Intricacies of aging and Down syndrome.

Down syndrome is the most frequently occurring genetic condition, with a substantial escalation in risk associated with advanced maternal age. The syndrome is characterized by a diverse range of phenotypes, affecting to some extent all levels of organization, and its progeroid nature - early manifestation of aspects of the senile phenotype. Despite extensive investigations, many aspects and mechanisms of the disease remain unexplored. The current review aims to provide an overview of the main causes and manifestations of Down syndrome, while also examining the phenomenon of accelerated aging and exploring potential therapeutic strategies.

Cognitive dysfunctions in the course of SARS­CoV­2 virus infection, including NeuroCOVID, frontal syndrome and cytokine storm (Review).

During the coronavirus disease 2019 (COVID-19) pandemic, cognitive impairment of varying degrees of severity began to be observed in a significant percentage of patients. The present study discussed the impact of immunological processes on structural and functional changes in the central nervous system and the related cognitive disorders. The purpose of the present review was to analyse and discuss available information from the scientific literature considering the possible relationship between severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) viral infection and cognitive impairment, including NeuroCOVID, frontal syndrome and cytokine storm. A systematic literature review was conducted using: Google Scholar, Elsevier and the PubMed database. When searching for materials, the following keywords were used: 'cognitive dysfunctions', 'SARS-CoV-2', 'COVID-19', 'Neuro-SARS2', 'NeuroCOVID', 'frontal syndrome', 'cytokine storm', 'Long COVID-19'. A total of 96 articles were included in the study. The analysis focused on the characteristics of each study's materials, methods, results and conclusions. SARS-CoV-2 infection may induce or influence existing cognitive disorders of various nature and severity. The influence of immunological factors related to the response against SARS-CoV-2 on the disturbance of cerebral perfusion, the functioning of nerve cells and the neuroprotective effect has been demonstrated. Particular importance is attached to the cytokine storm and the related difference between pro- and anti-inflammatory effects, oxidative stress, disturbances in the regulation of the hypothalamic-pituitary-adrenal axis and the stress response of the body.

Dynamics of Lateral Habenula-Ventral Tegmental Area Microcircuit on Pain-Related Cognitive Dysfunctions.

Chronic pain is a health problem that affects the ability to work and perform other activities, and it generally worsens over time. Understanding the complex pain interaction with brain circuits could help predict which patients are at risk of developing central dysfunctions. Increasing evidence from preclinical and clinical studies suggests that aberrant activity of the lateral habenula (LHb) is associated with depressive symptoms characterized by excessive negative focus, leading to high-level cognitive dysfunctions. The primary output region of the LHb is the ventral tegmental area (VTA), through a bidirectional connection. Recently, there has been growing interest in the complex interactions between the LHb and VTA, particularly regarding their crucial roles in behavior regulation and their potential involvement in the pathological impact of chronic pain on cognitive functions. In this review, we briefly discuss the structural and functional roles of the LHb-VTA microcircuit and their impact on cognition and mood disorders in order to support future studies addressing brain plasticity during chronic pain conditions.

Risk factors for post-COVID cognitive dysfunctions: the impact of psychosocial vulnerability.

BACKGROUND: Cognitive dysfunction is a well-established manifestation of the post-COVID syndrome. Psychological vulnerability to stressors can modify disease trajectories, causing long-term risk for negative outcomes. Nonetheless, how premorbid risk factors and response to stressor affect neuropsychological changes is still incompletely understood. In this study, we explored the impact of psychosocial variables on cognitive functioning in a post-COVID sample. METHODS: All subjects were submitted to a comprehensive neuropsychological battery and an assessment of perceived loneliness, post-traumatic stress, and changes in anxiety and depression levels. A social vulnerability index was also calculated. The set of psycho-social variables was reduced to two Principal Component Analysis (PCA) components: distress and isolation. RESULTS: Forty-five percent of individuals showed cognitive impairments, with predominant memory and executive deficits. Post-traumatic stress disorder was clinically relevant in 44% of the sample. Social vulnerability scores of the sample were comparable to those of general population. The individual performance in learning and response initiation/suppression was directly related to distress component, encasing anxiety, stress, and depression measures. CONCLUSION: These findings suggest that psychosocial assessment of post-COVID patients can detect fragile individuals at risk of cognitive impairments. Dedicated psychological support services may play a useful role in the prevention of post-COVID cognitive dysfunction.

The role of the salience network in cognitive and affective deficits.

Analysis and interpretation of studies on cognitive and affective dysregulation often draw upon the network paradigm, especially the Triple Network Model, which consists of the default mode network (DMN), the frontoparietal network (FPN), and the salience network (SN). DMN activity is primarily dominant during cognitive leisure and self-monitoring processes. The FPN peaks during task involvement and cognitive exertion. Meanwhile, the SN serves as a dynamic "switch" between the DMN and FPN, in line with salience and cognitive demand. In the cognitive and affective domains, dysfunctions involving SN activity are connected to a broad spectrum of deficits and maladaptive behavioral patterns in a variety of clinical disorders, such as depression, insomnia, narcissism, PTSD (in the case of SN hyperactivity), chronic pain, and anxiety, high degrees of neuroticism, schizophrenia, epilepsy, autism, and neurodegenerative illnesses, bipolar disorder (in the case of SN hypoactivity). We discuss behavioral and neurological data from various research domains and present an integrated perspective indicating that these conditions can be associated with a widespread disruption in predictive coding at multiple hierarchical levels. We delineate the fundamental ideas of the brain network paradigm and contrast them with the conventional modular method in the first section of this article. Following this, we outline the interaction model of the key functional brain networks and highlight recent studies coupling SN-related dysfunctions with cognitive and affective impairments.

IL-1ß and TNF-α play an important role in modulating the risk of periodontitis and Alzheimer's disease.

BACKGROUND: Systemic activation of the immune system can exert detrimental effects on the central nervous system. Periodontitis, a chronic disease of the oral cavity, is a common source of systemic inflammation. Neuroinflammation might be a result of this to accelerate progressive deterioration of neuronal functions during aging or exacerbate pre-existing neurodegenerative diseases, such as Alzheimer's disease. With advancing age, the progressive increase in the body's pro-inflammatory status favors the state of vulnerability to both periodontitis and Alzheimer's disease. In the present study, we sought to delineate the roles of cytokines in the pathogenesis of both diseases. METHODS: To examine the impacts of periodontitis on the onset and progression of Alzheimer's disease, 6-month-old female 3 × Tg-AD mice and their age-matched non-transgenic mice were employed. Periodontitis was induced using two different experimental models: heat-killed bacterial-induced periodontitis and ligature-induced periodontitis. To delineate the roles of pro-inflammatory cytokines in the pathogenesis of periodontitis and Alzheimer's disease, interleukin 1 beta (IL-1ß) and tumor necrosis factor-alpha (TNF-α) were also injected into the buccal mandibular vestibule of mice. RESULTS: Here, we show that IL-1ß and TNF-α were two of the most important and earliest cytokines upregulated upon periodontal infection. The systemic upregulation of these two cytokines promoted a pro-inflammatory environment in the brain contributing to the development of Alzheimer's disease-like pathology and cognitive dysfunctions. Periodontitis-induced systemic inflammation also enhanced brain inflammatory responses and subsequently exacerbated Alzheimer's disease pathology and cognitive impairment in 3 × Tg-AD mice. The role of inflammation in connecting periodontitis to Alzheimer's disease was further affirmed in the conventional magnetization transfer experiment in which increased glial responses resulting from periodontitis led to decreased magnetization transfer ratios in the brain of 3 × Tg-AD mice. CONCLUSIONS: Systemic inflammation resulting from periodontitis contributed to the development of Alzheimer's disease tau pathology and subsequently led to cognitive decline in non-transgenic mice. It also potentiated Alzheimer's disease pathological features and exacerbated impairment of cognitive function in 3 × Tg-AD mice. Taken together, this study provides convincing evidence that systemic inflammation serves as a connecting link between periodontitis and Alzheimer's disease.

Distinct Neuropsychological Correlates of Apathy Sub-Domains in Multiple Sclerosis.

BACKGROUND: Apathy is relatively frequent and significantly associated with clinical and cognitive outcomes in Multiple Sclerosis (MS), even if previous research has produced mixed results. This varied picture could be due to most studies treating apathy as a unitary construct, despite the evidence showing that apathy is a multifaceted syndrome including three different sub-domains (i.e., cognitive, affective, and behavioral). This study aims to investigate the neuropsychological correlates of apathy fractionated into its three sub-domains in participants with MS. METHODS: Eighty-five participants with MS underwent a comprehensive neuropsychological battery. The severity of apathy symptoms was assessed by the self-report version of the Apathy Evaluation Scale. RESULTS: Correlational analysis showed that cognitive apathy sub-domain scores had a high correlation with the performances obtained at cognitive tests tapping into inhibitory control (i.e., IML and Strop test-interference task), whereas the affective apathy sub-domain scores had a high correlation with the performances obtained at cognitive test tapping into the use of executive functions in visuospatial abilities (i.e., Clock Drawing Test). Moreover, linear regression analysis results showed that the cognitive apathy sub-domain scores predicted executive functioning domain scores and that the cognitive and affective apathy sub-domains scores predicted visuospatial abilities domain scores. CONCLUSION: These results confirm that apathy is a multidimensional concept with important neuropsychological correlates, visible only when it is fractionated into its sub-domains.

A Study of Neurological Soft Signs and Cognition in Schizophrenia.

INTRODUCTION: Neurological soft signs (NSS) are delicate neurological abnormalities that comprise deficits in motor coordination, problems with the sequencing of complex motor acts, and sensory integration difficulties. These are nonspecific with no specific localization in the brain. NSS are found in many patients with Schizophrenia. Cognitive dysfunctions are also present in more than two-thirds of patients with Schizophrenia. This study aims at assessing the NSS and its association with cognitive impairment in patients with Schizophrenia. METHODS:  A total of 100 Schizophrenia patients were included in the study. The Heidelberg scale was used for assessing the NSS. The Montreal Cognitive Assessment Scale (MoCA) for cognitive impairment, the Positive and Negative Syndrome Scale (PANSS) for Schizophrenia, and the Brief Psychiatric Rating Scale (BPRS) were used to assess the severity. Statistical analysis was performed by Pearson's Chi-square test, Kruskal-Wallis test, Wilcoxon rank tests and Spearman rank correlation along with mean and standard deviation. RESULTS:  NSS were present in 68% (N=68) of the patients with motor coordination being maximally affected. Cognitive impairment was found in 73% (N=73) of patients with a MoCA score <26. Patients with predominant negative symptoms had higher NSS scores and lower MoCA scores. A "statistically significant" correlation was observed between cognitive impairment and NSS. Most patients with NSS and impaired cognition were in the "markedly ill" category of BPRS. CONCLUSION:  A significant association was observed between cognitive deficits, negative symptoms, and NSS in Schizophrenia. NSS and cognitive dysfunctions are integral parts of Schizophrenia symptom domains and need to be assessed as the negative symptoms and severity of illness are associated with NSS, especially problems with motor coordination and cognitive dysfunctions.

Striatal ZBTB16 Is Associated With Cognitive Deficits in Alzheimer Disease Mice.

PURPOSE: In Alzheimer disease (AD), brain regions such as the cortex and the hippocampus show abundant amyloid load which correlates with cognitive function decline. Prior to the significant development of AD pathophysiology, patients report the manifestation of neuropsychiatric symptoms, indicating a functional interplay between basal ganglia structures and hippocampal regions. Zinc finger and BTB domain-containing protein 16 (ZBTB16) is a transcription factor that controls the expression of downstream genes and the involvement of ZBTB16 in the striatum undergoing pathological aging in AD and the resulting behavioral phenotypes has not yet been explored. METHODS: To study molecular alterations in AD pathogenesis, we analyzed the brain from amyloid precursor protein (APP)/ presenilin 1 (PS1) transgenic mice. The molecular changes in the striatal region of the brain were analyzed via the immunoblotting, and the quantitative RNA sequencing. The cognitive impairments of APP/PS1 mice were assessed via 3 behavioral tests: 3-chamber test, Y-maze test, and noble object recognition test. And multielectrode array experiments for the analysis of the neuronal activity of the striatum in APP/PS1 mice was performed. RESULTS: We found that the alteration in ZBTB16 levels that occurred in the early ages of the pathologically aging striatum coalesces with the disruption of transcriptional dysregulation while causing social memory deficits, anxiety-like behavior. The early ZBTB16 knockdown treatment in the striatum of APP/PS1 mice rescued cognition that continued into later age. CONCLUSION: This study demonstrates that perturbation of transcriptional regulation of ZBTB16 during pathological aging may influence cognitive impairments and reveals a potent approach to targeting the transcriptional regulation of the striatum for the treatment of AD.

[Complex diagnostics and treatment of cognitive dysfunctions in cerebral palsy]. / Kompleksnaya diagnostika i lechenie kognitivnykh narushenii pri detskom tserebral'nom paraliche.

The article details modern approaches to the comprehensive diagnosis and treatment of cognitive dysfunctions in children with cerebral palsy. It is shown that cognitive disorders in cerebral palsy are diverse and are represented by disorders of perception, memory, attention, visual-motor coordination, intelligence and speech. Diagnosis of cognitive dysfunctions in patients with cerebral palsy is a difficult task, due to their diverse combination with motor, speech and sensory pathology, which requires an integrated approach. The article highlights in detail the modern directions of complex rehabilitation (including medical, social, psychological and pedagogical correction) of cognitive dysfunctions in children with cerebral palsy, in accordance with modern clinical recommendations and treatment standards.

Drug Therapy in Cognitive Disorders and Its Effects on Oral Health.

Dementia and Alzheimer's disease are the two most characteristic cognitive disorders presenting numerous cognitive dysfunctions such as memory loss, functional impairment, speech impairment, and orientation problems. In India, there is an increased risk in the elderly population leading to the prevalence of Alzheimer's and dementia-related diseases. Therefore, it is not only general health care practitioners but also oral health care providers also play a major role in rehabilitating and treating this type of patient. So, it is necessary for oral health care providers to understand the pharmacologic agents used for the management of Alzheimer's and dementia-related diseases. This article gives an insight into the management of dementia and Alzheimer's disease and also an update on the drug therapies for AD and outlines their implications on oral health.

Serum neurofilament light reflects cognitive dysfunctions in children with obstructive sleep apnea.

BACKGROUND: In children, obstructive sleep apnea (OSA) can cause cognitive dysfunctions. Amyloid-beta and tau are elevated in OSA. Neurofilament light (NfL) is a marker of neuro-axonal damage, but there are no reports of NfL for OSA. The objective was to investigate the serum levels of NfL and tau in children with or without OSA and explore their relationship with cognitive dysfunctions caused by OSA. METHODS: This retrospective case-control study included children diagnosed with adenoid tonsil hypertrophy from July 2017 to September 2019 at the Second Affiliated Hospital of Xi'an Jiaotong University. Correlations between cognitive scores and tau and NfL were examined. RESULTS: Fifty-six OSA and 49 non-OSA children were included. The serum NfL levels were higher in the OSA group (31.68 (27.29-36.07) pg/ml) than in the non-OSA group (19.13 (17.32-20.95) pg/ml) (P < 0.001). Moreover, NfL was correlated with the course of the disease, apnea-hypopnea index (AHI), obstructive apnea index (OAI), obstructive apnea-hypopnea index (OAHI), average oxygen saturation (SaO2), respiratory arousal index (RAI), and cognitive dysfunctions evaluated by the Chinese Wechsler Intelligence Scale for Children (C-WISC) (all P < 0.05). The area under the receiver operating characteristics curve (AUC) of NfL was 0.816 (95%CI: 0.736-0.897). Multiple regression analysis revealed that NfL was significantly associated with verbal intelligence quotient (VIQ), performance intelligence quotient (PIQ) and full-scale intelligence quotient (FIQ) (P < 0.001, respectively). CONCLUSIONS: Serum NfL levels are associated with the severity of cognitive dysfunctions in children diagnosed with adenoid tonsil hypertrophy and might be a candidate noninvasive, objective marker to identify cognitive dysfunctions in children with OSA.

Relationship between apathy and cognitive dysfunctions in multiple sclerosis: A 4-year prospective longitudinal study.

BACKGROUND: Cognitive dysfunctions are highly prevalent in multiple sclerosis (MS) and negatively impact occupational and social functioning. OBJECTIVE: In the present longitudinal study, we aimed at modeling cognitive changes and at assessing whether apathy could be a predictor of cognitive decline in MS. METHODS: We assessed 67 people with MS at two-time points (baseline, T0; 4-year follow-up, T1), by means of several clinical, behavioural, and cognitive measures. We used a delta approach to measure cognitive decline during the follow-up period. We applied a mixed factorial design and a linear regression model to explore factors associated with cognitive changes over time. RESULTS: A higher level of apathy at baseline predicted the progressive cognitive decline at follow-up, whereas a higher level of depression did not. Among demographic and clinical characteristics, only low education level was significantly associated with cognitive decline over time. Interestingly, participants with persistent apathy (diagnosis of apathy at T0 and T1, A+A+) and those who developed apathy (A-A+) showed poorer inhibitory control and a larger decline in executive functioning during the 4-year follow-up than participants who had never received the diagnosis of apathy (A-A-). CONCLUSION: Apathy represents an early marker of cognitive decline in MS. These findings have important clinical and prognostic implications.

Cognitive and affective disturbances in patients with Parkinson's disease: Perspectives for classifying of motor/neuropsychiatric subtypes.

Parkinson's disease (PD) is a neurological disorder, related to rigidity, bradykinesia, and resting tremors, among other motor symptoms. It is noticed in the increasing frequency of neuropsychiatric disorders, which may be also caused by non-motor symptoms of PD. Treatment of PD is usually based on the classification of motor subtypes; however, it remains unclear whether motor subtypes have differences in the severity of psychiatric symptoms. It determines the importance of discovering possible neuropsychiatric subtypes of PD. We conducted a clinical study, which included group 1 - patients with postural instability and gait disorders dominant (PIGD) subtype, group 2 - patients with tremor dominant (TD) and indeterminate subtypes (non-PIGD), and group 3 - people who did not have CNS damage. We used the Montreal Cognitive Assessment, Russified 20-point version of the Toronto Alexithymia Scale, State-Trait Anxiety Inventory, and Beck Depression Inventory for assessment of the mental status. It was the first time that neuropsychiatric subtypes of PD had been investigated based on the condition of cognition and mood. Cluster analysis gave us the possibility to classify our patients by the following subtype: affective-cognitive PIGD, anxious PIGD, affective-cognitive non-PIGD, and non-PIGD without psychiatric symptoms. This indicates a closed link between psychiatric and motor symptoms, which can be used for the improved treatment of PD.

ß-Hydroxybutyric acid attenuates heat stress-induced neuroinflammation via inhibiting TLR4/p38 MAPK and NF-κB pathways in the hippocampus.

Heat stress causes many pathophysiological responses in the brain, including neuroinflammation and cognitive deficits. ß-Hydroxybutyric acid (BHBA) has been shown to have neuroprotective effects against inflammation induced by lipopolysaccharide. The aim of the present study was to evaluate the effects of BHBA on neuroinflammation induced by heat stress, as well as the underlying mechanisms. Mice were pretreated with vehicle, BHBA or minocycline (positive control group) and followed by heat exposure (43°C) for 15 min for 14 days. In mice subjected to heat stress, we found that treatment with BHBA or minocycline significantly decreased the level of serum cortisol, the expressions of heat shock protein 70 (HSP70), and the density of c-Fos+ cells in the hippocampus. Surprisingly, the ethological tests revealed that heat stress led to cognitive dysfunctions and could be alleviated by BHBA and minocycline administration. Further investigation showed that BHBA and minocycline significantly attenuated the activation of microglia and astrocyte induced by heat stress. Pro-inflammatory cytokines were attenuated in the hippocampus by BHBA and minocycline treatment. Importantly, compared with the heat stress group, mice in the BHBA treatment group and positive control group experienced a decrease in the expressions of toll-like receptor 4 (TLR4), phospho-p38 (p-p38), and nuclear factor kappa B (NF-κB). Our results elucidated that BHBA inhibits neuroinflammation induced by heat stress by suppressing the activation of microglia and astrocyte, and modulating TLR4/p38 MAPK and NF-κB pathways. This study provides new evidence that BHBA is a potential strategy for protecting animals from heat stress.

Dysfunction of striatal MeCP2 is associated with cognitive decline in a mouse model of Alzheimer's disease.

Rationale: Cerebral Methyl-CpG binding Protein 2 (MeCP2) is involved in several psychiatric disorders that are concomitant with cognitive dysfunction. However, the regulatory function of striatal MeCP2 and its association with Alzheimer's disease (AD) has been largely neglected due to the absence of amyloid plaque accumulation in the striatal region until the later stages of AD progression. Considerable evidence indicates that neuropsychiatric symptoms related to cognitive decline are involved with striatal dysfunction. To this respect, we investigated the epigenetic function of striatal MeCP2 paralleling the pathogenesis of AD. Methods: We investigated the brain from amyloid precursor protein (APP)/presenilin1 (PS1) transgenic mice and postmortem brain samples from normal subjects and AD patients. The molecular changes in the brain, particularly in the striatal regions, were analyzed with thioflavin S staining, immunohistochemistry, immunoblotting, and MeCP2 chromatin immunoprecipitation sequencing (ChIP-seq). The cognitive function of APP/PS1 mice was assessed via three behavioral tests: 3-chamber test (3CT), Y-maze test (YMT), and passive avoidance test (PA). A multi-electrode array (MEA) was performed to analyze the neuronal activity of the striatum in APP/PS1 mice. Results: Striatal MeCP2 expression was increased in the younger (6 months) and older (10 months) ages of APP/PS1 mice, and the genome-wide occupancy of MeCP2 in the younger APP/PS1 showed dysregulated binding patterns in the striatum. Additionally, we confirmed that APP/PS1 mice showed behavioral deficits in multiple cognitive behaviors. Notably, defective cognitive phenotypes and abnormal neuronal activity in old APP/PS1 mice were rescued through the knock-down of striatal MeCP2. Conclusion: We found that the MeCP2-mediated dysregulation of the epigenome in the striatum is linked to the defects in cognitive behavior and neuronal activity in the AD animal model, and that this alteration is initiated even in the very early stages of AD pathogenesis. Together, our data indicates that MeCP2 may be a potential target for the diagnosis and treatment of AD at asymptomatic and symptomatic stages.

The pathogenic effects of particulate matter on neurodegeneration: a review.

The increasing amount of particulate matter (PM) in the ambient air is a pressing public health issue globally. Epidemiological studies involving data from millions of patients or volunteers have associated PM with increased risk of dementia and Alzheimer's disease in the elderly and cognitive dysfunction and neurodegenerative pathology across all age groups, suggesting that PM may be a risk factor for neurodegenerative diseases. Neurodegenerative diseases affect an increasing population in this aging society, putting a heavy burden on economics and family. Therefore, understanding the mechanism by which PM contributes to neurodegeneration is essential to develop effective interventions. Evidence in human and animal studies suggested that PM induced neurodenegerative-like pathology including neurotoxicity, neuroinflammation, oxidative stress, and damage in blood-brain barrier and neurovascular units, which may contribute to the increased risk of neurodegeneration. Interestingly, antagonizing oxidative stress alleviated the neurotoxicity of PM, which may underlie the essential role of oxidative stress in PM's potential effect in neurodegeneration. This review summarized up-to-date epidemiological and experimental studies on the pathogenic role of PM in neurodegenerative diseases and discussed the possible underlying mechanisms.

ß-Hydroxybutyric acid improves cognitive function in a model of heat stress by promoting adult hippocampal neurogenesis.

Heat stress has multiple potential effects on the brain, such as neuroinflammation, neurogenesis defects, and cognitive impairment. ß-hydroxybutyric acid (BHBA) has been demonstrated to play neuroprotective roles in various models of neurological diseases. In the present study, we investigated the efficacy of BHBA in alleviating heat stress-induced impairments of adult hippocampal neurogenesis and cognitive function, as well as the underlying mechanisms. Mice were exposed to 43 ℃ for 15 min for 14 days after administration with saline, BHBA, or minocycline. Here, we showed for the first time that BHBA normalized memory ability in the heat stress-treated mice and attenuated heat stress-impaired hippocampal neurogenesis. Consistently, BHBA noticeably improved the synaptic plasticity in the heat stress-treated hippocampal neurons by inhibiting the decrease of synapse-associated proteins and the density of dendritic spines. Moreover, BHBA inhibited the expression of cleaved caspase-3 by suppressing endoplasmic reticulum (ER) stress, and increased the expression of brain-derived neurotrophic factor (BDNF) in the heat stress-treated hippocampus by activating the protein kinase B (Akt)/cAMP response element binding protein (CREB) and methyl-CpG binding protein 2 (MeCP2) pathways. These findings indicate that BHBA is a potential agent for improving cognitive functions in heat stress-treated mice. The action may be mediated by ER stress, and Akt-CREB-BDNF and MeCP2 pathways to improve adult hippocampal neurogenesis and synaptic plasticity.

Rehabilitation Outcomes of Cortical Blindness and Characteristics Secondary to Cardiac Arrest: A Review.

We reviewed the published literature on rehabilitation outcomes in patients with cortical blindness (CB) and highlighted the characteristic features and prognosis of CB due to cardiac arrest. The studies excluded were those involving the pediatric population (