the transsulfuration pathway. Hydrogen sulfide (H2S) levels are low in schizophrenia. H2S is synthesized by cystathionine β-synthase and cystathionine γ-lyase, which are the two enzymes in the transsulfuration pathway. Iron-sulfur proteins obtain sulfur from L-cysteine. The oxidative phosphorylation (OXPHOS) pathway has various iron-sulfur proteins. With low levels of L-cysteine, iron-sulfur cluster formation will be dysregulated leading to deficits in OXPHOS in schizophrenia. Molybdenum cofactor (MoCo) synthesis requires sulfur, which is obtained from L-cysteine. With low levels of MoCo synthesis, molybdenum-dependent sulfite oxidase (SUOX) will not be synthesized at appropriate levels. SUOX detoxifies sulfite from sulfur-containing amino acids. If sulfites are not detoxified, there can be sulfite toxicity. The transsulfuration pathway metabolizes selenomethionine, whereby selenium from selenomethionine can be used for selenoprotein synthesis. The low activity of the transsulfuration pathway decreases selenoprotein synthesis. Glutathione peroxidase (GPX), with various GPXs being selenoprotein, is low in schizophrenia. The dysregulations of selenoproteins would lead to oxidant stress, which would increase the methylation of genes and histones leading to epigenetic changes in TRS. An add-on treatment to mainline antipsychotics is proposed for TRS that targets the dysregulations of the transsulfuration pathway and the dysregulations of other pathways stemming from the transsulfuration pathway being dysregulated.

Future episodic thinking refers to the ability to imagine oneself in the future and project oneself into specific future events. This cognitive process is related to decision making and planning for the future. Although healthy populations commonly project themselves into the future (e.g. while planning a trip or career), patients with mood disorders show impairment in this ability. In this review article, we discuss the similarities and differences in future thinking among the following populations: major depressive disorder, dysphoria, anxiety, and post-traumatic stress disorder (PTSD). Importantly, we highlight the methodological variations in future episodic memory tasks in the literature that may explain the differences in the existing results.

Thanks to the current advances in the software analysis of facial expressions, there is a burgeoning interest in understanding emotional facial expressions observed during the retrieval of autobiographical memories. This review describes the research on facial expressions during autobiographical retrieval showing distinct emotional facial expressions according to the characteristics of retrieved memoires. More specifically, this research demonstrates that the retrieval of emotional memories can trigger corresponding emotional facial expressions (e.g. positive memories may trigger positive facial expressions). Also, this study demonstrates the variations of facial expressions according to specificity, self-relevance, or past versus future direction of memory construction. Besides linking research on facial expressions during autobiographical retrieval to cognitive and affective characteristics of autobiographical memory in general, this review positions this research within the broader context research on the physiologic characteristics of autobiographical retrieval. We also provide several perspectives for clinical studies to investigate facial expressions in populations with deficits in autobiographical memory (e.g. whether autobiographical overgenerality in neurologic and psychiatric populations may trigger few emotional facial expressions). In sum, this review paper demonstrates how the evaluation of facial expressions during autobiographical retrieval may help understand the functioning and dysfunctioning of autobiographical memory.

This study investigates the relationship between mindfulness, meditation, cognition and stress in people with Alzheimer's disease (AD), dementia, mild cognitive impairment and subjective cognitive decline. Accordingly, we explore how the use of meditation as a behavioural intervention can reduce stress and enhance cognition, which in turn ameliorates some dementia symptoms. A narrative review of the literature was conducted with any studies using meditation as an intervention for dementia or dementia-related memory conditions meeting inclusion criteria. Studies where moving meditation was the main intervention were excluded due to the possible confounding of exercise. Ten papers were identified and reviewed. There was a broad use of measures across all studies, with cognitive assessment, quality of life and perceived stress being the most common. Three studies used functional magnetic resonance imaging to measure functional changes to brain regions during meditation. The interventions fell into the following three categories: mindfulness, most commonly mindfulness-based stress reduction (six studies); Kirtan Kriya meditation (three studies); and mindfulness-based Alzheimer's stimulation (one study). Three of these studies were randomised controlled trials. All studies reported significant findings or trends towards significance in a broad range of measures, including a reduction of cognitive decline, reduction in perceived stress, increase in quality of life, as well as increases in functional connectivity, percent volume brain change and cerebral blood flow in areas of the cortex. Limitations and directions for future studies on meditation-based treatment for AD and stress management are suggested.

Neurodegenerative diseases, such as Alzheimer's disease, Huntington's disease, Parkinson's disease, prion disease, and amyotrophic lateral sclerosis, are a dissimilar group of disorders that share a hallmark feature of accumulation of abnormal intraneuronal or extraneuronal misfolded/unfolded protein and are classified as protein misfolding disorders. Cellular and endoplasmic reticulum (ER) stress activates multiple signaling cascades of the unfolded protein response (UPR). Consequently, translational and transcriptional alterations in target gene expression occur in response directed toward restoring the ER capacity of proteostasis and reestablishing the cellular homeostasis. Evidences from in vitro and in vivo disease models indicate that disruption of ER homeostasis causes abnormal protein aggregation that leads to synaptic and neuronal dysfunction. However, the exact mechanism by which it contributes to disease progression and pathophysiological changes remains vague. Downstream signaling pathways of UPR are fully integrated, yet with diverse unexpected outcomes in different disease models. Three well-identified ER stress sensors have been implicated in UPR, namely, inositol requiring enzyme 1, protein kinase RNA-activated-like ER kinase (PERK), and activating transcription factor 6. Although it cannot be denied that each of the involved stress sensor initiates a distinct downstream signaling pathway, it becomes increasingly clear that shared pathways are crucial in determining whether or not the UPR will guide the cells toward adaptive prosurvival or proapoptotic responses. We review a body of work on the mechanism of neurodegenerative diseases based on oxidative stress and cell death pathways with emphasis on the role of PERK.

In this review, we discuss the genetic etiologies of Alzheimer's disease (AD). Furthermore, we review genetic links to protein signaling pathways as novel pharmacological targets to treat AD. Moreover, we also discuss the clumps of AD-m ediated genes according to their single nucleotide polymorphism mutations. Rigorous data mining approaches justified the significant role of genes in AD prevalence. Pedigree analysis and twin studies suggest that genetic components are part of the etiology, rather than only being risk factors for AD. The first autosomal dominant mutation in the amyloid precursor protein (APP) gene was described in 1991. Later, AD was also associated with mutated early-onset (presenilin 1/2, PSEN1/2 and APP) and late-onset (apolipoprotein E, ApoE) genes. Genome-wide association and linkage analysis studies with identified multiple genomic areas have implications for the treatment of AD. We conclude this review with future directions and clinical implications of genetic research in AD.

In this review, we provide an overview of the relationship between cannabis use and the development of schizophrenia, using both animal and human studies. We further discuss the potential neural mechanism that may mediate the relationship between cannabis use and schizophrenia symptoms. We finally provide clinical implications and future studies that can further elucidate the relationship between cannabis and schizophrenia.

There are many factors that strongly influence the aetiology, development, and progression of cognitive decline in old age, mild cognitive impairment (MCI), and Alzheimer's disease (AD). These factors include not only different personality traits and moods but also lifestyle patterns (e.g. exercise and diet) and awareness levels that lead to cognitive decline in old age. In this review, we discuss how personality traits, mood states, and lifestyle impact brain and behaviour in older adults. Specifically, our review shows that these lifestyle and personality factors affect several brain regions, including the hippocampus, a region key for memory that is affected by cognitive decline in old age as well as AD. Accordingly, appropriate recommendations are presented in this review to assist individuals in decreasing chances of MCI, dementia, AD, and associated symptoms.

Given that achievement in learning mathematics at school correlates with work and social achievements, it is important to understand the cognitive processes underlying abilities to learn mathematics efficiently as well as reasons underlying the occurrence of mathematics anxiety (i.e. feelings of tension and fear upon facing mathematical problems or numbers) among certain individuals. Over the last two decades, many studies have shown that learning mathematical and numerical concepts relies on many cognitive processes, including working memory, spatial skills, and linguistic abilities. In this review, we discuss the relationship between mathematical learning and cognitive processes as well as the neural substrates underlying successful mathematical learning and problem solving. More importantly, we also discuss the relationship between these cognitive processes, mathematics anxiety, and mathematics learning disabilities (dyscalculia). Our review shows that mathematical cognition relies on a complex brain network, and dysfunction to different segments of this network leads to varying manifestations of mathematical learning disabilities.

Here, we provide a review of behavioural, cognitive, and neural studies of the thalamus, including its role in attention, consciousness, sleep, and motor processes. We further discuss neuropsychological and brain disorders associated with thalamus function, including Parkinson's disease, Alzheimer's disease, Korsakoff's syndrome, and sleep disorders. Importantly, we highlight how thalamus-related processes and disorders can be explained by the role of the thalamus as a relay station.

Parkinson's disease (PD) is primarily a motor disorder that involves the gradual loss of motor function. Symptoms are observed initially in the extremities, such as hands and arms, while advanced stages of the disease can effect blinking, swallowing, speaking, and breathing. PD is a neurodegenerative disease, with dopaminergic neuronal loss occurring in the substantia nigra pars compacta, thus disrupting basal ganglia functions. This leads to downstream effects on other neurotransmitter systems such as glutamate, γ-aminobutyric acid, and serotonin. To date, one of the main treatments for PD is levodopa. While it is generally very effective, prolonged treatments lead to levodopa-induced dyskinesia (LID). LID encompasses a family of symptoms ranging from uncontrolled repetitive movements to sustained muscle contractions. In many cases, the symptoms of LID can cause more grief than PD itself. The purpose of this review is to discuss the possible clinical features, cognitive correlates, neural substrates, as well as potential psychopharmacological and surgical (including nondopaminergic and deep brain stimulation) treatments of LID.

Parkinson's disease (PD) is characterized by a range of motor symptoms. Besides the cardinal symptoms (tremor, bradykinesia/akinesia, and rigidity), PD patients also show other motor deficits, including gait disturbance, speech deficits, and impaired handwriting. However, along with these key motor symptoms, PD patients also experience cognitive deficits in attention, executive function, working memory, and learning. Recent evidence suggests that these motor and cognitive deficits of PD are not completely dissociable, as aspects of cognitive dysfunction can impact motor performance in PD. In this article, we provide a review of behavioral and neural studies on the associations between motor symptoms and cognitive deficits in PD, specifically akinesia/bradykinesia, tremor, gait, handwriting, precision grip, and speech production. This review paves the way for providing a framework for understanding how treatment of cognitive dysfunction, for example cognitive rehabilitation programs, may in turn influence the motor symptoms of PD.

Postural instability (PI) is one of the most debilitating motor symptoms of Parkinson's disease (PD), as it is associated with an increased risk of falls and subsequent medical complications (e.g. fractures), fear of falling, decreased mobility, self-restricted physical activity, social isolation, and decreased quality of life. The pathophysiological mechanisms underlying PI in PD remain elusive. This short review provides a critical summary of the literature on PI in PD, covering the clinical features, the neural and cognitive substrates, and the effects of dopaminergic medications and deep brain stimulation. The delayed effect of dopaminergic medication combined with the success of extrastriatal deep brain stimulation suggests that PI involves neurotransmitter systems other than dopamine and brain regions extending beyond the basal ganglia, further challenging the traditional view of PD as a predominantly single-system neurodegenerative disease.

Introduction: Schizophrenia is a severe mental disorder with multiple psychopathological domains being affected. Several lines of evidence indicate that cognitive impairment serves as the key component of schizophrenia psychopathology. Although there have been a multitude of cognitive studies in schizophrenia, there are many conflicting results. We reasoned that this could be due to individual differences among the patients (i.e. variation in the severity of positive vs. negative symptoms), different task designs, and/or the administration of different antipsychotics., Methods: We thus review existing data concentrating on these dimensions, specifically in relation to dopamine function. We focus on most commonly used cognitive domains: learning, working memory, and attention., Results: We found that the type of cognitive domain under investigation, medication state and type, and severity of positive and negative symptoms can explain the conflicting results in the literature., Conclusions: This review points to future studies investigating individual differences among schizophrenia patients in order to reveal the exact relationship between cognitive function, clinical features, and antipsychotic treatment.