Hmm….
“This paper is interesting: it supports the finding that ADD is associated with higher density of dopamine transporter (DAT). It also suggests that nicotine has an effect similar to methylphenidate in patients with high DAT density.”
(Original reference: Lukas)
For those of us whose biology is a little out of date, and who are suffering from nicotine withdrawal, can you explain what this means? Thanks.
I fear this paper ist rather.. humm.. pointless.
They did not search for ADHD concernment by the mothers, and I fear this grade is higher than under Non-Smokers (Self-Medication).
Does this have any connection with visual stimulation that ADD folks crave as well?
look up hubel’s work on the visual cortex to peice this together: thats the key with the visual ADD thing.
also the key is with prefrontal genu function. this is also why persons with add have mood swings (or irrational rants): look at the diagrams some more and i could talk you through how those nerves work if you guys wish.
the corpus callosum when looked at sagitally, atrophies from a phenomena called diaschisis (spelling not sure, my wifes word, shes the radiologist), this happens in late life dementia. the ADD and dopamine idea is very interesting; most parkinsons or parkinsonian patients respond to either ritalin or provigil very well, and do not do well with your standard SSRI’s
i am troubled at the emphasis of the allele thing: too much emphasis on developing rv1021 reuptake modulators. this is a protein found in the brains of boston area engineering professors: pfizer is researching this towards making a new drug.
the nicotinic modulation was discovered by the fact that there is a coorelation of persons who smoke not to get idiopathic parkinsons. also the dementia drugs have some nicotinic modulation and that just smoking a little bit, helps with short term memory.
i have given aricept to a patient with tourette’s syndrome as well as ADD, the med worked like a charm, but i did not refill it because it is off off lable use. Pfizer is seriously now persuing ADD as an indication for treatment with Aricept.
ask specific questions and i can answer to the best of my ability.
i am working on a blog entry over at my blog on the poetics of glogging: met with blogdiva from culture kitchen over at john barlows and we discussed this a bit. i will finish that entry by tomorrow and edit it a bit. this all has to do with corpus callosum function interacting with the two hemisheres during the production of kanji like language with broca’s and wernike’s. Kana like language touches on the visual prosthetic.
the idea is to stimulate the brain towards healing; i find that social interaction may be more better at preserving the memory when compared to treatment with aricept. the same may be true with medicines for ADD. that the appropriate social interactions for those children are time consuming and that the quick fix meds will cause a fundamental restructuring of brain architecture nessecitating a life time dependency of psychotropic medications.
isa gordon has something that is like a memory prosthetic center down in arizona, but i do not know much about it.
a more serious researcher is by the name of elizabeth gould from princeton; great article in the june 23 2001 edition of the new yorker that talks about the new consept of brain architecture. she did a classical experiment where she cut the hippocampii of cats, put some on prozac, and others on a placebo. the cats where attached to an ocillator and the signal demonstrating a reconnection with the cats on the prozac.
the limbic system is parallel to the striatum and basal ganglion.
also another good thing to look up is the proceding from the 2003 international symposium on wearable computing where the keynote speaker whas a Dr Okun from the university of florida who discussed deep brain stimulation for the treatment of parkinsonian tremors: during this lecture, the discription of the multiple layers of brain tissue was discussed and the different signals being given was demonstrated.
so if you think about all of the above in concert, as a multidirectional oprah, you can understand at what point all this is tangental, and at what point it is a concerted discription of multiple pathways within the brain.
if anyone is further interested, look up robins work over at hypertextual ontology: she is very good at making stuff like this make more sense.
stef
PS danah, are you still mad at me?
look up hubel’s work on the visual cortex to peice this together: thats the key with the visual ADD thing.
also the key is with prefrontal genu function. this is also why persons with add have mood swings (or irrational rants): look at the diagrams some more and i could talk you through how those nerves work if you guys wish.
the corpus callosum when looked at sagitally, atrophies from a phenomena called diaschisis (spelling not sure, my wifes word, shes the radiologist), this happens in late life dementia. the ADD and dopamine idea is very interesting; most parkinsons or parkinsonian patients respond to either ritalin or provigil very well, and do not do well with your standard SSRI’s
i am troubled at the emphasis of the allele thing: too much emphasis on developing rv1021 reuptake modulators. this is a protein found in the brains of boston area engineering professors: pfizer is researching this towards making a new drug.
the nicotinic modulation was discovered by the fact that there is a coorelation of persons who smoke not to get idiopathic parkinsons. also the dementia drugs have some nicotinic modulation and that just smoking a little bit, helps with short term memory.
i have given aricept to a patient with tourette’s syndrome as well as ADD, the med worked like a charm, but i did not refill it because it is off off lable use. Pfizer is seriously now persuing ADD as an indication for treatment with Aricept.
ask specific questions and i can answer to the best of my ability.
i am working on a blog entry over at my blog on the poetics of glogging: met with blogdiva from culture kitchen over at john barlows and we discussed this a bit. i will finish that entry by tomorrow and edit it a bit. this all has to do with corpus callosum function interacting with the two hemisheres during the production of kanji like language with broca’s and wernike’s. Kana like language touches on the visual prosthetic.
the idea is to stimulate the brain towards healing; i find that social interaction may be more better at preserving the memory when compared to treatment with aricept. the same may be true with medicines for ADD. that the appropriate social interactions for those children are time consuming and that the quick fix meds will cause a fundamental restructuring of brain architecture nessecitating a life time dependency of psychotropic medications.
isa gordon has something that is like a memory prosthetic center down in arizona, but i do not know much about it.
a more serious researcher is by the name of elizabeth gould from princeton; great article in the june 23 2001 edition of the new yorker that talks about the new consept of brain architecture. she did a classical experiment where she cut the hippocampii of cats, put some on prozac, and others on a placebo. the cats where attached to an ocillator and the signal demonstrating a reconnection with the cats on the prozac.
the limbic system is parallel to the striatum and basal ganglion.
also another good thing to look up is the proceding from the 2003 international symposium on wearable computing where the keynote speaker whas a Dr Okun from the university of florida who discussed deep brain stimulation for the treatment of parkinsonian tremors: during this lecture, the discription of the multiple layers of brain tissue was discussed and the different signals being given was demonstrated.
so if you think about all of the above in concert, as a multidirectional oprah, you can understand at what point all this is tangental, and at what point it is a concerted discription of multiple pathways within the brain.
if anyone is further interested, look up robins work over at hypertextual ontology: she is very good at making stuff like this make more sense.
stef
PS danah, are you still mad at me?
Stefanos: so basically, if the flux capacitor reaches 1.1 Giga Watts, it’s all ok from there onwards?
Stefanos: so basically, if the flux capacitor reaches 1.1 Giga Watts, it’s all ok?
Stefanos: so basically, if the flux capacitor reaches 1.1 Giga Watts, it’s all ok?