Results: The accumulating evidence from large studies and meta-analyses allows us to understand the role of CRP in major psychiatric disorders and increase our understanding of specific symptoms and subtypes of disorders.

CRP may be considered a 'psychiatric biomarker' which can alert clinicians about neuroinflammation, adverse effects of medications, cardiometabolic status, co-morbidities, and may also predict clinical outcomes and guide optimal treatment selection.

Based on what CRP itself is, there is an obvious link between this protein and inflammation. Because of this, high CRP levels are a concern as well, primarily because they can be an indicator of chronic inflammation. This is true especially if high CRP levels remain for long periods of time without receding.

Chronic inflammation can be incredibly harmful to the body. Why is this? Inflammation signals white blood cells to release “free radicals” into the body and kill harmful stimuli.

The problem with this is that the free radicals damage the surrounding areas of where a harmful stimuli might be, harming and even killing our cells. This process, when prolonged, greatly increases the risk for cancer cells to develop.

This type of research has discovered that chronic inflammation plays a role in the development of many different diseases and health conditions. Some of these include arthritis, diabetes, heart disease, lupus, neurodegeneration like Alzheimer’s, and even Parkinson’s disease. Recent research indicates it might even be linked to depression.

Unfortunately, there is still much more research to be done in regards to actually treating and preventing chronic inflammation, and in turn keeping CRP levels low. As it stands, Johns Hopkins Medicine states that treating chronic ailments, like high CRP levels,is a challenge.

Conclusion and relevance:Our results suggest sex-specific long-term effects in brain morphology after MIA [Maternal Immune Activation].

Categorical analyses suggest that this association might be driven by acute infections or or other sources of severe inflammation, which is of clinical relevance given that the COVID-19 pandemic is currently affecting millions of pregnant women worldwide. 

Cytokines and neurodevelopment

In the past several decades, inflammation has been increasingly recognized as an important contributor to central nervous system (CNS) injury in both the developing and adult brain.

The brain is particularly vulnerable in utero as well as during infancy and early childhood, and insults that occur during these critical periods have the potential to cause long-term damage.

Several neurodevelopmental disorders have been linked to early life immune activation and inflammation, including autism spectrum disorders (ASD), schizophrenia, cerebral palsy, epilepsy, cognitive impairment, and depression .

Methods: The 12-month prevalence of specific psychopathological syndromes among 1772 adults from the general population was estimated by a structured interview.

Additionally, participants underwent spirometry and were asked about obstructive lung disease in the year prior to the study.

Logistic and linear regression models were used to relate obstructive lung disease and spirometrically defined airway obstruction to mental health problems.

Results: Mental health problems were found in 35.7% of the participants. After adjusted for sociodemographic, clinical and life-style factors, asthma and chronic bronchitis were associated with almost all domains of mental health problems. In contrast, independent of its definition, spirometric airflow limitation was only related to generalized anxiety (odds ratios ranging from 2.3 to 2.7).

A reduced ratio of forced expiratory volume in one second to forced vital capacity was associated with mental health problems in general and panic and general anxiety in particular.

Conclusion: Our findings suggest an association of objective measure of airflow limitation to generalized anxiety and panic.

While the causal relationship between obstructive lung disease, airflow limitation and anxiety remains to be determined, clinicians should pay diagnostic attention to the significant overlap of these conditions.

Abstract

This article describes the history of the diagnostic class of neurodevelopmental disorders (NDDs) up to DSM-5.

We further analyze how the development of genetics will transform the classification and diagnosis of NDDs. In DSM-5, NDDs include intellectual disability (ID), autism spectrum disorder (ASD), and attention-deficit/hyperactivity disorder (ADHD).

Physicians in German-, French- and English-speaking countries (eg, Weikard, Georget, Esquirol, Down, Asperger, and Kanner) contributed to the phenomenological definitions of these disorders throughout the 18th and 20th centuries.

These diagnostic categories show considerable comorbidity and phenotypic overlap. NDDs are one of the chapters of psychiatric nosology most likely to benefit from the approach advocated by the National Institute of Mental Health’s Research Domain Criteria project.

Genetic research supports the hypothesis that ID, ASD, ADHD, schizophrenia, and bipolar disorder lie on a neurodevelopmental continuum.

The identification of recurrently observed copy number variants and disruptive gene variants in ASD (eg, CDH8, 16p11.2, SCN2A) led to the adoption of the genotype-first approach to characterize individuals at the etiological level.


Reams of relevant research (including our own) proves Jobs right. Innovators excel at connecting the unconnected. They engage in associational thinking.

At Apple (or at any innovative company), they take a little bit of this, sprinkle in a little bit of that and that and that to churn out market-busting ideas such as iTunes, and the iPod, iPhone, and iPad (along with a few market disasters like the G4 Cube computer).

Abstractin English, Spanish, French

This article describes the history of the diagnostic class of neurodevelopmental disorders (NDDs) up to DSM-5.

We further analyze how the development of genetics will transform the classification and diagnosis of NDDs. In DSM-5, NDDs include intellectual disability (ID), autism spectrum disorder (ASD), and attention-deficit/hyperactivity disorder (ADHD).

Physicians in German-, French- and English-speaking countries (eg, Weikard, Georget, Esquirol, Down, Asperger, and Kanner) contributed to the phenomenological definitions of these disorders throughout the 18th and 20th centuries.

These diagnostic categories show considerable comorbidity and phenotypic overlap.

NDDs are one of the chapters of psychiatric nosology most likely to benefit from the approach advocated by the National Institute of Mental Health's Research Domain Criteria project.

Genetic research supports the hypothesis that ID, ASD, ADHD, schizophrenia, and bipolar disorder lie on a neurodevelopmental continuum.

The identification of recurrently observed copy number variants and disruptive gene variants in ASD (eg, CDH8, 16p11.2, SCN2A) led to the adoption of the genotype-first approach to characterize individuals at the etiological level. .

Abstract

Events in fetal life impact long-term health outcomes. The placenta is the first organ to form and is the site of juxtaposition between the maternal and fetal circulations.

Most diseases of pregnancy are caused by, impact, or are reflected in the placenta.

The purpose of this review is to describe the main inflammatory processes in the placenta, discuss their immunology, and relate their short- and long-term disease associations.

Acute placental inflammation (API), including maternal and fetal inflammatory responses corresponds to the clinical diagnosis of chorioamnionitis and is associated with respiratory and neurodevelopmental diseases.

The chronic placental inflammatory pathologies (CPI), include chronic villitis of unknown etiology, chronic deciduitis, chronic chorionitis, eosinophilic T-cell vasculitis, and chronic histiocytic intervillositis.

These diseases are less-well studied, but have complex immunology and show mechanistic impacts on the fetal immune system.

Overall, much work remains to be done in describing the long-term impacts of placental inflammation on offspring health.

Abstract

Maternal infection and inflammation during pregnancy are associated with neurodevelopmental disorders in offspring, but little is understood about the molecular mechanisms underlying this epidemiologic phenomenon.

Here, we leveraged single-cell RNA sequencing to profile transcriptional changes in the mouse fetal brain in response to maternal immune activation (MIA) and identified perturbations in cellular pathways associated with mRNA translation, ribosome biogenesis and stress signaling.

We found that MIA activates the integrated stress response (ISR) in male, but not female, MIA offspring in an interleukin-17a-dependent manner, which reduced global mRNA translation and altered nascent proteome synthesis.

Moreover, blockade of ISR activation prevented the behavioral abnormalities as well as increased cortical neural activity in MIA male offspring.

Our data suggest that sex-specific activation of the ISR leads to maternal inflammation-associated neurodevelopmental disorders.