anonymous asked:

I took an IQ test when I was six and just recently and apparently my processing speed went up like 25 points??

That’s awesome! Were there any differences, like were you medicated this time, or was the only difference that you’re older now?


People with developmental disorders often notice that their IQ scores improve over time. Since IQs are calculated by comparing you to your peers, it would be lower when you were younger and then get higher as your brain develops to be more like your peers’.


Please don’t play neurodevelopmental disorders if you don’t have them or understand them on a personal level. ADHD is not just being hyper or acting silly, schizophrenia is not just hearing voices. Give me poor motor skills, auditory issues, sensory disorder, no motivation, confusion, stimming, tantrums, special interests, tic movements when upset. If you don’t know what some of those are, you shouldn’t be playing the disorder. Don’t drown out those who suffer because you think it’s quirky.

Neurobiologists restore youthful vigor to adult brains

They say you can’t teach an old dog new tricks. The same can be said of the adult brain. Its connections are hard to change, while in children, novel experiences rapidly mold new connections during critical periods of brain development.

UC Irvine neurobiologist Sunil Gandhi and colleagues wanted to know whether the flexibility of the juvenile brain could be restored to the adult brain. Apparently, it can: They’ve successfully re-created a critical juvenile period in the brains of adult mice. In other words, the researchers have reactivated brain plasticity – the rapid and robust changes in neural pathways and synapses as a result of learning and experience.

And in doing so, they’ve cleared a trail for further study that may lead to new treatments for developmental brain disorders such as autism and schizophrenia. Results of their study appear online in Neuron.

The scientists achieved this by transplanting a certain type of embryonic neuron into the brains of adult mice. The transplanted neurons express GABA, a chief inhibitory neurotransmitter that aids in motor control, vision and many other cortical functions.

Much like older muscles lose their youthful flexibility, older brains lose plasticity. But in the Gandhi study, the transplanted GABA neurons created a new period of heightened plasticity that allowed for vigorous rewiring of the adult brain. In a sense, old brain processes became young again.

In early life, normal visual experience is crucial to properly wire connections in the visual system. Impaired vision during this time leads to a long-lasting visual deficit called amblyopia. In an attempt to restore normal sight, the researchers transplanted GABA neurons into the visual cortex of adult amblyopic mice.

“Several weeks after transplantation, when the donor animal’s visual system would be going through its critical period, the amblyopic mice started to see with normal visual acuity,” said Melissa Davis, a postdoctoral fellow and lead author of the study.

These results raise hopes that GABA neuron transplantation might have future clinical applications. This line of research is also likely to shed light on the basic brain mechanisms that create critical periods.

“These experiments make clear that developmental mechanisms located within these GABA cells control the timing of the critical period,” said Gandhi, an assistant professor of neurobiology & behavior.

He added that the findings point to the use of GABA cell transplantation to enhance retraining of the adult brain after injury. Furthermore, this work sparks new questions as to how these transplanted GABA neurons reactivate plasticity, the answers to which might lead to therapies for currently incurable brain disorders.

Multiple neurodevelopmental disorders have a common molecular cause

Neurodevelopmental disorders such as Down syndrome and autism-spectrum disorder can have profound, lifelong effects on learning and memory, but relatively little is known about the molecular pathways affected by these diseases. A study published by Cell Press October 9th in the American Journal of Human Genetics shows that neurodevelopmental disorders caused by distinct genetic mutations produce similar molecular effects in cells, suggesting that a one-size-fits-all therapeutic approach could be effective for conditions ranging from seizures to attention-deficit hyperactivity disorder.

“Neurodevelopmental disorders are rare, meaning trying to treat them is not efficient,” says senior study author Carl Ernst of McGill University. “Once we fully define the major common pathways involved, targeting these pathways for treatment becomes a viable option that can affect the largest number of people.”

A large fraction of neurodevelopmental disorders are associated with variation in specific genes, but the genetic factors responsible for these diseases are very complex. For example, whereas common variants in the same gene have been associated with two or more different disorders, mutations in many different genes can lead to similar diseases. As a result, it has not been clear whether genetic mutations that cause neurodevelopmental disorders affect distinct molecular pathways or converge on similar cellular functions.

To address this question, Ernst and his team used human fetal brain cells to study the molecular effects of reducing the activity of genes that are mutated in two distinct autism-spectrum disorders. Changes in transcription factor 4 (TCF4) cause 18q21 deletion syndrome, which is characterized by intellectual disability and psychiatric problems, and mutations in euchromatic histone methyltransferase 1 (EHMT1) cause similar symptoms in a disease known as 9q34 deletion syndrome.

Interfering with the activity of TCF4 or EHMT1 produced similar molecular effects in the cells. Strikingly, both of these genetic modifications resulted in molecular patterns that resemble those of cells that are differentiating, or converting from immature cells to more specialized cells. “Our study suggests that one fundamental cause of disease is that neural stem cells choose to become full brain cells too early,” Ernst says. “This could affect how they incorporate into cellular networks, for example, leading to the clinical symptoms that we see in kids with these diseases.”

Journal Reference: Chen et al. Molecular convergence of neurodevelopmental disorders. American Journal of Human Genetics, October 2014

Now THIS Is a Synapse

Every time I read about the synapse, the all-important junction between two neurons, the cartoon above pops into my head. It shows the gist of how a synapse works: An electrical pulse enters the cell on the left and activates those little blue balls, called vesicles, to release their chemical contents, called neurotransmitters. The neurotransmitters spill out into the space between the cells, called the cleft, and activate those blue rectangles, called ion channels. The channels trigger the cell on the right to fire its own electrical pulse, or action potential, and this message travels on to the next cell. It’s pretty neat. Our brains are full of trillions of synapses, each with the capability of converting an electrical signal into a chemical one and back again.

My doodle is conceptually useful for understanding many neuroscience studies. It helped me visualize, for example, how researchers record the messages of brain cells, and how the synapse plays a role in developmental disorders, and how the firing patterns of all of these synapses provide our brains with a sophisticated coding scheme.

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Neurodevelopment Disorders: *Cue CBS Laugh Track*

CBS and Chuck Lorre’s The Big Bang Theory dominates as the most popular show on scripted television. Currently in its eighth season, the multi-camera sitcom has aired nearly 200 episodes and ranks as thesecond most watched show on TV with a twenty million viewer pull. Ashow with this much notoriety has the rare opportunity to legitimately influence American culture in a positive way, but unfortunately The Big Bang Theory chooses not to. The premier scripted show in TV ratings happens to present some of the nastiest minority stereotypes on television. Aside from the token minority, Raj, and the dumb blonde stereotype, Penny, The Big Bang Theory’s most insidious reinforcement of stereotypes lie in the character Sheldon Cooper, played by Emmy Award winning actor Jim Parsons.

As a white, cisgender male, Sheldon seems an unlikely candidate to embody a minority. Yet, he displays behaviors consistent with a person with Asperger’s and thus he has become an unintentional representative of the mentally handicapped. Though denied by CBS and Jim Parsons himself, several Internet theorists, including Autism Speaks, Autism Daily, and Psychology Today, have insisted that the character Sheldon presents the characteristics of a person with Asperger’s syndrome. Individuals with Asperger’s Syndrome (a mild form of Autism), sometimes called “Aspies,” possess deficits in social interaction yet find themselves gifted with above average IQ levels and one interest that they predominantly excel in. Ordinarily, individuals with Asperger’s think literally, obsess over routine, and struggle to assess social cues.

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  • My thoughts on the whole 'not-vaccinating-my-child-so-they-don't-get-Autism' thing:firstly, you know as well as I know that there is no proven link between the two and secondly, do you mean to tell me that you'd rather risk your child getting sick and dying from a preventable disease and/or spreading said deadly disease to other children, therein making them sick and die than have a disabled/differently abled child? I understand the worry in your child being different than most other children & being made fun of for it and I even kind of get the worry over their 'quality' of life because parents always worry but you know what, Autism isn't even a bad thing to have and who are you to assume the quality of life for an Autistic individual is any less than a non-Autistic individual? It's rather telling that you'd rather risk your child's life/the lives of other children than even THINK of having an Autistic child. And by 'telling,' I mean horribly Ableist and disgusting.
  • *sidenote:I updated this post as I was made aware of how my specific usage of differently abled to replace the term disabled was problematic because it could be read as invalidating for those who DO identify as disabled.
Three UC San Diego Researchers Receive New CIRM Grants

Three UC San Diego Researchers Receive New CIRM Grants

Researchers at the University of California, San Diego School of Medicine are principal investigators in three of nine new grants approved today by the governing board of the California Institute for Regenerative Medicine (CIRM).

All of the grants are part of CIRM’s Human Induced Pluripotent Stem Cell (hiPSC) Initiative, an effort to develop and advance research into reprogramming cells, such as skin, into pluripotent stem cells that can then be differentiated into other functional cell types, such as neurons. In this case, the grants focus upon creating and operating long-term repositories of high quality stem cell lines representing different diseases that can be used by researchers everywhere.

The CIRM board approved nine grant proposals to create and store 9,000 cell lines from 3,000 individuals representing 11 diseases at a total cost of $32.3 million. Three of the proposals are based at UC San Diego and total more than $2.5 million. They are:

Kang Zhang, MD, PhD
Blinding eye diseases/$1,034,453
Blindness or impaired vision affects 3.3 million Americans over the age of 40, according to the National Institutes of Health. It’s a phenomenon that increases with age. The NIH projects 5.5 million blind or vision-impaired Americans by 2020.

Chief among vision afflictions are diseases like age-related macular degeneration (AMD), primary open-angle glaucoma (POAG) and proliferative diabetic retinopathy (PDR). Kang Zhang, MD, PhD, professor of ophthalmology and human genetics at the Shiley Eye Center and director of the Institute for Genomic Medicine, both at UC San Diego, and colleagues propose to obtain skin biopsies from patients with AMD, POAG and PDR and develop retina cell lines derived from differentiated hiPSCs. These lines will help researchers better understand the mechanisms of blinding diseases and aid drug development screening and testing. Ultimately, the hiPSCs might be used to replace degenerated or damaged retinal cells and restore vision.

Joseph Gleeson MD
Childhood neurodevelopmental disorders/$874,135
Many children with brain disorders have symptoms combining autism, cerebral palsy and epilepsy, suggesting underlying and shared mechanisms of dysfunction. In this project, principal investigator Joseph G. Gleeson, MD, professor of neurosciences and pediatrics at UC San Diego School of Medicine, and colleagues aim to identify 500 patients with these disorders, primarily from Rady Children’s Hospital-San Diego.  The goal is to develop a database of biological, medical, radiographic and genetic information that can be used to study stem cell mechanisms of disease and design therapeutic interventions. Please call 858-822-3538 for information or to participate.

Douglas Galasko, MD
Alzheimer’s disease/$643,693
Alzheimer’s disease (AD) is the most common form of dementia in the elderly, affecting more than 5 million Americans, among them 600,000 Californians. There are no treatments to slow the progression or prevent the neurological disorder. With colleagues, Douglas Galasko, MD, director of the Shiley-Marcos Alzheimer’s Disease Research Center at UC San Diego, will obtain skin cells from 220 persons with AD and 120 controls whose genetic backgrounds have been extensively studied. These cells will be preserved and made available to researchers, in particular hiPSC projects parsing the mechanisms and genetic risk of AD and for screening and testing new AD drugs.

The May 19 grants bring UC San Diego’s total to more than $ 133 million in CIRM funding since the first awards in 2006.

A Brain System that Appears To Compensate for Autism, OCD, and Dyslexia

Individuals with five neurodevelopmental disorders — autism spectrum disorder, obsessive-compulsive disorder, Tourette syndrome, dyslexia, and specific language impairment (SLI) — appear to compensate for dysfunction by relying on a single powerful and nimble system in the brain known as declarative memory.

This hypothesis being proposed by a Georgetown University Medical Center neuroscientist is based on decades of research. It is published online and will be in the April issue of Neuroscience and Biobehavioral Reviews.

The proposed compensation allows individuals with autism to learn scripts for navigating social situations; helps people with obsessive-compulsive disorder or Tourette syndrome to control tics and compulsions; and provides strategies to overcome reading and language difficulties in those diagnosed with dyslexia, autism, or SLI, a developmental disorder of language.

“There are multiple learning and memory systems in the brain, but declarative memory is the superstar,” says Michael Ullman, PhD, professor of neuroscience at Georgetown and director of the Brain and Language Laboratory. He explains that declarative memory can learn explicitly (consciously) as well as implicitly (non-consciously).

“It is extremely flexible, in that it can learn just about anything. Therefore it can learn all kinds of compensatory strategies, and can even take over for impaired systems,” says Ullman.

“Nevertheless, in most circumstances, declarative memory won’t do as good a job as these systems normally do, which is an important reason why individuals with the disorders generally still have noticeable problems despite the compensation,” he adds.

Knowing that individuals with these disorders can rely on declarative memory leads to insights on how to improve diagnosis and treatment of these conditions. It could improve treatment in two ways, Ullman says. First, designing treatments that rely on declarative memory, or that improve learning in this system, could enhance compensation. Conversely, treatments that are designed to avoid compensation by declarative memory may strengthen the dysfunctional systems.

Ullman says compensation by declarative memory may also help explain an observation that has long puzzled scientists — the fact that boys are diagnosed with these disorders more frequently than girls. “Studies suggest that girls and women are better than boys and men, on average, in their use of declarative memory. Therefore females are likely to compensate more successfully than males, even to the point of compensating themselves out of diagnosis more often than males,” Ullman says.

Declarative memory may also compensate for dysfunctions in other disorders, he adds, including attention deficit hyperactivity disorder (ADHD) and even adult-onset disorders such as aphasia or Parkinson’s disease.

The hypothesis may thus have powerful clinical and other implications for a wide variety of disorders, Ullman says.

Can Early Intervention Prevent Autism?

By Sujata Gupta 

Even before he was born, Kristin Hinson knew her son Noah’s odds of developing autism were high. When a child is diagnosed with the disorder, a younger sibling has a heightened risk of receiving the same diagnosis. That risk is further magnified when one has two older siblings on the spectrum. Noah has three older siblings, and two of them have autism.

When I reach Hinson over the phone, she’s cutting the kids’ hair (she has 5). She’s currently working on Justin, her second oldest, now 11, whom she periodically shushes as she tells her story. Her oldest child Amelia, says Hinson, a stay-at-home mom in Lincoln, California, was a typical child so it never occurred to her to worry about Justin. In retrospect, she says, he showed some warning signs as a young toddler, such as a weird obsession with things that opened and closed, like buckles, windows, and doors, and delayed talking, but he wasn’t diagnosed until age three. By the time Simon came along a few years later, Hinson had started to recognize those early red flags and she soon enrolled him in a study focusing on the younger siblings of autistic children at the University of California, Davis MIND Institute. Younger siblings like Simon are almost 15 times more likely to wind up on the spectrum than children in the general population. Simon was diagnosed with autism at just 15 months.

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Highlights of Changes from DSM-IV-TR to DSM-5: Neurodevelopmental Disorders

Really great summary (albeit a long one) of what’s different between the two editions. I cannot for the life of me figure out how to link to the pdf file but all you have to do is search “changes from dsm 4 to dsm 5” and it was my first result. For those who would like the brief(-er) version, continue reading on! I was going to publish my entire synopsis but the post would have been painfully long, so instead I’m breaking it up into diagnostic categories, starting with…


Intellectual Disability (Intellectual Developmental Disorder)

  • Previously mental retardation but still considered a mental disorder
  • Severity now determined by adaptive functioning rather than IQ score

Communication Disorders

  • Language Disorder: combines DSM-IV expressive and mixed receptive-expressive language disorders
  • Speech Sound Disorder: new name for phonological disorder
  • Childhood-Onset Fluency Disorder: new name for stuttering
  • Social (Pragmatic) Communication Disorder: new condition for persistent difficulties in the social uses of verbal and nonverbal communication. Cannot be diagnosed in the presence of restricted repetitive behaviors, interests, and activities (which would be make the disorder an Autism Spectrum Disorder). The symptoms of some patients diagnosed with DSM-IV pervasive developmental disorder not otherwise specified may meet the DSM-V criteria for this disorder

Autism Spectrum Disorder

  • Reflects a scientific consensus that four previously separate disorders are actually a single condition with different levels of symptom severity in two core domains
  • Now encompasses the previous DSM-IV autistic disorder (autism), Asperger’s disorder, childhood disintegrative disorder, and pervasive developmental disorder not otherwise specified.
  • ASD is characterized by 1) deficits in social communication and social interaction and 2) restricted repetitive behaviors, interests, and activities (RRBs).

Attention-Deficit/Hyperactivity Disorder

  • The same 18 symptoms are used as in DSM-IV, and continue to be divided into two symptom domains (inattention and hyperactivity/impulsivity), of which at least six symptoms in one domain are required for diagnosis. However, several changes have been made in DSM-5, including 1) the onset criterion has been changed from “symptoms that caused impairment were present before age 7 years” to “several inattentive or hyperactive-impulsive symptoms were present prior to age 12; 2) a comorbid diagnosis with autism spectrum disorder is now allowed; and 3) a symptom threshold change has been made for adults, to reflect their substantial evidence of clinically significant ADHD impairment, with the cutoff for ADHD of five symptoms, instead of six required for younger persons, both for inattention and for hyperactivity and impulsivity.
  • ADHD was placed in the neurodevelopmental disorders chapter to reflect brain developmental correlates with ADHD (is this a typo? do they mean ASD?) and the DSM-5 decision to eliminate the DSM-IV chapter that includes all diagnoses usually first made in infancy, childhood, or adolescence.

Specific Learning Disorder

  • Combines the DSM-IV diagnoses of reading disorder, mathematics disorder, disorder of written expression, and learning disorder NOS

Motor Disorders

  • Developmental Coordination Disorder
  • Stereotypic Movement Disorder
  • Tourette’s Disorder
  • Persistent (Chronic) Motor or Vocal Tic Disorder
  • Provisional Tic Disorder
  • Other Specified Tic disorder
  • Unspecified Tic Disorder
This study supports an association between increasing exposure from thimerosal containing childhood vaccines and the subsequent risk of specific delays in development among males and females.

PMID:  N Am J Med Sci. 2014 Oct ;6(10):519-31. PMID: 25489565 Abstract Title:  Thimerosal-containing hepatitis B vaccination and the risk for diagnosed specific delays in development in the United States: a case-control study in the vaccine safety datalink. Abstract:  BACKGROUND: Within the first 3 years of life, the brain develops rapidly. Its development is characterized by critical developmental periods for speech, vision, hearing, language, balance, etc.; and alteration in any of the processes occurring in those critical periods can lead to specific delays in development.AIMS: The present study evaluated the potential toxic effects of organic-mercury exposure from Thimerosal (49.55% mercury by weight) in childhood vaccines and its hypothesized possible relationship with specific delays in development.MATERIALS AND METHODS: A hypothesis testing case-control study was undertaken to evaluate the relationship between exposure to Thimerosal-containing hepatitis B vaccines administered at specific intervals in the first 6 months among cases diagnosed with specific delays in development and controls born between 1991-2000, utilizing data in the Vaccine Safety Datalink database.RESULTS: Cases were significantly more likely than controls to have received increased organic-mercury from Thimerosal-containing hepatitis B vaccine administered in the first, second, and sixth month of life.CONCLUSION: Though routine childhood vaccination may be an important public health tool to reduce the morbidity and mortality associated with infectious diseases, the present study supports an association between increasing organic-mercury exposure from Thimerosal-containing childhood vaccines and the subsequent risk of specific delays in development among males and females.

(Image caption: Fluorescent microphotograph of neurons. The green dye stains for a specialized synaptic protein and the red dye stains for actin, the polymeric protein that forms microfilaments and is a major component in the cytoskeleton. Credit: Adam Wegner, Webb Lab / Vanderbilt)

New insight into how brain makes memories

Every time you make a memory, somewhere in your brain a tiny filament reaches out from one neuron and forms an electrochemical connection to a neighboring neuron.

A team of biologists at Vanderbilt University, headed by Associate Professor of Biological Sciences Donna Webb, studies how these connections are formed at the molecular and cellular level.

The filaments that make these new connections are called dendritic spines and, in a series of experiments described in the April 17 issue of the Journal of Biological Chemistry, the researchers report that a specific signaling protein, Asef2, a member of a family of proteins that regulate cell migration and adhesion, plays a critical role in spine formation. This is significant because Asef2 has been linked to autism and the co-occurrence of alcohol dependency and depression.

“Alterations in dendritic spines are associated with many neurological and developmental disorders, such as autism, Alzheimer’s disease and Down Syndrome,” said Webb. “However, the formation and maintenance of spines is a very complex process that we are just beginning to understand.”

Neuron cell bodies produce two kinds of long fibers that weave through the brain: dendrites and axons. Axons transmit electrochemical signals from the cell body of one neuron to the dendrites of another neuron. Dendrites receive the incoming signals and carry them to the cell body. This is the way that neurons communicate with each other.

As they wait for incoming signals, dendrites continually produce tiny flexible filaments called filopodia. These poke out from the surface of the dendrite and wave about in the region between the cells searching for axons. At the same time, biologists think that the axons secrete chemicals of an unknown nature that attract the filopodia. When one of the dendritic filaments makes contact with one of the axons, it begins to adhere and to develop into a spine. The axon and spine form the two halves of a synaptic junction. New connections like this form the basis for memory formation and storage.

(Image caption: Fluorescent microphotograph of neurons that shows filapodia extending out from dendrite. Credit: Webb Lab / Vanderbilt)

Autism has been associated with immature spines, which do not connect properly with axons to form new synaptic junctions. However, a reduction in spines is characteristic of the early stages of Alzheimer’s disease. This may help explain why individuals with Alzheimer’s have trouble forming new memories.

The formation of spines is driven by actin, a protein that produces microfilaments and is part of the cytoskeleton. Webb and her colleagues showed that Asef2 promotes spine and synapse formation by activating another protein called Rac, which is known to regulate actin activity. They also discovered that yet another protein, spinophilin, recruits Asef2 and guides it to specific spines.

“Once we figure out the mechanisms involved, then we may be able to find drugs that can restore spine formation in people who have lost it, which could give them back their ability to remember,” said Webb.

VAERS had significantly higher ORs than autism following thimerosal containing DTaP vaccines in comparison to thimerosal free DTaP vaccines.

PMID:  Behav Brain Res. 2011 Sep 30 ;223(1):107-18. Epub 2011 Apr 28. PMID: 21549155 Abstract Title:  Persistent behavioral impairments and alterations of brain dopamine system after early postnatal administration of thimerosal in rats. Abstract:  The neurotoxic organomercurial thimerosal (THIM), used for decades as vaccine preservative, is a suspected factor in the pathogenesis of some neurodevelopmental disorders. Previously we showed that neonatal administration of THIM at doses equivalent to those used in infant vaccines or higher, causes lasting alterations in the brain opioid system in rats. Here we investigated neonatal treatment with THIM (at doses 12, 240, 1440 and 3000μg Hg/kg) on behaviors, which are characteristically altered in autism, such as locomotor activity, anxiety, social interactions, spatial learning, and on the brain dopaminergic system in Wistar rats of both sexes. Adult male and female rats, which were exposed to the entire range of THIM doses during the early postnatal life, manifested impairments of locomotor activity and increased anxiety/neophobia in the open field test. In animals of both sexes treated with the highest THIM dose, the frequency of prosocial interactions was reduced, while the frequency of asocial/antisocial interactionswas increased in males, but decreased in females. Neonatal THIM treatment did not significantly affect spatial learning and memory. THIM-exposed rats also manifested reduced haloperidol-induced catalepsy, accompanied by a marked decline in the density of striatal D₂ receptors, measured by immunohistochemical staining, suggesting alterations to the brain dopaminergic system. Males were more sensitive than females to some neurodisruptive/neurotoxic actions of THIM. These data document that early postnatal THIM administration causes lasting neurobehavioral impairments and neurochemical alterations in the brain, dependent on dose and sex. If similar changes occur in THIM/mercurial-exposed children, they could contribute do neurodevelopmental disorders.

Neurobiology of Attention Deficit/Hyperactivity Disorder

Attention deficit/hyperactivity disorder (ADHD), a prevalent neurodevelopmental disorder, has been associated with various structural and functional CNS abnormalities but findings about neurobiological mechanisms linking genes to brain phenotypes are just beginning to emerge. Despite the high heritability of the disorder and its main symptom dimensions, common individual genetic variants are likely to account for a small proportion of the phenotype’s variance. Recent findings have drawn attention to the involvement of rare genetic variants in the pathophysiology of ADHD, some being shared with other neurodevelopmental disorders. Traditionally, neurobiological research on ADHD has focused on catecholaminergic pathways, the main target of pharmacological treatments. However, more distal and basic neuronal processes in relation with cell architecture and function might also play a role, possibly accounting for the coexistence of both diffuse and specific alterations of brain structure and activation patterns. This article aims to provide an overview of recent findings in the rapidly evolving field of ADHD neurobiology with a focus on novel strategies regarding pathophysiological analyses.

Culmination of the research that examines the effects of thimerosal in humans indicates that it is a poison at minute levels with a plethora of deleterious consequences.

PMID:  Clin Chim Acta. 2015 Apr 15 ;444:212-220. Epub 2015 Feb 21. PMID: 25708367 Abstract Title:  Thimerosal: Clinical, epidemiologic and biochemical studies. Abstract:  INTRODUCTION: Thimerosal (or Thiomersal) is a trade name for an organomercurial compound (sodium ethyl-mercury (Hg) thiosalicylate) that is 49.55% Hg by weight, which rapidly decomposes in aqueous saline solutions into ethyl-Hg hydroxide and ethyl-Hg chloride. Developed in 1927, it has been and is still being used as a preservative in some cosmetics, topical pharmaceuticals, and biological drug products, including vaccines. Concerns have been voiced about its use because it is toxic to human cells. Although it is banned in several countries, it continues to be added to some vaccines in the United States and many vaccines in the developing world.DISCUSSION: This critical review focuses on the clinical, epidemiological, and biochemical studies of adverse effects from Thimerosal in developing humans. This review will include research that examines fetal, infant, and childhood death; birth defects; neurodevelopmental testing deficits in children; and neurodevelopmental disorders (attention deficit/hyperactivity disorder, autism spectrum disorder, tic disorder, and specific developmental delays). The review will also look at the research that examined the outcomes of acute accidental ethyl-Hg poisoning in humans. The studies that examine the underlying biochemical insights into the neuronal cellular damage will also be explored.CONCLUSION: The culmination of the research that examines the effects of Thimerosal in humans indicates that it is a poison at minute levels with a plethora of deleterious consequences, even at the levels currently administered in vaccines.