Have YOU been tested for Neanderthal genes?
11 Jan 2013, 6:11 pm
I strongly doubt it. It is very long since they died out and within larger areas it would be practically the same percentage for the entire population as people have mixed so much since then. However the neanderthals did as far as i understand have lower skills than modern humans when it come to social relations, although they were equally or more intelligent than modern humans on other areas.
11 Jan 2013, 11:07 pm
eric76 wrote:
Furthermore, forget "traits". Those are nothing but indirection. Autism and Asperger's are the results of the neurons and their connectivity in the brain.
I have to admit I'm not familar with the above theory. Do you have a link I can check out?
_________________
Our first challenge is to create an entire economic infrastructure, from top to bottom, out of whole cloth.
-CEO Nwabudike Morgan, "The Centauri Monopoly"
Sid Meier's Alpha Centauri (Firaxis Games)
12 Jan 2013, 1:15 am
AgentPalpatine wrote:
eric76 wrote:
Furthermore, forget "traits". Those are nothing but indirection. Autism and Asperger's are the results of the neurons and their connectivity in the brain.
I have to admit I'm not familar with the above theory. Do you have a link I can check out?
That the brains of people with Autism are different in some respects has been known for some time (I don't know how long), there is certainly ongoing research into the topics. One thing to note in particular that the cause of the differences is by no means sure.
Anyway, here are a few of the many reports of the differences found between that of Autistic children and their control groups.
Neuroimaging studies reported structural differences in language-related regions between individuals with autism and controls. A larger total brain volume has been consistently reported in children with autism, with some studies showing that this overall volume difference may persist through to adulthood.
Abnormal asymmetry in frontal and temporal areas has been reported by a number of studies, although the direction of regional abnormalities is somewhat inconsistent. For example, a reversal of the usual left–right asymmetry (in typically developing individuals) has been found in the right inferior frontal gyrus, with larger volumes in the right hemisphere of individuals with autism.
...
A recent study compared a relatively homogenous group of participants (atypical language development with average IQ) with matched controls. Increases in cortical thickness were found in the autism group in areas that are implicated in social cognition and communication, such as the inferior frontal gyrus, superior temporal sulcus, inferior parietal lobule and fusiform gyrus. Thus, it appears that structural abnormalities are apparent in brains of individuals with autism, particularly in areas that underlie core features such as communication problems of the disorder.
...
To fully characterize the neural underpinnings of autism, it may be necessary to view it as a disorder of connections between brain regions rather than at the level of a single region. From this perspective, the language deficits in autism may be due to problems integrating a set of brain functions into a coherent concept even though the ability to execute individual functions may be relatively preserved. Indeed, it has been reported that some high-functioning children with autism have unusual strengths in processing single words, whereas their ability to process the meaning of complex sentences is significantly impaired.
...
In addition to abnormal long-range connectivity across brain regions, researchers suggested that there may be increased short-range connectivity in autism. Post-mortem studies reported increased density of cortical mini-columns in brains of individuals with autism, suggesting a greater proportion of short range (as opposed to long-range) fibers. Similarly, Herbert and colleagues used a white matter parcellation technique and found increased radiate white matter in the autism group, which contains predominately short association fibers. Thus, these findings indicate abnormal microstructure of white matter in autism.
Abnormal asymmetry in frontal and temporal areas has been reported by a number of studies, although the direction of regional abnormalities is somewhat inconsistent. For example, a reversal of the usual left–right asymmetry (in typically developing individuals) has been found in the right inferior frontal gyrus, with larger volumes in the right hemisphere of individuals with autism.
...
A recent study compared a relatively homogenous group of participants (atypical language development with average IQ) with matched controls. Increases in cortical thickness were found in the autism group in areas that are implicated in social cognition and communication, such as the inferior frontal gyrus, superior temporal sulcus, inferior parietal lobule and fusiform gyrus. Thus, it appears that structural abnormalities are apparent in brains of individuals with autism, particularly in areas that underlie core features such as communication problems of the disorder.
...
To fully characterize the neural underpinnings of autism, it may be necessary to view it as a disorder of connections between brain regions rather than at the level of a single region. From this perspective, the language deficits in autism may be due to problems integrating a set of brain functions into a coherent concept even though the ability to execute individual functions may be relatively preserved. Indeed, it has been reported that some high-functioning children with autism have unusual strengths in processing single words, whereas their ability to process the meaning of complex sentences is significantly impaired.
...
In addition to abnormal long-range connectivity across brain regions, researchers suggested that there may be increased short-range connectivity in autism. Post-mortem studies reported increased density of cortical mini-columns in brains of individuals with autism, suggesting a greater proportion of short range (as opposed to long-range) fibers. Similarly, Herbert and colleagues used a white matter parcellation technique and found increased radiate white matter in the autism group, which contains predominately short association fibers. Thus, these findings indicate abnormal microstructure of white matter in autism.
n a small, preliminary study that included 13 male children, those with autism had an average 67 percent more prefrontal brain neurons and larger than average brain weight, than children without autism, according to a study in the November 9 issue of JAMA.
Brain and head overgrowth in children with autism and neural dysfunction are evident at young ages in multiple brain regions, including the prefrontal cortex (PFC), that are involved in higher-order social, emotional, communication, and cognitive development. "Therefore, knowledge of the neural basis of overgrowth could point to early causal mechanisms in autism and elucidate the neural functional defects that engender autistic symptoms. In the first magnetic resonance imaging (MRI) report of early brain overgrowth in autism a decade ago, it was theorized that excess numbers of neurons could be an underlying cause, perhaps due to prenatal dysregulation of proliferation, apoptosis [cell death], or both. However, the neural basis of early overgrowth remains unknown and can only be known from direct quantitative studies of the young postmortem autistic brain," according to background information in the article.
...
The researchers found statistically significant differences in neuron counts in the PFC in the autistic children compared with controls. There were 79 percent more neurons in DL-PFC in the autistic cases compared with the control cases and 29 percent more in M-PFC. The average DL-PFC count in the autistic children was 1.57 billion neurons compared with an average of 0.88 billion neurons in control children. The average M-PFC count in the autistic group was 0.36 billion neurons compared with an average of 0.28 billion neurons in controls. "Together, these 2 subdivisions gave a total combined prefrontal neuron count that was 67 percent greater in the autistic children compared with controls," the authors write.
The researchers also found that the brain weight in the autistic sample deviated from normative average weight for age by 17.6 percent, while control brains deviated from age-based norms by 0.2 percent.
Brain and head overgrowth in children with autism and neural dysfunction are evident at young ages in multiple brain regions, including the prefrontal cortex (PFC), that are involved in higher-order social, emotional, communication, and cognitive development. "Therefore, knowledge of the neural basis of overgrowth could point to early causal mechanisms in autism and elucidate the neural functional defects that engender autistic symptoms. In the first magnetic resonance imaging (MRI) report of early brain overgrowth in autism a decade ago, it was theorized that excess numbers of neurons could be an underlying cause, perhaps due to prenatal dysregulation of proliferation, apoptosis [cell death], or both. However, the neural basis of early overgrowth remains unknown and can only be known from direct quantitative studies of the young postmortem autistic brain," according to background information in the article.
...
The researchers found statistically significant differences in neuron counts in the PFC in the autistic children compared with controls. There were 79 percent more neurons in DL-PFC in the autistic cases compared with the control cases and 29 percent more in M-PFC. The average DL-PFC count in the autistic children was 1.57 billion neurons compared with an average of 0.88 billion neurons in control children. The average M-PFC count in the autistic group was 0.36 billion neurons compared with an average of 0.28 billion neurons in controls. "Together, these 2 subdivisions gave a total combined prefrontal neuron count that was 67 percent greater in the autistic children compared with controls," the authors write.
The researchers also found that the brain weight in the autistic sample deviated from normative average weight for age by 17.6 percent, while control brains deviated from age-based norms by 0.2 percent.
Brain overgrowth in autism during a critical time in development: implications for frontal pyramidal neuron and interneuron development and connectivity
...
Abstract
While abnormalities in head circumference in autism have been observed for decades, it is only recently that scientists have begun to focus in on the developmental origins of such a phenomenon. In this article we review past and present literature on abnormalities in head circumference, as well as recent developmental MRI studies of brain growth in this disorder. We hypothesize that brain growth abnormalities are greatest in frontal lobes, particularly affecting large neurons such as pyramidal cells, and speculate how this abnormality might affect neurofunctional circuitry in autism. The relationship to clinical characteristics and other disorders of macrencephaly are discussed.
...
Abstract
While abnormalities in head circumference in autism have been observed for decades, it is only recently that scientists have begun to focus in on the developmental origins of such a phenomenon. In this article we review past and present literature on abnormalities in head circumference, as well as recent developmental MRI studies of brain growth in this disorder. We hypothesize that brain growth abnormalities are greatest in frontal lobes, particularly affecting large neurons such as pyramidal cells, and speculate how this abnormality might affect neurofunctional circuitry in autism. The relationship to clinical characteristics and other disorders of macrencephaly are discussed.
Neuron Number and Size in Prefrontal Cortex of Children With Autism
...
Conclusion In this small preliminary study, brain overgrowth in males with autism involved an abnormal excess number of neurons in the PFC.
Clinical signs of autism are often preceded by or emerge concurrently with a period of abnormal brain and head overgrowth. This early neurobiological signal of abnormal development has been reported to begin at 9 to 18 months of age.
Overgrowth and neural dysfunction are evident at young ages in multiple brain regions, including the prefrontal cortex (PFC), that are involved in higher-order social, emotional, communication, and cognitive development. Therefore, knowledge of the neural basis of overgrowth could point to early causal mechanisms in autism and elucidate the neural functional defects that engender autistic symptoms. In the first magnetic resonance imaging (MRI) report of early brain overgrowth in autism a decade ago, it was theorized that excess numbers of neurons could be an underlying cause, perhaps due to prenatal dysregulation of proliferation, apoptosis, or both.
However, the neural basis of early overgrowth remains unknown and can only be known from direct quantitative studies of the young postmortem autistic brain. In one study, 4 postmortem cases of 4- to 11-year-olds with autism had approximately 53% more Von Economo neurons in the frontoinsular cortex than 3 controls. In another study, the brain of a 3-year-old with autism had 58% more Von Economo neurons than that of a 2-year old control. Since the total number of Von Economo neurons in the brain is small, an excess of these specific cell types cannot account for early brain overgrowth.
...
In this small, preliminary study, male children with autism had a mean 67% more prefrontal neurons than those in the control group. The excess was greater within DL-PFC than in M-PFC, a difference that parallels MRI volumetric data showing greater deviance in DL-PFC than M-PFC in living autistic toddlers.6 MRI studies show that enlargement is not restricted to DL-PFC and M-PFC; whether increased neuron counts in autism extend beyond these 2 major prefrontal subdivisions to include other cortical areas remains to be determined.
The autistic group also had larger than average brain weight. In 6 of the 7 cases, neuron numbers equaled or exceeded predictions based on brain weight compared with controls. These data indicate that a pathological increase in neuron numbers may be a key contributor to brain overgrowth in autism. However, our data also illustrated a strong positive correlation between total neuron numbers and brain weight in the control cases that was not found in the autistic cases. Thus, the autistic brains exhibited a substantial disturbance in the normal linear relationship between neuron quantity and overall brain weight. Neuron counts in the autistic children should have been accompanied by brain weights considerably larger than was observed, reaching 29.4% enlargement rather than the observed 17.6% enlargement. Thus, the size of the autistic brain, overlarge though it is, might actually underestimate the pathology of excess neuron numbers.
Because cortical neurons are not generated in postnatal life, this pathological increase in neuron numbers in autistic children indicates prenatal causes, including unchecked proliferation, reduced apoptosis, or both. Proliferation of cortical neurons is exponential between 10 and 20 weeks gestation and normally results in a net overabundance of neurons by as much as 100%.32 In animal models, dysregulation of genetic mechanisms are known that cause an even greater neuron overabundance and lead to increased head, brain, and cortical size, as is found in young children with autism. Functional analyses of genes located within copy number variation regions in autism also raise the possibility of dysregulation of proliferation during development.
Apoptotic mechanisms during the third trimester and early postnatal life normally remove subplate neurons, which comprise about half the neurons produced in the second trimester. A failure of that key early developmental process could also create a pathological excess of cortical neurons. A failure of subplate apoptosis might additionally indicate abnormal development of the subplate itself. The subplate plays a critical role in the maturation of layer 4 inhibitory functioning as well as in the early stages of thalamocortical and corticocortical connectivity development. Reduced inhibitory functioning and defects of functional and structural connectivity are characteristic of autism, but the causes have remained elusive. The possibility of abnormal development of the subplate in autism merits investigation.
Future studies of neuron numbers and underlying molecular and genetic mechanisms in autism face many limitations, as encountered in the present study. For example, the sample of postmortem tissue from children with autism—all that were available at the time of the study—was small. Despite the small sample size, evidence of excess neuron numbers in our autistic cases was statistically robust and occurred in cases with varying characteristics, such as with less severe and more severe autistic symptoms, and with and without intellectual disability. None of the causes of death for autistic cases in this study produce an increase in postmortem brain weight or neuron numbers. Most of the autistic and control children died of acute global ischemic hypoxia. Nearly every autistic and control case came from a full-term pregnancy. A history of medication and adverse medical conditions was not present in most of the cases, particularly for the 4 youngest autistic cases, each of whom had substantial excess neuron counts. Conversely, the lowest prefrontal neuron number in the autism group was found in a 7-year-old boy with a seizure disorder, which may explain why he had fewer counts than other autistic children. The potential effect of seizures on cellular and molecular measures in autism is important to investigate further.
...
Conclusion In this small preliminary study, brain overgrowth in males with autism involved an abnormal excess number of neurons in the PFC.
Clinical signs of autism are often preceded by or emerge concurrently with a period of abnormal brain and head overgrowth. This early neurobiological signal of abnormal development has been reported to begin at 9 to 18 months of age.
Overgrowth and neural dysfunction are evident at young ages in multiple brain regions, including the prefrontal cortex (PFC), that are involved in higher-order social, emotional, communication, and cognitive development. Therefore, knowledge of the neural basis of overgrowth could point to early causal mechanisms in autism and elucidate the neural functional defects that engender autistic symptoms. In the first magnetic resonance imaging (MRI) report of early brain overgrowth in autism a decade ago, it was theorized that excess numbers of neurons could be an underlying cause, perhaps due to prenatal dysregulation of proliferation, apoptosis, or both.
However, the neural basis of early overgrowth remains unknown and can only be known from direct quantitative studies of the young postmortem autistic brain. In one study, 4 postmortem cases of 4- to 11-year-olds with autism had approximately 53% more Von Economo neurons in the frontoinsular cortex than 3 controls. In another study, the brain of a 3-year-old with autism had 58% more Von Economo neurons than that of a 2-year old control. Since the total number of Von Economo neurons in the brain is small, an excess of these specific cell types cannot account for early brain overgrowth.
...
In this small, preliminary study, male children with autism had a mean 67% more prefrontal neurons than those in the control group. The excess was greater within DL-PFC than in M-PFC, a difference that parallels MRI volumetric data showing greater deviance in DL-PFC than M-PFC in living autistic toddlers.6 MRI studies show that enlargement is not restricted to DL-PFC and M-PFC; whether increased neuron counts in autism extend beyond these 2 major prefrontal subdivisions to include other cortical areas remains to be determined.
The autistic group also had larger than average brain weight. In 6 of the 7 cases, neuron numbers equaled or exceeded predictions based on brain weight compared with controls. These data indicate that a pathological increase in neuron numbers may be a key contributor to brain overgrowth in autism. However, our data also illustrated a strong positive correlation between total neuron numbers and brain weight in the control cases that was not found in the autistic cases. Thus, the autistic brains exhibited a substantial disturbance in the normal linear relationship between neuron quantity and overall brain weight. Neuron counts in the autistic children should have been accompanied by brain weights considerably larger than was observed, reaching 29.4% enlargement rather than the observed 17.6% enlargement. Thus, the size of the autistic brain, overlarge though it is, might actually underestimate the pathology of excess neuron numbers.
Because cortical neurons are not generated in postnatal life, this pathological increase in neuron numbers in autistic children indicates prenatal causes, including unchecked proliferation, reduced apoptosis, or both. Proliferation of cortical neurons is exponential between 10 and 20 weeks gestation and normally results in a net overabundance of neurons by as much as 100%.32 In animal models, dysregulation of genetic mechanisms are known that cause an even greater neuron overabundance and lead to increased head, brain, and cortical size, as is found in young children with autism. Functional analyses of genes located within copy number variation regions in autism also raise the possibility of dysregulation of proliferation during development.
Apoptotic mechanisms during the third trimester and early postnatal life normally remove subplate neurons, which comprise about half the neurons produced in the second trimester. A failure of that key early developmental process could also create a pathological excess of cortical neurons. A failure of subplate apoptosis might additionally indicate abnormal development of the subplate itself. The subplate plays a critical role in the maturation of layer 4 inhibitory functioning as well as in the early stages of thalamocortical and corticocortical connectivity development. Reduced inhibitory functioning and defects of functional and structural connectivity are characteristic of autism, but the causes have remained elusive. The possibility of abnormal development of the subplate in autism merits investigation.
Future studies of neuron numbers and underlying molecular and genetic mechanisms in autism face many limitations, as encountered in the present study. For example, the sample of postmortem tissue from children with autism—all that were available at the time of the study—was small. Despite the small sample size, evidence of excess neuron numbers in our autistic cases was statistically robust and occurred in cases with varying characteristics, such as with less severe and more severe autistic symptoms, and with and without intellectual disability. None of the causes of death for autistic cases in this study produce an increase in postmortem brain weight or neuron numbers. Most of the autistic and control children died of acute global ischemic hypoxia. Nearly every autistic and control case came from a full-term pregnancy. A history of medication and adverse medical conditions was not present in most of the cases, particularly for the 4 youngest autistic cases, each of whom had substantial excess neuron counts. Conversely, the lowest prefrontal neuron number in the autism group was found in a 7-year-old boy with a seizure disorder, which may explain why he had fewer counts than other autistic children. The potential effect of seizures on cellular and molecular measures in autism is important to investigate further.
12 Jan 2013, 7:38 am
norwegianman1972 wrote:
Of course the brain works different for people with an autism diagnosis. Otherwise we wouldn´t have had the diagnosis in the first place...
And the brain works differently because there are differences in the brain itself. If the brain was the same as everyone else, then it would work the same as everyone else.
The question is not whether the brain is different, but why is it different? And there are a great number of possibilities for that.
12 Jan 2013, 9:12 am
eric76 wrote:
That the brains of people with Autism are different in some respects has been known for some time (I don't know how long), there is certainly ongoing research into the topics. One thing to note in particular that the cause of the differences is by no means sure.
Anyway, here are a few of the many reports of the differences found between that of Autistic children and their control groups.
Anyway, here are a few of the many reports of the differences found between that of Autistic children and their control groups.
Thank you. I was'nt able to read details on the first article, and my understanding of the 3rd article is limited. For the 2nd and 4th article, it appears that these are studies of deceased individuals, who (presumably) had a DX while they were alive. Even if we go by DSM-IV standards, Autism can have false positives, and I would think the risk of a false positive would be highest when dealing with individuals who unfortunately were not able to provide information for the interview that is generally required for a formal DX, nor have observed social maladjustment.
I'm also trying to understand how researchers have ruled out ASD "traits", when the DSM-IV and DSM-5 standards both seem to rely on traits to issue a DX.
_________________
Our first challenge is to create an entire economic infrastructure, from top to bottom, out of whole cloth.
-CEO Nwabudike Morgan, "The Centauri Monopoly"
Sid Meier's Alpha Centauri (Firaxis Games)
12 Jan 2013, 1:46 pm
AgentPalpatine wrote:
Thank you. I was'nt able to read details on the first article, and my understanding of the 3rd article is limited. For the 2nd and 4th article, it appears that these are studies of deceased individuals, who (presumably) had a DX while they were alive. Even if we go by DSM-IV standards, Autism can have false positives, and I would think the risk of a false positive would be highest when dealing with individuals who unfortunately were not able to provide information for the interview that is generally required for a formal DX, nor have observed social maladjustment.
I'm also trying to understand how researchers have ruled out ASD "traits", when the DSM-IV and DSM-5 standards both seem to rely on traits to issue a DX.
I'm also trying to understand how researchers have ruled out ASD "traits", when the DSM-IV and DSM-5 standards both seem to rely on traits to issue a DX.
The brains used in the research came from individuals who were diagnosed with Autism.
It is the behavior or traits of the individuals that received the attention of the doctors who classify a set of seemingly related traits as a specific condition. The implicit assumption is that a common set of seemingly related traits in different individuals reflects a condition that they all have in common.
I don't know how much the old time psychologists and psychiatrists recognized the traits as being based on unusual variations of the brain. It sounds to me like they often thought that the brains were the same as anyone else's and that the behavior was somehow learned. The result was "treatments" that did nothing but create hell for the patients. Fortunately, these quacks seem to be fewer and fewer in numbers.
In the old days, it pretty much took a complaint by a patient for the doctor to even have an idea of where to look for a problem. Today, more and more conditions are detectable by a doctor who can make a diagnosis even if the patient has no complaints. For example, every routine visit to the doctor includes a measurement of your blood pressure. Medications can be prescribed to try to bring high blood pressure down. There was a time in the past where that capability did not exist -- the first time the doctor and patient would know anything was wrong was when the patient had a stroke.
I think that it is well recognized now that the traits reflect differences in the structure of the brain. But the diagnosis still depends on the traits. The doctors must rely on these traits for the diagnosis because that is what they have available to work with. A doctor cannot take core samples of living patients brains to look for the reasons for the traits to make a diagnosis. They can do some brain scans, but those scans cannot show the fine structure of the brain in detail.
In the future, it might become possible to scan the brain of an individual and see enough detail in the underlying structure to diagnose Autism. If that happens, there may be no reliance on the traits at all.
What I expect will happen is that researchers will zero in on the causes of Autism and will watch for those causes and will perhaps be able to treat them and greatly reduce the number of children born with Autism.
12 Jan 2013, 4:21 pm
eric76 wrote:
What I expect will happen is that researchers will zero in on the causes of Autism and will watch for those causes and will perhaps be able to treat them and greatly reduce the number of children born with Autism.
How would you propose to treat what you are indicating are neuron differences in the brain?
_________________
Our first challenge is to create an entire economic infrastructure, from top to bottom, out of whole cloth.
-CEO Nwabudike Morgan, "The Centauri Monopoly"
Sid Meier's Alpha Centauri (Firaxis Games)
12 Jan 2013, 7:13 pm
AgentPalpatine wrote:
eric76 wrote:
What I expect will happen is that researchers will zero in on the causes of Autism and will watch for those causes and will perhaps be able to treat them and greatly reduce the number of children born with Autism.
How would you propose to treat what you are indicating are neuron differences in the brain?
The point of treatment, if treatment is possible, would need to be of the mother while she is pregnant with the developing baby.
For example, making sure that pregnant women have sufficient amounts of folic acid greatly reduces the risk that their babies will be born with spina bifida.
12 Jan 2013, 7:35 pm
eric76 wrote:
The point of treatment, if treatment is possible, would need to be of the mother while she is pregnant with the developing baby.
For example, making sure that pregnant women have sufficient amounts of folic acid greatly reduces the risk that their babies will be born with spina bifida.
For example, making sure that pregnant women have sufficient amounts of folic acid greatly reduces the risk that their babies will be born with spina bifida.
Are you indicating that there is an enviromental cause of the hypothetical neuron "differences" that you mentioned in earlier posts? This does seem different than preventing the introduction of toxins or encouraging good nutrition.
_________________
Our first challenge is to create an entire economic infrastructure, from top to bottom, out of whole cloth.
-CEO Nwabudike Morgan, "The Centauri Monopoly"
Sid Meier's Alpha Centauri (Firaxis Games)
12 Jan 2013, 8:40 pm
AgentPalpatine wrote:
eric76 wrote:
The point of treatment, if treatment is possible, would need to be of the mother while she is pregnant with the developing baby.
For example, making sure that pregnant women have sufficient amounts of folic acid greatly reduces the risk that their babies will be born with spina bifida.
For example, making sure that pregnant women have sufficient amounts of folic acid greatly reduces the risk that their babies will be born with spina bifida.
Are you indicating that there is an enviromental cause of the hypothetical neuron "differences" that you mentioned in earlier posts? This does seem different than preventing the introduction of toxins or encouraging good nutrition.
No. I'm saying that Autism appears to be related to the development of the brain of the baby prior to birth. If there is going to be a treatment to reduce the risk of Autism, any treatment is surely going to have to be prior to birth.
12 Jan 2013, 8:46 pm
eric76 wrote:
No. I'm saying that Autism appears to be related to the development of the brain of the baby prior to birth. If there is going to be a treatment to reduce the risk of Autism, any treatment is surely going to have to be prior to birth.
Even if we accepted the hypothetical neuron theory, would'nt that be more genetic than some sort of developmental "issue" during development?
_________________
Our first challenge is to create an entire economic infrastructure, from top to bottom, out of whole cloth.
-CEO Nwabudike Morgan, "The Centauri Monopoly"
Sid Meier's Alpha Centauri (Firaxis Games)
13 Jan 2013, 12:02 am
AgentPalpatine wrote:
eric76 wrote:
No. I'm saying that Autism appears to be related to the development of the brain of the baby prior to birth. If there is going to be a treatment to reduce the risk of Autism, any treatment is surely going to have to be prior to birth.
Even if we accepted the hypothetical neuron theory, would'nt that be more genetic than some sort of developmental "issue" during development?
Remember that when we are talking about Autism or Asperger's, we are talking about the brain. The brain is different. The question is not whether or not the brain is involved, but what is different about the brain and how it got that way. If it is genetic, then it is because the proteins encoded somehow helped cause the way the brain is formed to be somewhat different than for others or made it more susceptible to be formed differently.
In other words, whatever causes Autism, it is doing something to the brain and it certainly appears that whatever it is, it results in differences to the brain during gestation.
As far as the cause, it could be quite a few different things or many things working together. It might be that genetics. It might be a Vitamin D deficiency. It might be viral. It might be all of these. It might be none of these. But whatever it is, it causes the brain to be developed differently.
13 Jan 2013, 10:44 am
http://blog.23andme.com/ancestry/find-your-inner-neanderthal
I will know within a few weeks. Just mailed off my saliva sample a few days ago, and apparently 23andme tests for Neanderthal ancestry. (Though I'm most interested in the psychology-related genes as well as my risk of breast/ovarian cancer.)
13 Jan 2013, 11:21 am
Ettina wrote:
http://blog.23andme.com/ancestry/find-your-inner-neanderthal
I will know within a few weeks. Just mailed off my saliva sample a few days ago, and apparently 23andme tests for Neanderthal ancestry. (Though I'm most interested in the psychology-related genes as well as my risk of breast/ovarian cancer.)
I will know within a few weeks. Just mailed off my saliva sample a few days ago, and apparently 23andme tests for Neanderthal ancestry. (Though I'm most interested in the psychology-related genes as well as my risk of breast/ovarian cancer.)
Wow!
Keep us posted about the neanderthal part- if you dont mind revealing your dna in public.
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