Names | |
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IUPAC name hexadecanal | |
Other names Hexadecanal; AI3-24252; EINECS 211-111-0; UNII-WQD27655QE | |
Identifiers | |
3D model (JSmol) | |
1772756 | |
ChEBI | |
ChEMBL | |
ChemSpider | |
DrugBank | |
ECHA InfoCard | 100.010.102 |
EC Number |
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722456 | |
KEGG | |
PubChem CID | |
UNII | |
CompTox Dashboard (EPA) | |
| |
| |
Properties | |
C16H32O | |
Molar mass | 240.428 g/mol |
Hazards | |
GHS labelling: | |
Warning | |
H315, H319, H335 | |
P261, P264, P271, P280, P302+P352, P304+P340, P305+P351+P338, P312, P321, P332+P313, P337+P313, P362, P403+P233, P405, P501 | |
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa). |
Hexadecanal is an organic compound with the chemical formula C16H32O.
Hexadecanal is found in human skin, saliva, and feces. It has a calming effect on mice. [1]
A 2017 study found that non-autistic men demonstrate an increase in electrodermal activity when exposed to subliminal levels of hexadecanal while men with autism spectrum disorder do not. [2] [3]
In 2021, inhalation of hexadecanal was found to reduce aggression in men but to trigger aggression in women. [4] Hexadecanal is one of the most abundant substances emitted by human babies from their heads, which may be an evolutionary survival mechanism to induce mothers to defend the baby and fathers to not attack it. But it is not yet known whether the amount of hexadecanal emitted by humans is sufficient to affect other humans. [5]
Asperger syndrome (AS), also known as Asperger's syndrome or Asperger's, is a diagnostic label that has been used to describe a neurodevelopmental disorder characterized by significant difficulties in social interaction and nonverbal communication, along with restricted, repetitive patterns of behavior and interests. Asperger syndrome has been merged with other conditions into autism spectrum disorder (ASD) and is no longer a diagnosis in the WHO's ICD-11 or the APA's DSM-5-TR. It was considered milder than other diagnoses which were merged into ASD due to relatively unimpaired spoken language and intelligence.
A gluten-free casein-free diet, also known as a gluten-free dairy-free diet, is a diet that does not include gluten, and casein. Despite an absence of scientific evidence, there have been advocates for the use of this diet as a treatment for autism and related conditions.
Sir Simon Philip Baron-Cohen is a British clinical psychologist and professor of developmental psychopathology at the University of Cambridge. He is the director of the university's Autism Research Centre and a Fellow of Trinity College.
Sex differences in psychology are differences in the mental functions and behaviors of the sexes and are due to a complex interplay of biological, developmental, and cultural factors. Differences have been found in a variety of fields such as mental health, cognitive abilities, personality, emotion, sexuality, friendship, and tendency towards aggression. Such variation may be innate, learned, or both. Modern research attempts to distinguish between these causes and to analyze any ethical concerns raised. Since behavior is a result of interactions between nature and nurture, researchers are interested in investigating how biology and environment interact to produce such differences, although this is often not possible.
Mind-blindness, mindblindness or mind blindness is a theory initially proposed in 1990 that claims that all autistic people have a lack or developmental delay of theory of mind (ToM), meaning they are less able to attribute mental states to others. According to the theory, a lack of ToM is considered equivalent to a lack of both cognitive and affective empathy. In the context of the theory, mind-blindness implies being unable to predict behavior and attribute mental states including beliefs, desires, emotions, or intentions of other people. The mind-blindness theory asserts that children who delay in this development will often develop autism.
Autism has multiple causes. This article focuses on heritable causes. The heritability of autism is the proportion of differences in expression of autism that can be explained by genetic variation; if the heritability of a condition is high, then the condition is considered to be primarily genetic. Autism has a strong genetic basis. Although the genetics of autism are complex, autism spectrum disorder (ASD) is explained more by multigene effects than by rare mutations with large effects.
Monoamine oxidase A, also known as MAO-A, is an enzyme that in humans is encoded by the MAOA gene. This gene is one of two neighboring gene family members that encode mitochondrial enzymes which catalyze the oxidative deamination of amines, such as dopamine, norepinephrine, and serotonin. A mutation of this gene results in Brunner syndrome. This gene has also been associated with a variety of other psychiatric disorders, including antisocial behavior. Alternatively spliced transcript variants encoding multiple isoforms have been observed.
Many causes of autism, including environmental and genetic factors, have been recognized or proposed, but understanding of the theory of causation of autism is incomplete. Attempts have been made to incorporate the known genetic and environmental causes into a comprehensive causative framework. ASD is a neurodevelopmental disorder marked by impairments in communicative ability and social interaction, as well as restricted and repetitive behaviors, interests, or activities not suitable for the individual's developmental stage. The severity of symptoms and functional impairment vary between individuals.
The empathising–systemising (E–S) theory is a theory on the psychological basis of autism and male–female neurological differences originally put forward by clinical psychologist Simon Baron-Cohen. It classifies individuals based on abilities in empathic thinking (E) and systematic thinking (S). It attempts to explain the social and communication symptoms in autism spectrum disorders as deficits and delays in empathy combined with intact or superior systemising.
Neurexins (NRXN) are a family of presynaptic cell adhesion proteins that have roles in connecting neurons at the synapse. They are located mostly on the presynaptic membrane and contain a single transmembrane domain. The extracellular domain interacts with proteins in the synaptic cleft, most notably neuroligin, while the intracellular cytoplasmic portion interacts with proteins associated with exocytosis. Neurexin and neuroligin "shake hands," resulting in the connection between the two neurons and the production of a synapse. Neurexins mediate signaling across the synapse, and influence the properties of neural networks by synapse specificity. Neurexins were discovered as receptors for α-latrotoxin, a vertebrate-specific toxin in black widow spider venom that binds to presynaptic receptors and induces massive neurotransmitter release. In humans, alterations in genes encoding neurexins are implicated in autism and other cognitive diseases, such as Tourette syndrome and schizophrenia.
Teashirt homolog 3 is a protein that in humans is encoded by the TSHZ3 gene. In mice, it is a necessary part of the neural circuitry that controls breathing. The gene is also a homolog of the Drosophila melanogaster teashirt gene, which encodes a zinc finger transcription factor important for development of the trunk.
Autism spectrum disorder (ASD), or simply autism, is a neurodevelopmental disorder "characterized by persistent deficits in social communication and social interaction across multiple contexts" and "restricted, repetitive patterns of behavior, interests, or activities". Sensory abnormalities are also included in the diagnostic manuals. Common associated traits such as motor coordination impairment are typical of the condition but not required for diagnosis. A formal diagnosis requires that symptoms cause significant impairment in multiple functional domains; in addition, the symptoms must be atypical or excessive for the person's age and sociocultural context.
The imprinted brain hypothesis is an unsubstantiated hypothesis in evolutionary psychology regarding the causes of autism spectrum and schizophrenia spectrum disorders, first presented by Bernard Crespi and Christopher Badcock in 2008. It claims that certain autistic and schizotypal traits are opposites, and that this implies the etiology of the two conditions must be at odds.
Autism spectrum disorder (ASD) refers to a variety of conditions typically identified by challenges with social skills, communication, speech, and repetitive sensory-motor behaviors. The 11th International Classification of Diseases (ICD-11), released in January 2021, characterizes ASD by the associated deficits in the ability to initiate and sustain two-way social communication and restricted or repetitive behavior unusual for the individual's age or situation. Although linked with early childhood, the symptoms can appear later as well. Symptoms can be detected before the age of two and experienced practitioners can give a reliable diagnosis by that age. However, official diagnosis may not occur until much older, even well into adulthood. There is a large degree of variation in how much support a person with ASD needs in day-to-day life. This can be classified by a further diagnosis of ASD level 1, level 2, or level 3. Of these, ASD level 3 describes people requiring very substantial support and who experience more severe symptoms. ASD-related deficits in nonverbal and verbal social skills can result in impediments in personal, family, social, educational, and occupational situations. This disorder tends to have a strong correlation with genetics along with other factors. More research is identifying ways in which epigenetics is linked to autism. Epigenetics generally refers to the ways in which chromatin structure is altered to affect gene expression. Mechanisms such as cytosine regulation and post-translational modifications of histones. Of the 215 genes contributing, to some extent in ASD, 42 have been found to be involved in epigenetic modification of gene expression. Some examples of ASD signs are specific or repeated behaviors, enhanced sensitivity to materials, being upset by changes in routine, appearing to show reduced interest in others, avoiding eye contact and limitations in social situations, as well as verbal communication. When social interaction becomes more important, some whose condition might have been overlooked suffer social and other exclusion and are more likely to have coexisting mental and physical conditions. Long-term problems include difficulties in daily living such as managing schedules, hypersensitivities, initiating and sustaining relationships, and maintaining jobs.
The development of an animal model of autism is one approach researchers use to study potential causes of autism. Given the complexity of autism and its etiology, researchers often focus only on single features of autism when using animal models.
Sex and gender differences in autism exist regarding prevalence, presentation, and diagnosis.
Mark Firman Bear is an American neuroscientist. He is currently the Picower Professor of Neuroscience at The Picower Institute for Learning and Memory at Massachusetts Institute of Technology. He is a former Howard Hughes Medical Institute Investigator; an Elected Fellow of the American Association for the Advancement of Science and the American Academy of Arts and Sciences; and a Member of the National Academy of Medicine.
R. Suzanne Zukin is an American neuroscientist and a professor of neuroscience who directs a research lab as a F. M. Kirby Chair in Neural Repair and Protection and director of the Neuropsychopharmacology Center at Albert Einstein College of Medicine. Zukin's areas of research include neurodegenerative disorders, ischemia, epigenetics and autism and uses molecular biology approaches to research these disorders. Zukin has made seminal contributions to the understanding of NMDA and AMPA receptor function and activity.
Nadine Gogolla is a Research Group Leader at the Max Planck Institute of Neurobiology in Martinsried, Germany as well as an Associate Faculty of the Graduate School for Systemic Neuroscience. Gogolla investigates the neural circuits underlying emotion to understand how the brain integrates external cues, feeling states, and emotions to make calculated behavioral decisions. Gogolla is known for her discovery using machine learning and two-photon microscopy to classify mouse facial expressions into emotion-like categories and correlate these facial expressions with neural activity in the insular cortex.
Richard Carl Elciario Dolmetsch is a Colombian-American neuroscientist, educator and biotechnology entrepreneur. Dolmetsch is the president of Tempero Bio, a biotech company seeking to cure substance use disorders, and an adjunct professor at Stanford University.