The *Journal of the American Geriatrics Society* issued the followingnews release about a study ("Cumulative Anticholinergic Exposure IsAssociated with Poor Memory and Executive Function in Older Men")
A study published in Journal of the American Geriatrics Societysuggested that the use of certain medications in elderly populations maybe associated with cognitive decline. The study examined the effects ofexposure to anticholinergic medications, a type of drug used to treat avariety of disorders that include respiratory and gastrointestinalproblems, on over 500 relatively healthy men aged 65 years or older withhigh blood pressure.
Older people often take several drugs to treat multiple healthconditions. As some of these drugs also have properties that affectneurotransmitters in the brain that are important to overall brainfunction, the researchers examined the total effects of all medicationstaken by the patients, both prescription and over-the-counter, that werebelieved to affect the function of a particular neurotransmitter,acetylcholine.The findings show that chronic use of medications with anticholinergicproperties may have detrimental effects on memory and the ability toperform daily living tasks, such as shopping and managing finances.Participants showed deficits in both memory and daily function when theytook these medications over the course of a year. The degree of memorydifficulty and impairment in daily living tasks also increasedproportionally to the total amount of drug exposure, based on a ratingscale the authors developed to assess anticholinergicity of the drugs.According to study co-author Dr. Ling Han of the Yale UniversityDepartment of Internal Medicine, elderly patients may be more vulnerableto these types of medications due to neurological and pharmacokineticalchanges related to aging."This study extends our previous findings on acute cognitive impairmentfollowing recent anticholinergic exposure in older medical inpatients,"says Han. "Prescribing for older adults who take multiple prescriptionand over-the-counter medications requires careful attention to minimizethe risk of potential harms of the drugs while maximizing their healthbenefits."
Monday, January 26, 2009
Saturday, January 24, 2009
Popular Songs Can Cure Specific Memories
ScienceDaily (Jan. 23, 2009) — Whether the soundtrack of your youth was doo-wop or disco, new wave or Nirvana, psychology research at Kansas State University shows that even just thinking about a particular song can evoke vivid memories of the past.
"We thought that actually hearing the song would bring back the most vivid memories," said Richard Harris, professor of psychology at K-State. "But in our study there wasn't a lot of difference in memory between those who heard the song and those who didn't. What we determined was happening is that you already know the song and you're hearing it in your mind."
Harris and Elizabeth Cady, a 2006 K-State doctoral graduate in psychology, recently published a study of music as a memory cue in the journal Psychology of Music. J. Bret Knappenberger, a 2004 K-State bachelor's graduate in psychology, also was co-author.
Harris said the study fit his other research on the intersection of media and memory. In another project, Harris explored why people like to quote movies. He said the project with Cady was one of the first times his research delved into the medium of music.
"Most people have this idea that music can be a powerful memory cue," Harris said. "You hear a song on the radio and it brings up memories of senior prom or graduation. That's why oldies stations are so popular -- not because the music is good but because it reminds us of specific times in our lives."
The researchers wanted to understand whether memories were cued by actually hearing the song or by thinking about it in other ways. They tested 124 subjects between the ages of 18-20 in spring 2003. A pilot study had the subjects list songs from five stages of life: early childhood, grade school, middle school, high school and college.
In the second part of the study, the subjects were given a short list of the songs that were chosen with the most frequency in the pilot study. The subjects were asked to pick one song from each category that had a strong memory attached to it, write about the memory and rate how vivid it was.
Harris said that he and Cady were surprised at how many participants reported strong memories associated with the same song. For the grade-school era, 26 percent of participants had strong memories associated with Vanilla Ice's song "Ice Ice Baby." For middle school, 36 percent reported strong memories associated with Coolio's "Gangsta's Paradise."
A control group was given only the names of the songs, while test groups either heard short clips of the songs, read the lyrics or saw art from the album or a photo of the artist. Harris said the vividness of memories didn't vary much from one group to another, leading the researchers to determine that the subjects we're "hearing" the song by being reminded of it in one way or another.
"Music is a very emotional stimulus," he said. "It's autobiographical in that we remember events from a long time ago with strong emotion. These pop songs were played many times, so there's a lot of repeat presentation."
Although many of the songs, like "Gangsta's Paradise," for instance, place the memories at a particular point in time, Harris said some of the responses reflected music that is popular during a certain stage of life -- the "Happy Birthday" song in childhood, for instance. Even though "Eye of the Tiger" was released in 1982, before the subjects were born, 24 percent reported that it provoked a strong memory of high school sporting events.
Harris said that music can be a powerful memory cue because it's multimodal. That is, it combines words and instrumentation, for which we generally use different sides of our brains. "Music is a rich stimulus," Harris said. "If we can't remember the words, we remember the music. I can remember advertising jingles from my childhood, but I don't remember the slogans without the music. Music may be something that our brains are primed to understand and enjoy in the same way we're primed to understand language, although language is much more fundamental."
"We thought that actually hearing the song would bring back the most vivid memories," said Richard Harris, professor of psychology at K-State. "But in our study there wasn't a lot of difference in memory between those who heard the song and those who didn't. What we determined was happening is that you already know the song and you're hearing it in your mind."
Harris and Elizabeth Cady, a 2006 K-State doctoral graduate in psychology, recently published a study of music as a memory cue in the journal Psychology of Music. J. Bret Knappenberger, a 2004 K-State bachelor's graduate in psychology, also was co-author.
Harris said the study fit his other research on the intersection of media and memory. In another project, Harris explored why people like to quote movies. He said the project with Cady was one of the first times his research delved into the medium of music.
"Most people have this idea that music can be a powerful memory cue," Harris said. "You hear a song on the radio and it brings up memories of senior prom or graduation. That's why oldies stations are so popular -- not because the music is good but because it reminds us of specific times in our lives."
The researchers wanted to understand whether memories were cued by actually hearing the song or by thinking about it in other ways. They tested 124 subjects between the ages of 18-20 in spring 2003. A pilot study had the subjects list songs from five stages of life: early childhood, grade school, middle school, high school and college.
In the second part of the study, the subjects were given a short list of the songs that were chosen with the most frequency in the pilot study. The subjects were asked to pick one song from each category that had a strong memory attached to it, write about the memory and rate how vivid it was.
Harris said that he and Cady were surprised at how many participants reported strong memories associated with the same song. For the grade-school era, 26 percent of participants had strong memories associated with Vanilla Ice's song "Ice Ice Baby." For middle school, 36 percent reported strong memories associated with Coolio's "Gangsta's Paradise."
A control group was given only the names of the songs, while test groups either heard short clips of the songs, read the lyrics or saw art from the album or a photo of the artist. Harris said the vividness of memories didn't vary much from one group to another, leading the researchers to determine that the subjects we're "hearing" the song by being reminded of it in one way or another.
"Music is a very emotional stimulus," he said. "It's autobiographical in that we remember events from a long time ago with strong emotion. These pop songs were played many times, so there's a lot of repeat presentation."
Although many of the songs, like "Gangsta's Paradise," for instance, place the memories at a particular point in time, Harris said some of the responses reflected music that is popular during a certain stage of life -- the "Happy Birthday" song in childhood, for instance. Even though "Eye of the Tiger" was released in 1982, before the subjects were born, 24 percent reported that it provoked a strong memory of high school sporting events.
Harris said that music can be a powerful memory cue because it's multimodal. That is, it combines words and instrumentation, for which we generally use different sides of our brains. "Music is a rich stimulus," Harris said. "If we can't remember the words, we remember the music. I can remember advertising jingles from my childhood, but I don't remember the slogans without the music. Music may be something that our brains are primed to understand and enjoy in the same way we're primed to understand language, although language is much more fundamental."
Monday, January 19, 2009
Switchboard InTthe Brain Helps Us Learn and Remember At The Same Time
ScienceDaily (Jan. 16, 2009) — The healthy brain is in a constant struggle between learning new experiences and remembering old experiences, a new study in this week's PLoS Biology reports. Virtually all social interactions require the rapid exchange of new and old information. For instance, normal conversation requires that while listening to the new information another person is providing, we are already retrieving information in preparation of an appropriate reply. Yet, some memory theories assume that these different modes of memory cannot happen at the same time and compete for priority within our brain.
Brain researchers now provide the first clear evidence supporting a competition between learning and remembering. Their findings also suggest that one brain region can resolve the conflict by improving the rapid switch between learning and remembering. The researchers included Willem Huijbers, Cyriel Pennartz, and Sander Daselaar of the Netherlands' University of Amsterdam, and Roberto Cabeza of Duke University.
The researchers used a novel memory task that forced learning and remembering to occur within a brief period of time. In the study, a group of adults in their 20's looked at a set of regular words presented in the middle of a screen. Participants rapidly tried to remember whether the words had previously been studied or not. Simultaneously, a set of colorful pictures were presented in the background. Meanwhile, the participants' brains were scanned with functional magnetic resonance imaging (fMRI). After brain scanning, participants were surprised with another memory test including the colorful background pictures instead of the words.
In support of a memory competition, the surprise test showed that learning the pictures is much more difficult when simultaneously remembering a word. At the same time, learning the pictures becomes easier when a word is forgotten.
The brain scans revealed that the brain areas involved in learning of the pictures were also less activated when words were simultaneously remembered. In other words, the process of remembering appears to suppress the brain regions involved in learning, the authors note.
The researchers also found one region in the left frontal part of the brain that was only active when both learning and remembering succeeded. Interestingly, activity in this region was specific to those participants that showed minimal suppression of learning activity. In other words, whether they simultaneously remembered a word or not, it did not influence their brain activity during the learning of the background pictures.
This frontal region could function as a switchboard in the brain, the researchers suggest. As learning and remembering cannot happen at the same time, this region might help us to rapidly switch the state of our brain between "learn" and "remember" modes.
It was already thought from patient studies that this frontal region is important for rapid switching between tasks and rules. Patients with damage to this area have problems in rapidly adapting to new situations and tend to persevere in old rules. The same region is also affected in older adults.
Future research should reveal the extent and practical implications of impairments in switching between learning and remembering in patients and older adults, and whether we can improve our switchboard through training.
Brain researchers now provide the first clear evidence supporting a competition between learning and remembering. Their findings also suggest that one brain region can resolve the conflict by improving the rapid switch between learning and remembering. The researchers included Willem Huijbers, Cyriel Pennartz, and Sander Daselaar of the Netherlands' University of Amsterdam, and Roberto Cabeza of Duke University.
The researchers used a novel memory task that forced learning and remembering to occur within a brief period of time. In the study, a group of adults in their 20's looked at a set of regular words presented in the middle of a screen. Participants rapidly tried to remember whether the words had previously been studied or not. Simultaneously, a set of colorful pictures were presented in the background. Meanwhile, the participants' brains were scanned with functional magnetic resonance imaging (fMRI). After brain scanning, participants were surprised with another memory test including the colorful background pictures instead of the words.
In support of a memory competition, the surprise test showed that learning the pictures is much more difficult when simultaneously remembering a word. At the same time, learning the pictures becomes easier when a word is forgotten.
The brain scans revealed that the brain areas involved in learning of the pictures were also less activated when words were simultaneously remembered. In other words, the process of remembering appears to suppress the brain regions involved in learning, the authors note.
The researchers also found one region in the left frontal part of the brain that was only active when both learning and remembering succeeded. Interestingly, activity in this region was specific to those participants that showed minimal suppression of learning activity. In other words, whether they simultaneously remembered a word or not, it did not influence their brain activity during the learning of the background pictures.
This frontal region could function as a switchboard in the brain, the researchers suggest. As learning and remembering cannot happen at the same time, this region might help us to rapidly switch the state of our brain between "learn" and "remember" modes.
It was already thought from patient studies that this frontal region is important for rapid switching between tasks and rules. Patients with damage to this area have problems in rapidly adapting to new situations and tend to persevere in old rules. The same region is also affected in older adults.
Future research should reveal the extent and practical implications of impairments in switching between learning and remembering in patients and older adults, and whether we can improve our switchboard through training.
Scientists Discover Gene Responsible for Brain's Aging
ScienceDaily (Jan. 18, 2009) — Will scientists one day be able to slow the aging of the brain and prevent diseases such as Alzheimer's and Parkinson's? Perhaps -- at least once the genetic coding associated with neuronal degeneration has been unraveled.
According to a new study published in The Journal of Neuroscience, a research team from the Université de Montréal, Maisonneuve-Rosemont Hospital and Lawrence Berkeley National Laboratory has taken a giant step in this direction by identifying a gene that controls the normal and pathological aging of neurons in the central nervous system: Bmi1.
The primary risk factor for diseases such as macular degeneration, Parkinson's and Alzheimer's is age. Although many researchers have sought to better understand the genetics and pathophysiology of these diseases, few studies have focused on the basic molecular mechanisms that control neuronal aging.
Dr. Gilbert Bernier, of the Université de Montréal and Maisonneuve-Rosemont Hospital, led a team that identified a mutation in mice that dramatically accelerates the process of aging in the brain and the eye. The new study reveals that neurons in the retina and cerebral cortex require a gene called Bmi1 to prevent activation of the p53 pathway and the accumulation of free radicals.
"Overall, we have now established that the Bmi1 gene is a direct regulator of cell aging in brain and retinal neurons of mammals through its action on the defense mechanisms against free radicals," says Dr. Bernier.
The article is the work of Dr. Gilbert Bernier in collaboration with Wassim Chatoo, Mohammed Abdouh, Jocelyn David, Marie-Pier Champagne, José Ferreira from the Université de Montréal and Maisonneuve-Rosemont Hospital with Francis Rodier from the Lawrence Berkeley National Laboratory, San Francisco, U.S.
Journal reference:
Chatoo et al. The Polycomb Group Gene Bmi1 Regulates Antioxidant Defenses in Neurons by Repressing p53 Pro-Oxidant Activity. Journal of Neuroscience, 2009; 29 (2): 529 DOI: 10.1523/JNEUROSCI.5303-08.2009
According to a new study published in The Journal of Neuroscience, a research team from the Université de Montréal, Maisonneuve-Rosemont Hospital and Lawrence Berkeley National Laboratory has taken a giant step in this direction by identifying a gene that controls the normal and pathological aging of neurons in the central nervous system: Bmi1.
The primary risk factor for diseases such as macular degeneration, Parkinson's and Alzheimer's is age. Although many researchers have sought to better understand the genetics and pathophysiology of these diseases, few studies have focused on the basic molecular mechanisms that control neuronal aging.
Dr. Gilbert Bernier, of the Université de Montréal and Maisonneuve-Rosemont Hospital, led a team that identified a mutation in mice that dramatically accelerates the process of aging in the brain and the eye. The new study reveals that neurons in the retina and cerebral cortex require a gene called Bmi1 to prevent activation of the p53 pathway and the accumulation of free radicals.
"Overall, we have now established that the Bmi1 gene is a direct regulator of cell aging in brain and retinal neurons of mammals through its action on the defense mechanisms against free radicals," says Dr. Bernier.
The article is the work of Dr. Gilbert Bernier in collaboration with Wassim Chatoo, Mohammed Abdouh, Jocelyn David, Marie-Pier Champagne, José Ferreira from the Université de Montréal and Maisonneuve-Rosemont Hospital with Francis Rodier from the Lawrence Berkeley National Laboratory, San Francisco, U.S.
Journal reference:
Chatoo et al. The Polycomb Group Gene Bmi1 Regulates Antioxidant Defenses in Neurons by Repressing p53 Pro-Oxidant Activity. Journal of Neuroscience, 2009; 29 (2): 529 DOI: 10.1523/JNEUROSCI.5303-08.2009
Sunday, January 18, 2009
Diabetes Associated With Different Type of Brain Injury In Patients With Dementia
ScienceDaily (Jan. 17, 2009) — Patients with dementia and diabetes appear to display a different pattern of injuries in their brains than patients with dementia but without diabetes, according to an article posted online today that will appear in the March print issue of Archives of Neurology, one of the JAMA/Archives journals.
"The association between diabetes mellitus and increased risk for dementia in the elderly is well documented," the authors write as background information in the article. Several possible mechanisms have been proposed for this association, including the direct effects of high blood glucose and insulin, the build-up of beta-amyloid plaques in the brain and the effects of diabetes-related vascular disease on blood vessels in the brain.
Joshua A. Sonnen, M.D., of the University of Washington, Seattle, and colleagues studied 196 individuals who were part of the Adult Changes in Thought Study, a community-based investigation of dementia. After the participants died, their brains were autopsied and their cases were divided into four groups based on clinical information: those with diabetes and dementia, those with diabetes but not dementia, those with dementia but not diabetes and those without either disease.
In the 125 patients without dementia, neuropathological and biochemical factors did not differ based on diabetes status. However, among the 71 with dementia, two patterns of injury emerged based on whether the patients had diabetes and received diabetes treatment. Those without diabetes had larger amounts of beta-amyloid buildup and greater free radical damage, whereas those with diabetes had more microvascular infarcts (microscopic injury to small blood vessels in the brain known as arterioles) and more inflammation in neural tissue. This pattern was related to diabetes treatment, in that patients with dementia receiving treatment for diabetes had more microvascular infarcts, and untreated diabetic patients with dementia had beta-amyloid build-up similar to non-diabetic patients with dementia.
"These novel characterizations of two apparently different patterns of injury in dementia depending on diabetes mellitus status may have important etiologic and therapeutic implications," the authors conclude.
This work was supported by grants from the National Institutes of Health; by the Nancy and Buster Alvord Endowment; and by the U.S. Department of Veterans Affairs.
"The association between diabetes mellitus and increased risk for dementia in the elderly is well documented," the authors write as background information in the article. Several possible mechanisms have been proposed for this association, including the direct effects of high blood glucose and insulin, the build-up of beta-amyloid plaques in the brain and the effects of diabetes-related vascular disease on blood vessels in the brain.
Joshua A. Sonnen, M.D., of the University of Washington, Seattle, and colleagues studied 196 individuals who were part of the Adult Changes in Thought Study, a community-based investigation of dementia. After the participants died, their brains were autopsied and their cases were divided into four groups based on clinical information: those with diabetes and dementia, those with diabetes but not dementia, those with dementia but not diabetes and those without either disease.
In the 125 patients without dementia, neuropathological and biochemical factors did not differ based on diabetes status. However, among the 71 with dementia, two patterns of injury emerged based on whether the patients had diabetes and received diabetes treatment. Those without diabetes had larger amounts of beta-amyloid buildup and greater free radical damage, whereas those with diabetes had more microvascular infarcts (microscopic injury to small blood vessels in the brain known as arterioles) and more inflammation in neural tissue. This pattern was related to diabetes treatment, in that patients with dementia receiving treatment for diabetes had more microvascular infarcts, and untreated diabetic patients with dementia had beta-amyloid build-up similar to non-diabetic patients with dementia.
"These novel characterizations of two apparently different patterns of injury in dementia depending on diabetes mellitus status may have important etiologic and therapeutic implications," the authors conclude.
This work was supported by grants from the National Institutes of Health; by the Nancy and Buster Alvord Endowment; and by the U.S. Department of Veterans Affairs.
Friday, January 16, 2009
MIdlife Coffee and Tea Drinking May Protect Against Late-life Dementia
ScienceDaily (Jan. 15, 2009) — Stockholm, Sweden -- Midlife coffee drinking can decrease the risk of dementia/Alzheimer's disease (AD) later in life. This conclusion is made in a Finnish Cardiovascular Risk Factors, Aging and Dementia (CAIDE) Study published in the Journal of Alzheimer's Disease.
This study has been conducted at the University of Kuopio, Finland in collaboration with Karolinska Institutet, Stockholm, Sweden, and the National Public Health Institute, Helsinki, Finland. The study included participants from the survivors of population-based cohorts previously surveyed within the North Karelia Project and the FINMONICA study in 1972, 1977, 1982 or 1987 (midlife visit). After an average follow-up of 21 years, 1409 individuals (71%) aged 65 to 79 completed the re-examination in 1998. A total of 61 cases were identified as demented (48 with AD).
"We aimed to study the association between coffee and tea consumption at midlife and dementia/AD risk in late-life, because the long-term impact of caffeine on the central nervous system was still unknown, and as the pathologic processes leading to Alzheimer's disease may start decades before the clinical manifestation of the disease," says lead researcher, associate professor Miia Kivipelto, from the University of Kuopio, Finland and Karolinska Institutet, Stockholm, Sweden.
At the midlife examination, the consumption of coffee and tea was assessed with a previously validated semi-quantitative food-frequency questionnaire. Coffee drinking was categorized into three groups: 0-2 cups (low), 3-5 cups (moderate) and >5 cups (high) per day. Further, the question concerning tea consumption was dichotomized into those not drinking tea (0 cup/day) vs. those drinking tea (≥1 cup/day).
The study found that coffee drinkers at midlife had lower risk for dementia and AD later in life compared to those drinking no or only little coffee. The lowest risk (65% decreased) was found among moderate coffee drinkers (drinking 3-5 cups of coffee/day). Adjustments for various confounders did not change the results. Tea drinking was relatively uncommon and was not associated with dementia/AD.
Kivipelto also notes that, "Given the large amount of coffee consumption globally, the results might have important implications for the prevention of or delaying the onset of dementia/AD. The finding needs to be confirmed by other studies, but it opens the possibility that dietary interventions could modify the risk of dementia/AD. Also, identification of mechanisms of how coffee exerts its protection against dementia/AD might help in the development of new therapies for these diseases."
This study has been conducted at the University of Kuopio, Finland in collaboration with Karolinska Institutet, Stockholm, Sweden, and the National Public Health Institute, Helsinki, Finland. The study included participants from the survivors of population-based cohorts previously surveyed within the North Karelia Project and the FINMONICA study in 1972, 1977, 1982 or 1987 (midlife visit). After an average follow-up of 21 years, 1409 individuals (71%) aged 65 to 79 completed the re-examination in 1998. A total of 61 cases were identified as demented (48 with AD).
"We aimed to study the association between coffee and tea consumption at midlife and dementia/AD risk in late-life, because the long-term impact of caffeine on the central nervous system was still unknown, and as the pathologic processes leading to Alzheimer's disease may start decades before the clinical manifestation of the disease," says lead researcher, associate professor Miia Kivipelto, from the University of Kuopio, Finland and Karolinska Institutet, Stockholm, Sweden.
At the midlife examination, the consumption of coffee and tea was assessed with a previously validated semi-quantitative food-frequency questionnaire. Coffee drinking was categorized into three groups: 0-2 cups (low), 3-5 cups (moderate) and >5 cups (high) per day. Further, the question concerning tea consumption was dichotomized into those not drinking tea (0 cup/day) vs. those drinking tea (≥1 cup/day).
The study found that coffee drinkers at midlife had lower risk for dementia and AD later in life compared to those drinking no or only little coffee. The lowest risk (65% decreased) was found among moderate coffee drinkers (drinking 3-5 cups of coffee/day). Adjustments for various confounders did not change the results. Tea drinking was relatively uncommon and was not associated with dementia/AD.
Kivipelto also notes that, "Given the large amount of coffee consumption globally, the results might have important implications for the prevention of or delaying the onset of dementia/AD. The finding needs to be confirmed by other studies, but it opens the possibility that dietary interventions could modify the risk of dementia/AD. Also, identification of mechanisms of how coffee exerts its protection against dementia/AD might help in the development of new therapies for these diseases."
Sunday, January 11, 2009
Protein That Protects Against Alzheimer's?
ScienceDaily (Jan. 10, 2009) — Research on the mechanisms involved in neurodegenerative diseases such as Alzheimer's, stroke, dementia, Parkinson's and multiple sclerosis, to name a few, has taken a step forward thanks to the work of biological sciences Ph.D. student Sonia Do Carmo, supervised by Professor Éric Rassart of the Université du Québec à Montreal (UQAM) Biological Sciences Department, in collaboration with researchers at the Armand-Frappier Institute and the University of Valladolid in Spain.
Do Carmo and her collaborators have successfully demonstrated the protective and reparative role of apolipoprotein D, or ApoD, in neurodegenerative diseases. Their discovery suggests interesting avenues for preventing and slowing the progression of this type of illness.
These studies were inspired by work done ten years ago by Professor Rassart's team, who then discovered increased levels of ApoD in the brains of people with several types of neurodegenerative disorders, including Alzheimer's.
The team hypothesized that this protein might play a protective and restorative role but were unable to demonstrate this at the time.
The experiments
To establish the protective and reparative role of ApoD, the researchers used two types of genetically modified mice: one type with increased levels of ApoD in the brain and a second type with no ApoD. The mice were then exposed to neurodegenerative agents. A group of the modified mice and a control group (unmodified) were exposed to paraquat, a widely used herbicide that has been shown to increase the risk of Parkinson's. Then the same type of experiment was performed by injecting two groups with a virus that causes encephalitis. In both cases, the mice modified for increased levels of ApoD had the best outcomes, with a better ability to combat the diseases and a higher survival rate than the unmodified mice. The knockout mice with no ApoD displayed the poorest outcomes.
These experiments serve to illustrate the protective and reparative role of this protein.
When can we expect medication?
A number of steps remain before this research can translate into effective drugs against neurodegenerative conditions.
The original investigator, Professor Éric Rassart, explains, “You cannot simply inject ApoD, as it has to enter the brain in order for it to be active. We have successfully demonstrated the role of ApoD, but now we need to understand the action of this protein. Only then will we be able to think about creating a drug to prevent these types of diseases and to slow their progression. All the same, this discovery by Sonia Do Carmo and her collaborators is a significant breakthrough, as we know very little about the mechanisms of neurodegenerative diseases.”
The discovery has aroused considerable interest among the molecular biology community. Two major scientific journals have already published the research findings: Aging Cell (Vol. 7: 506-515, 2008) and Journal of Neuroscience (Vol. 28: 10330-10338, 2008
Do Carmo and her collaborators have successfully demonstrated the protective and reparative role of apolipoprotein D, or ApoD, in neurodegenerative diseases. Their discovery suggests interesting avenues for preventing and slowing the progression of this type of illness.
These studies were inspired by work done ten years ago by Professor Rassart's team, who then discovered increased levels of ApoD in the brains of people with several types of neurodegenerative disorders, including Alzheimer's.
The team hypothesized that this protein might play a protective and restorative role but were unable to demonstrate this at the time.
The experiments
To establish the protective and reparative role of ApoD, the researchers used two types of genetically modified mice: one type with increased levels of ApoD in the brain and a second type with no ApoD. The mice were then exposed to neurodegenerative agents. A group of the modified mice and a control group (unmodified) were exposed to paraquat, a widely used herbicide that has been shown to increase the risk of Parkinson's. Then the same type of experiment was performed by injecting two groups with a virus that causes encephalitis. In both cases, the mice modified for increased levels of ApoD had the best outcomes, with a better ability to combat the diseases and a higher survival rate than the unmodified mice. The knockout mice with no ApoD displayed the poorest outcomes.
These experiments serve to illustrate the protective and reparative role of this protein.
When can we expect medication?
A number of steps remain before this research can translate into effective drugs against neurodegenerative conditions.
The original investigator, Professor Éric Rassart, explains, “You cannot simply inject ApoD, as it has to enter the brain in order for it to be active. We have successfully demonstrated the role of ApoD, but now we need to understand the action of this protein. Only then will we be able to think about creating a drug to prevent these types of diseases and to slow their progression. All the same, this discovery by Sonia Do Carmo and her collaborators is a significant breakthrough, as we know very little about the mechanisms of neurodegenerative diseases.”
The discovery has aroused considerable interest among the molecular biology community. Two major scientific journals have already published the research findings: Aging Cell (Vol. 7: 506-515, 2008) and Journal of Neuroscience (Vol. 28: 10330-10338, 2008
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