Developments & Research
Please see our new site located at https://rccx.me
Since RCCX Theory was born — Which speculates the majority of our ailments are due to environmental triggers and a genetic deposition 10–20% of the population carries — mutations in mysterious chimeric genes which are critical in genome evolution — passed down, creating a huge range of physical and psychiatric conditions across families.
A vast amount of revent developments support it’s hypothesis.
- C4 being linked with schizophrenia (C4 often co-segregates with CYP21A2)
- CRH being found to be elevated in fibromyalgia
- Physical findings indicating that the various populations of people with chronic illness are actually united by one disease process which is stress-induced: similar white matter lesions in MS, EDS and CAH; raised ICP throughout these populations, small fiber polyneuropathy in EDS, Gulf War veterans, fibromyalgia, CFS
- Indications that Cell Danger Response (mitochondrial shutdown, Naviaux MD PhD) as the final common pathway in CFS/ME, etc.
- Immune disorders associated to mutations in MHC region [source]
- corticotropin-releasing hormone (CRH), which is secreted under stress, is high in children with ASD and stimulates both mast cells and microglia
- ADHD might be a (non)-allergic hypersensitivity disorder caused by an environmental trigger.
- Mast cells, histamines, and these disorders are being repeatedly linked not only in correlation but in mechanism. The evidence for a link between ADHD/EDS/POTS/MCAS/ASD is so great that it can no longer be ignored and research interest is accelerating.
HERV-K and HERV-W transcriptional activity in Myalgic Encephalomyelitis/ Chronic Fatigue Syndrome (2019)
Genetics
Chronic Fatigue Syndrome / Myalgic Encephalomyelitis (CFS / MS) is an incapacitating chronic disease that dramatically compromise the life quality. The CFS/ME pathogenesis is multifactorial, and it is believed that immunological, metabolic and environmental factors play a role. It is well documented an increased activity of Human endogenous retroviruses (HERVs) from different families in autoimmune and neurological diseases, making these elements good candidates for biomarkers or even triggers for such diseases. Here the expression of Endogenous retroviruses K and W (HERV–K and HERV–W) was determined in blood from moderately and severely affected ME/CFS patients. HERV-K was overexpressed only in moderately affected individuals and HERV-W showed no difference. This is the first report about HERV-K differential expression in moderate ME/CFS.
Immune, Autonomic, and Endocrine Dysregulation in Autism and Ehlers-Danlos Syndrome/Hypermobility Spectrum Disorders Versus Unaffected Controls (2019)
Correlation. [source]
These data suggest that EDS/HSD and autism share aspects of immune/autonomic/endocrine dysregulation, pain, and some tissue fragility, which is typically more severe in the former. This overlap, as well as documented comorbidity, suggests some forms of autism may be hereditary connective tissue disorders (HCTD).
Hypermobility and autonomic hyperacitivty (2019)
Correlation + mechanism [source]
We demonstrate for the first time that rates of hypermobility and symptoms of autonomic dysfunction are particularly high in adults with neurodevelopmental diagnoses. It is likely that the importance of hypermobility and autonomic dysfunction to the generation and maintenance of psychopathology in neurodevelopmental disorders is poorly appreciated. Work underway(autonomic testing, fMRI) will test the hypothesis that autonomic reactivity and interoceptive sensitivity predispose to the expression of psychiatric symptoms, particularly anxiety. It is further hypothesized that inefficient neural co-ordination of efferent autonomic drive with imprecise interoceptive representations may be amplified in hypermobile individuals. In hypermobility, this mechanism might explain increased vulnerability to stress sensitive and developmental neuropsychiatric conditions. [source]
Clustering of co-occurring conditions in autism spectrum disorder during early childhood: A retrospective analysis of medical claims data. (2019)
Analysis / Correlation [source]
The first cluster was characterized by generally high rates of COC diagnosis and comprised 23.7% (n = 776) of the cohort. Diagnoses of developmental delays were dominant in the second cluster containing 26.5% (n = 870) of the cohort. Children in the third cluster, making up 49.8% (n = 1,632) of the cohort, had the lowest rates of COC diagnosis, which were slightly higher than rates observed in the POP cohort. A secondary analysis using these data found that gastrointestinal and immune disorders showed similar longitudinal patterns of prevalence, as did seizure and sleep disorders. These findings may help to better inform the development of diagnostic workup and treatment protocols for COCs in children with ASD. [source]
Effect of stress on learning and motivation-relevance to autism spectrum disorder (2019)
Evidence. ASD have aggravated response to stress. [source]
Stress is well known to affect learning and motivation. However, patients with ASD have aggrevated tresponses to stress, especially fear response. There is extensive literature connecting the amygdala to social behavior and to pathophysiologic responses to stress. The amygdala regulate the responses to stress, and anatomical changes in amygdala have been reported in ASD. In particular, corticotropin-releasing hormone (CRH), which is secreted under stress, is high in children with ASD and stimulates both mast cells and microglia, thus providing possible targets for therapy. Factors and/or circumstances that could interfere with the neurodevelopmental pathways involved in learning and motivation are clearly important and should be recognized early.
Attention-deficit/hyperactivity disorder, joint hypermobility-related disorders and pain: expanding body-mind connections to the developmental age. (2018)
Attention-deficit/hyperactivity disorder (ADHD) and generalized joint hypermobility (JH) are two separated conditions, assessed, and managed by different specialists without overlapping interests. Recently, some researchers highlighted an unexpected association between these two clinical entities. This happens in a scenario of increasing awareness on the protean detrimental effects that congenital anomalies of the connective tissue may have on human health and development. Impaired coordination and proprioception, fatigue, chronic pain, and dysautonomia are identified as potential bridges between ADHD and JH. Based on these findings, a map of the pathophysiological and psychopathological pathways connecting both conditions is proposed. Although ADHD and JH are traditionally separated human attributes, their association may testify for the dyadic nature of mind-body connections during critical periods of post-natal development. Such a mixed picture has potentially important consequences in terms of disability and deserves more clinical and research attention. — [source]
Mast cells in early rheumatoid arthritis associate with disease severity and support B cell autoantibody production. (2018)
recent evidence suggests that MC contribution to autoimmune diseases can be complex and multifaceted. Several studies point to the relevance of MCs in RA and their role as novel markers of synovial inflammation and helps to identify patients with a severe clinical phenotype. — [source]
A Cohort Study Comparing Women with Autism Spectrum Disorder with and without Generalized Joint Hypermobility (2018)
While this study cannot address rates of ASD and GJH co-occurrence because of the way in which respondents were recruited, the comorbidity itself reinforces etiological links between autism and connective tissue disorders. Both cytokines and hormones play recognized roles in neurogenesis, neuritogenesis, synaptogenesis, and ongoing plasticity [81,82,83,84]. In addition, some researchers have proposed that autoantibodies to brain-specific proteins may also disrupt neurodevelopment, leading to increased autism risk [85]. Finally, endocrine disruption, either via endogenous or exogenous effectors, is likewise a growing area of research into autism’s etiology [12,86]. All of these topics highlight the crosstalk between the immune and endocrine systems and strengthen their combined links to ASD. — [source]
Rationale for Dietary Antioxidant Treatment of ADHD (2018)
Correlation + mechanism. [source]
The potential involvement of the immune system in ADHD has long been suspected due to the increased prevalence of allergic diseases including atopic dermatitis, asthma and rhinitis in patients with ADHD [69].
ADHD might thus be a (non) allergic hypersensitivity disorder caused by an environmental trigger, based on a non-IgE dependent histamine release from mast cells and basophilic granulocytes, since the histamine H3 receptor is involved in hyperactivity and promotes dopamine release in the frontal cortex. Moreover, polymorphisms in the histamine N-methyl transferase (HNMT) gene, impairing histamine clearance, were found to affect the behavioral responses to food additives, which increase histamine levels [76]. [source]
Application of immunotherapy for neurological manifestations in hypermobile Ehlers–Danlos syndrome (2018)
Evidence, correlation & response to treatment.
It has recently been proposed that the diverse clinical features of EDS, including neurological and immunological manifestations, can be attributed to mast cell activation.9,10 Roles of mast cells have also been indicated in the pathogenesis of autoimmune diseases, MS, and rheumatoid arthritis.11 On the other hand, elevated basal serum tryptase levels have been exclusively associated with duplication of the TPSAB1 gene encoding α-tryptase, followed by mast cell activation.12 In both the present cases, serum tryptase levels were normal, with the blood samples obtained not in the exacerbation but in the remission phase.
These case reports and case series suggest that the pathogenesis of hEDS can be partly associated with an autoimmune mechanism. While the underlying mechanisms of hEDS remain unclear, autoimmunity and mast cell activation may play key roles. Further clinical investigations are needed to elucidate how autoimmune mechanisms influence the pathogenesis of hEDS and evaluate the efficacy of immunotherapy. [source]
Autism, Joint Hypermobility-Related Disorders and Pain (Dec 2018)
There is increasing evidence suggesting that these co-occur more often than expected by chance. [source]
Successful treatment of postural orthostatic tachycardia and mast cell activation syndromes using naltrexone, immunoglobulin and antibiotic treatment (2018)
In a chart review of 33 additional patients with POTS in our GI clinic, 27 had lactulose breath testing (26 women, 1 men, mean age 35 years). These patients had MCAS in 27% and EDS in 42%. GI symptoms were present in all patients: mid/lower abdominal pain (96%), bloating (92%), nausea (85%), constipation (73%), diarrhoea (58%) and heartburn (58%). LBT was abnormal in 69% versus abnormal testing in 10% of volunteers in a prior control study.24
A Review on the Role of Inflammation in Attention-Deficit/Hyperactivity Disorder. (2018)
Although a strong neurobiological basis has been demonstrated, the pathophysiology of ADHD is still poorly understood. The evaluation of serum inflammatory markers has provided mixed results, likely due to the small sample sizes and high heterogeneity between biomarkers. However, there is evidence that increased inflammation during the early development may be a risk factor for ADHD symptoms. Although genetic studies have demonstrated a potential role for inflammation in this disorder, there is no clear evidence. To sum up, inflammation may be an important mechanism in ADHD pathophysiology, but more studies are still needed for a more precise conclusion. [source]
Psychological vulnerability to stress in carriers of congenital adrenal hyperplasia due to 21-hydroxylase deficiency
This is important to understand. There are studies showing carriers to be more stress efficient — but this one shows what I’ve observed to be true with CYP21A2 carriers (along with high rate for bipolar disorder).
Also as an aside those with CAH1 who are treated early with steroids will NOT have CAPS as the brain development won’t be the same.
Conclusions: Carriers of 21-OHD may be predisposed to the development of anxiety disorders.[source]
Mast cell disorders in Ehlers-Danlos syndrome. (2017)
This report reviews basic biology of mast cells and mast cell activation as well as recent research efforts, which implicate a role of MC dysregulation beyond atopic disorders and in a cluster of Ehlers-Danlos Syndromes, non-IGE mediated hypersensitivity disorders, and dysautonomia. [source]
Neuroinflammation Induces Neurodegeneration (2017)
The role of neuroinflammation in neuronal degeneration has been studied extensively in the last decade. The available evidences convincingly demonstrate that neuroinflammation is a crucial factor in the onset and progression of neurodegeneration and neuronal loss in neurodegenerative diseases. Additionally, peripheral inflammation also augments neuroinflammatory pathways by activating glial cells, neurons, and increase in BBB permeability. Moreover, peripheral immune and inflammatory cells migrate to the brain through the defective BBB. These migrated immune cells can proliferate in the brain at the site of inflammation and further augment neuroinflammation either directly or through glial cells and neuronal cells. Suppression of neuroinflammation can ameliorate neurodegenerative disease symptoms and reduce the extent of neurodegeneration. However, it is necessary to find newer therapeutic agents to repair the damaged neurons, and to regenerate new neurons at the site of neuronal damage in the CNS.
Mast Cell Activation in Brain Injury, Stress, and Post-traumatic Stress Disorder and Alzheimer’s Disease Pathogenesis (2017)
Mast cell activation is implicated in neuroinflammation, brain injuries, and various stress conditions. We suggest that mast cells participate in the pathogenesis of AD, and this process could be accelerated and worsened in brain injury, stress, and PTSD comorbidity. Inhibition of mast cell-associated inflammatory pathways in brain injury, stress, and PTSD could be explored as a new therapeutic target to inhibit or prevent the pathogenesis and potentially delay the onset of AD. Though the evidence is currently limited, investigating the role of mast cell activation in brain injuries, stress, and PTSD comorbidity in the onset and progression of AD is an important emerging new area to understand and to effectively treat neuroinflammatory disorders including AD. [source]
A connective tissue disorder may underlie ESSENCE problems in childhood. (2017)
Children with EDS-HT/JHS present ESSENCE problems that often coexist and tend to be recognized before the HDCT. Clinicians encountering children with ESSENCE problems should consider the possibility of an underlying HDCT such as EDS-HT/JHS, probably influencing neurodevelopmental attributes in a subgroup of children. Awareness of these interconnected clinical problems might help improve early referral, diagnosis and treatment of EDS-HT/JHS.
Generalised joint hypermobility and neurodevelopmental traits in a non-clinical adult population (2017)
Although GJH is overrepresented in clinical cases with neurodevelopmental disorders, such an association seems absent in a normal population. Thus, if GJH serves as a biomarker cutting across diagnostic boundaries, this association is presumably limited to clinical populations.
Histamine: The Missing Link in the Pathogenesis of Some Brain Disorders (2016)
Phenome-wide association study maps new diseases to the human major histocompatibility complex region (2016)
Over 160 disease phenotypes have been mapped to the major histocompatibility complex (MHC) region on chromosome 6 by genome-wide association study (GWAS), suggesting that the MHC region as a whole may be involved in the aetiology of many phenotypes, including unstudied diseases.
Findings showed that expected associations previously identified by GWAS could be identified by PheWAS (eg, psoriasis, ankylosing spondylitis, type I diabetes and coeliac disease) with some having strong cross-phenotype associations potentially driven by pleiotropic effects. Importantly, novel associations with eight diseases not previously assessed by GWAS
(eg, lichen planus) were also identified and replicated in an independent population. Many of these associated diseases appear to be immune-related disorders. Further assessment of these diseases in 16 484 Marshfield Clinic twins suggests that some of these diseases, including lichen planus, may have genetic aetiologies.[source]
Histamine H3 receptor as a potential target for cognitive symptoms in neuropsychiatric diseases (2016)
The potential contributions of the brain histaminergic system in neurodegenerative diseases, and the possiblity of histamine-targeting treatments is attracting considerable interests. The histamine H3 receptor (H3R) is expressed mainly in the central nervous system, and is, consequently, an attractive pharmacological target. Although recently described clinical trials have been disappointing in attention deficit hyperactivity disorder (ADHD) and schizophrenia (SCH), numerous H3R antagonists, including pitolisant, demonstrate potential in the treatment of narcolepsy, excessive daytime sleepiness associated with cognitive impairment, epilepsy, and Alzheimer’s disease (AD). This review focuses on the recent preclinical as well as clinical results that support the relevance of H3R antagonists for the treatment of cognitive symptoms in neuropsychiatric diseases, namely AD, epilepsy and SCH. [source]
Are mast cells important in diabetes? (2016)
Diabetes is a metabolic disorder characterized by hyperglycemia and associated with microvascular and macrovascular syndromes mediated by mast cells. Mast cells are activated through cross-linking of their surface high affinity receptors for IgE (FcRI) or other antigens, leading to degranulation and release of stored inflammatory mediators, and cytokines/chemokines without degranulation. Mast cells are implicated in innate and acquired immunity, inflammation and metabolic disorders such as diabetes. Histamine and tryptase genes in mast cells are overexpressed in pancreatic tissue of type 2 diabetes mellitus (T2DM) patients. Histamine is a classic inflammatory mediator generated by activated receptors of mast cells from the histamine-forming enzyme histidine decarboxylase (HDC), which can be activated by two inflammatory chemokines, RANTES and MPC1, when injected intramuscularly or intradermally in mice. This activation is inhibited in genetically mast cell-deficient W/Wv mice, which show higher insulin sensitivity and glucose tolerance. This study contributes to understanding the mechanism by which mast cells profoundly affect diabetes, and their manipulation could represent a new therapeutic strategy. However, further studies are needed to clarify the role of mast cells in inflammation and metabolic disorders such as diabetes.[source]
Identification of a common neurobiological substrate for mental illness. (2015)
We identified a concordance across psychiatric diagnoses in terms of integrity of an anterior insula/dorsal anterior cingulate-based network, which may relate to executive function deficits observed across diagnoses. This concordance provides an organizing model that emphasizes the importance of shared neural substrates across psychopathology, despite likely diverse etiologies, which is currently not an explicit component of psychiatric nosology. — [source]
Brain structure and joint hypermobility: relevance to the expression of psychiatric symptoms (2014)
Differences in the structural integrity of temporal and parietal cortices may underlie wider behavioural phenotypical expression of hypermobility: abnormalities in superior temporal cortex are also seen in autism.11 Inferior parietal cortex can affect proprioceptive awareness and hypermobility is itself linked to dyspraxia.1 Our findings suggest that processes compromising function in neuro-developmental conditions may occur in individuals with hypermobility, putatively enhancing vulnerability to stress and anxiety. — [source]
Morton’s foot and pyridoxal 5'-phosphate deficiency: genetically linked traits. (2014)
Vitamin B6 is an essential vitamin needed for many chemical reactions in the human body. It exists as several vitamins forms but pyridoxal 5'-phosphate (PLP) is the phosphorylated form needed for transamination, deamination, and decarboxylation. PLP is important in the production of neurotransmitters, acts as a Schiff base and is essential in the metabolism of homocysteine, a toxic amino acid involved in cardiovascular disease, stroke, thrombotic and Alzheimer’s disease. This report announces the connection between a deficit of PLP with a genetically linked physical foot form known as the Morton’s foot. Morton’s foot has been associated with fibromyalgia/myofascial pain syndrome. Another gene mutation methylenetetrahydrofolate reductase (MTHFr) is now being recognized much commonly than previous with chronic fatigue, chronic Lyme diseases and as “the missing link” in other chronic diseases. PLP deficiency also plays a role in impaired glucose tolerance and may play a much bigger role in the obesity, diabetes, fatty liver and metabolic syndrome. Without the Schiff-base of PLP acting as an electron sink, storing electrons and dispensing them in the mitochondria, free radical damage occurs! The recognition that a phenotypical expression (Morton’s foot) of a gene resulting in deficiency of an important cofactor enzyme pyridoxal 5'-phosphate will hopefully alert physicians and nutritionist to these phenomena. Supplementation with PLP, L5-MTHF, B12 and trimethylglycine should be used in those patients with hyperhomocysteinemia and/or MTHFR gene mutation.
Familial Occurrence of Systemic Mast Cell Activation Disease (2013)
In conclusion, our data provide evidence for common familial occurrence of MCAD. This makes the future application of systematic molecular genetic studies, such as genome-wide association studies, to MCAD very promising. Together with findings of previous studies, which suggested that almost all KIT mutations were somatic rather than germline (reviewed in [3]), our present data support the idea that in familial cases (i.e., the majority of MCAD) mutated disease-related operator and/or regulator genes could be responsible for the development of somatic mutations in KIT and other proteins involved in the regulation of mast cell activity [3]. Accordingly, the immunohistochemically different subtypes of MCAD (MCAS and SM) should be more accurately regarded as varying presentations of a common generic root process of mast cell dysfunction, than as distinct diseases [1], [3].
Histamine and neuroinflammation: insights from murine experimental autoimmune encephalomyelitis (2012)
Histamine receptors play multiple roles in immune reactions and autoimmune disorders. Strategies aimed at interfering with the histamine axis may have relevance in the therapy of autoimmune diseases of the CNS as histamine may determine, through different receptor activation pathways, a shift in T helper cell subpopulation, may influence migration of lymphocytes and myeloid cells during CNS invasion, interfere with antigen presentation at the immune synapse level and finally, determine variations in normal neuronal functions. It will be of paramount importance to define the temporal sequence of histamine receptor activation during disease initiation in peripheral tissues and during CNS invasion. Hopefully, this will help the scientific community to put the sometimes confusing and contradictory observations reviewed here into better focus and provide a perspective for evaluating potential therapeutic interventions using histaminergic compounds.
Recent Insights in the Epidemiology of Autoimmune Diseases: Improved Prevalence Estimates and Understanding of Clustering of Diseases (2009)
Rapid expansion of knowledge related to the genetics of autoimmune disease is currently underway. Data from twin, linkage and association studies point to a complex mode of inheritance, and indicate that genes involved in autoimmune disorders are pleiotropic rather than disease specific. Becker describes the “common variant/multiple disease” hypothesis stating that common alleles manifesting in a given disorder under particular genetic/environmental conditions may have the potential to give rise to alternate clinical phenotypes when combined with a different set of genetic and environmental factors [164]. Accumulating data support the premise that clinically distinct autoimmune diseases may have common susceptibility genes. For instance, a major United Kingdom–based genome-wide association study published in 2007 identified several loci with associations to more than one autoimmune disease { 2007 #432}. As summarized by Lettre and Rioux, at least 68 genetic risk variants have now been associated with various autoimmune diseases, in contrast to only 15 that were recognized prior to 2006 [166].
Significance of Conversation between Mast Cells and Nerves (2005)
The role of this bidirectional communication between mast cells and nerves appears to be multifactorial. Mast cells are thought to play a major role in resistance to infection and are extensively involved in inflammation and subsequent tissue repair. The communication with the nervous system allows the peripheral and central nervous systems to be involved in the regulation of defence mechanisms, inflammation, and response to infection. The involvement of mast cell-nerve communication in the response to stress, for instance, points to an extensive communication between the nervous and immune systems. — [source]
Genetics of infectious diseases.
Infectious diseases represent a major health problem worldwide, both in terms of morbidity and mortality. A complex combination of environmental, pathogen and host genetic factors plays a role in determining both susceptibility to particular microbes and the course of infection. Numerous studies have now mapped and identified relevant genes using a variety of both family-based and population-based approaches. Much interest has been focused on susceptibility to malaria, HIV/AIDS and mycobacterial infection, but other bacterial, viral and parasitic diseases are receiving increasing attention. Some major genes have been identified by genome scans of multi-case families, and mouse genetics has contributed to mapping and identification of a few genes. However, the great majority of known susceptibility loci emerged from screening of likely candidate genes. The emerging picture is of highly polygenic diseases, with occasional major genes, along with significant inter-population heterogeneity. This genetic architecture likely reflects the role that evolutionary selection has played in generating and maintaining a diverse repertoire of susceptibility/resistance loci, most with individually small effects. Genome-wide association studies with large sample sizes will be required to define the majority of the relevant polygenes. [source]
The 1,4-benzodiazepine Ro5–4864 (4-chlorodiazepam) suppresses multiple pro-inflammatory mast cell effector functions
In conclusion, the present data demonstrate that the 1,4-benzodiazepine Ro5–4864 significantly suppresses pro-inflammatory MC responses downstream of differential ligand/receptor systems, most likely by attenuating SFK activity by direct inhibition of the respective SFK and/or indirectly by acting at a so far unknown upstream plasmalemnal recognition site. Hence, Ro5–4864 and structurally related compounds might be applicable as effective MC stabilizing drugs in different MC-dependent diseases, such as allergies, asthma, and systemic MCAD. It is however mandatory to identify and characterize the direct molecular target(s) to exclude unwanted side effects on other immune and non-immune cells. For certain MC-dependent diseases, however, topical administration as cream, eye drops or nasal spray could be options for first applications.
To Organise
Here are the most common conditions self-reported from the RCCX and Chronic Illness discussion page.
https://me-pedia.org/wiki/RCCX_Genetic_Module_Theory
Chronic idiopathic urticaria and post-traumatic stress disorder (PTSD): an under-recognized comorbidity. (2012)
https://www.ncbi.nlm.nih.gov/m/pubmed/22507051/
Pharmacological effects of berberine on mood disorders (2019)
Based on the published findings, we conclude that berberine may be a potential treatment for mood disorders. Berberine in various mood disorders and its mechanism of action are summarized in Table 1. Schematic representation of the mechanism of berberine involved with depression is shown in Figure 1. Further research into the safety profile of berberine is required before its clinical application. — [source]
Does Prenatal Stress Shape Postnatal Resilience? — An Epigenome-Wide Study on Violence and Mental Health in Humans (2019)
We provide human evidence that children exposed to prenatal stress may experience resilience driven by epigenome-wide interactions. This plausibly translates animal findings and suggests that prenatal psychiatric risk factors may have different, and maybe even opposite, consequences in different world populations. Our findings therefore call for more research on personalizing psychiatric practices according to social and community backgrounds. By studying the gene–environment interactions in some of these world populations, we have also discovered a novel phenomenon that may be refined into a biomarker for mental burden, namely the stress-induced methylome switch. We hope that this discovery may lead to innovative molecular diagnostic tools in psychiatry, with profound impact on our understanding and treatment of mental disorders. — [source]
Prenatal Programming of Neuropsychiatric Disorders Across the Lifespan
Histamine H3 receptor as a potential target for cognitive symptoms in neuropsychiatric diseases
