Posts
In the January issue of Archives of General Psychiatry, there is an article (1) titled "Influence of Cognitive Status, Age, and APOE-4 Genetic Risk on Brain FDDNP Positron-Emission Tomography Imaging in Persons Without Dementia." The purpose of this study was to determine if the above-mentioned variables are associated "with increased cerebral FDDNP-Pet binding." What is FDDNP? it stands for 2-(1-{6-[(2-[F-18]fluoroethyl)methyl)amino]-2-naphthyl}ethylidene)malononitrile. Kind of just roles off the toungue doesn't it.
The researchers of this article and this other article (2) are responsible for developing this molecule, which binds to both amyloid plaques and tau tangles, the neuropathological hallmarks of Alzheimer's disease (AD is actually more than just the presence of these two abnormalities, but I'll get into at a later date). In their most recent study, they demonstrated that cognitive status, age, and APOE status were all associated with increased cerebral FDDNP uptake, which means that the above-mentioned variables are associated with increased deposition of amyloid plaques and tau tangles. As the authors state, "the results are consistent with our hypothesis and with previous clinical and postmortem studies demonstrating a relationship between such risk factors and amyloid plaque and tau tangle formation in the brain." The objective of this study was not add to this specific literature (pathology), but to demonstrate that their molecule worked, which it apparently did.
If you read the piece over at Sciencedaily.com (3), you would think the objective was something else. I know I piss on this site frequently, but it's a good barometer for how the media (mis)represents science news. Their piece is titled, "Scientists See Brain Aging Before Symptoms Appear." Sounds way cooler than the journal title. However, that was not the aim of study; determining if their tracer worked was the real aim. Remember, all of the findings regarding pathology were already known. The researchers even cite that research in their article.
So why the hyperbole? This stuff is only interesting to a select group of people (e.g., radiologists). Why try to make the uninteresting, interesting? Marketing, "UCLA scientists have used innovative brain-scan technology developed at UCLA, along with patient-specific information on Alzheimer's disease risk, to help diagnose brain aging, often before symptoms appear." I guess before this "innovative brain-scan technology," diagnosing presymptomatic brain ageing was difficult, right? Not really, (4, 5, 6, 7, 8, 9, 10). Again, the purpose of the study was to demonstrate the utility of the tracer.
In the journal article's financial disclosure section it says, "The University of California, Los Angeles, owns a US patent (6,274,119) titled 'Methods for Labeling B-Amyloid Plaques and Neurofibrillary Tangles...Drs Small, Huang, Cole, and Barrio reported that they are among the inventors, have received royalties, and will receive royalties on future sales." They're pimping their invention. Nothing wrong with that. But is all the BS necessary? Even the lead researcher joins in on the BS game, "Combining key patient information with a brain scan may give us better predictive power in targeting those who may benefit from early interventions, as well as help test how well treatments are working...this type of scan offers an opportunity to see what is really going on in the brain." The picture included with post is a FDDNP-PET image. Clear as mud, right? Not to be a nit-pick, but the study wasn't designed to determine if the stated variables can be utilized to predict onset, course, impairment, etc.
Here is more subtle advertising:
"Eventually, this imaging method, together with patient information like age, cognitive status and genetics, may help us better manage brain aging"
"PET, combined with the FDDNP probe, is the only imaging technology that offers a full profile of neurodegeneration that includes measures of both plaques and tangles"
This one is my favorite, "According to Small, in the future (cue music from Sagan's Cosmos), brain aging may be controlled similarly to high cholesterol or high blood pressure. Patients would receive a brain scan and perhaps a genetic test to predict their risk. Medications and other interventions could be prescribed, if necessary, to prevent or delay future neurodegeneration, allowing doctors to protect a healthy brain before extensive damage occurs. The brain scans may also prove helpful in tracking the effectiveness of treatments." What a prognosticator. Granted Dr. Small's utopia is a cliche and a bit hackneyed, but I still get this warm and fuzzy feeling inside the cockles of my heart.
Once again, the purpose of this study was "to determine if impaired cognitive status, older age, apolipoprotein E-4 (APOE-4) genetic risk for Alzheimer disease, family history of dementia, and less education are associated with increased regional cerebral FDDNP-PET binding." This is one of those study where the researchers knew the answer before going in (2, 11). The subjects involved were the same subjects involved in their previous study (2).
Hey, did any know that people want to revise the diagnostic criteria for Alzheimer's disease? These researchers sure did, "these criteria (referring to the revised criteria) include the presence of...1 or more abnormal biomarkers such as molecular neuroimaging with PET...FDDNP-PET might be a useful tool in applying such revised research diagnostic criteria."
I'm not faulting these people for pimping their product. That's expected. Just don't pretend that you're doing something otherwise.
The researchers of this article and this other article (2) are responsible for developing this molecule, which binds to both amyloid plaques and tau tangles, the neuropathological hallmarks of Alzheimer's disease (AD is actually more than just the presence of these two abnormalities, but I'll get into at a later date). In their most recent study, they demonstrated that cognitive status, age, and APOE status were all associated with increased cerebral FDDNP uptake, which means that the above-mentioned variables are associated with increased deposition of amyloid plaques and tau tangles. As the authors state, "the results are consistent with our hypothesis and with previous clinical and postmortem studies demonstrating a relationship between such risk factors and amyloid plaque and tau tangle formation in the brain." The objective of this study was not add to this specific literature (pathology), but to demonstrate that their molecule worked, which it apparently did.
If you read the piece over at Sciencedaily.com (3), you would think the objective was something else. I know I piss on this site frequently, but it's a good barometer for how the media (mis)represents science news. Their piece is titled, "Scientists See Brain Aging Before Symptoms Appear." Sounds way cooler than the journal title. However, that was not the aim of study; determining if their tracer worked was the real aim. Remember, all of the findings regarding pathology were already known. The researchers even cite that research in their article.
So why the hyperbole? This stuff is only interesting to a select group of people (e.g., radiologists). Why try to make the uninteresting, interesting? Marketing, "UCLA scientists have used innovative brain-scan technology developed at UCLA, along with patient-specific information on Alzheimer's disease risk, to help diagnose brain aging, often before symptoms appear." I guess before this "innovative brain-scan technology," diagnosing presymptomatic brain ageing was difficult, right? Not really, (4, 5, 6, 7, 8, 9, 10). Again, the purpose of the study was to demonstrate the utility of the tracer.
In the journal article's financial disclosure section it says, "The University of California, Los Angeles, owns a US patent (6,274,119) titled 'Methods for Labeling B-Amyloid Plaques and Neurofibrillary Tangles...Drs Small, Huang, Cole, and Barrio reported that they are among the inventors, have received royalties, and will receive royalties on future sales." They're pimping their invention. Nothing wrong with that. But is all the BS necessary? Even the lead researcher joins in on the BS game, "Combining key patient information with a brain scan may give us better predictive power in targeting those who may benefit from early interventions, as well as help test how well treatments are working...this type of scan offers an opportunity to see what is really going on in the brain." The picture included with post is a FDDNP-PET image. Clear as mud, right? Not to be a nit-pick, but the study wasn't designed to determine if the stated variables can be utilized to predict onset, course, impairment, etc.
Here is more subtle advertising:
"Eventually, this imaging method, together with patient information like age, cognitive status and genetics, may help us better manage brain aging"
"PET, combined with the FDDNP probe, is the only imaging technology that offers a full profile of neurodegeneration that includes measures of both plaques and tangles"
This one is my favorite, "According to Small, in the future (cue music from Sagan's Cosmos), brain aging may be controlled similarly to high cholesterol or high blood pressure. Patients would receive a brain scan and perhaps a genetic test to predict their risk. Medications and other interventions could be prescribed, if necessary, to prevent or delay future neurodegeneration, allowing doctors to protect a healthy brain before extensive damage occurs. The brain scans may also prove helpful in tracking the effectiveness of treatments." What a prognosticator. Granted Dr. Small's utopia is a cliche and a bit hackneyed, but I still get this warm and fuzzy feeling inside the cockles of my heart.
Once again, the purpose of this study was "to determine if impaired cognitive status, older age, apolipoprotein E-4 (APOE-4) genetic risk for Alzheimer disease, family history of dementia, and less education are associated with increased regional cerebral FDDNP-PET binding." This is one of those study where the researchers knew the answer before going in (2, 11). The subjects involved were the same subjects involved in their previous study (2).
Hey, did any know that people want to revise the diagnostic criteria for Alzheimer's disease? These researchers sure did, "these criteria (referring to the revised criteria) include the presence of...1 or more abnormal biomarkers such as molecular neuroimaging with PET...FDDNP-PET might be a useful tool in applying such revised research diagnostic criteria."
I'm not faulting these people for pimping their product. That's expected. Just don't pretend that you're doing something otherwise.
No comments:
Post a Comment