"With Alzheimer's disease it is all about establishing patterns of behavior. Whether it is the pee pee war, poop war, or sleeping you have to get into a pattern. You have to establish a pattern of behavior that is conducive to accomplishing a mission...."
Every so often I receive an email asking for advice on the Alzheimer's patient and sleeping. Some dememtia sufferers get up frequently at night, and others stay up all night.
When I receive these emails, I am immediately concerned. There is a very high correlation between sleep deprivation and depression. In the case of the Alzheimer's caregiver, the combination of stress and not getting a good night's sleep can lead to depression. This helps explain, in part, why 40 percent of Alzheimer's caregivers suffer from depression.
In this most recent email, our reader explains that his mother is staying up all night. The first solution the doctor offered was to put his mother on antipsychotic drugs. Yikes. Fortunately, our reader has his eye on the ball and has learned that the combination of Alzheimer's and antipsychotic drugs in not only a bad idea -- its dangerous.
See...Antipsychotics, Aricept, and a Good Point Guard
I am not a doctor, and I don't pretend to be a doctor. The potential solution I am offering here is as a fellow Alzheimer's caregiver.
The first question I always ask is, is the Alzheimer's patient sleeping during the day. Usually the answer is Yes. Well, you can only sleep so much in any 24 hour day. If you get 3 or more hours of sleep during the day, it is likely that you won't sleep much at night or that you will wake up in the very early AM. In order to sleep 6 hours or more, through the night, this pattern needs to be changed.
With my mother the question I have learned to ask myself in every situation is -- what is the pattern? What is the pattern of behavior?
In the pee pee war, I finally realized I had to get my mother into the bathroom every two hours. I learned by simple observation that when my mother said those magic words -- I have to pee -- it was too late. She is older and she can't hold it in. Her pee pee muscle is weak. I'll interject here. I learned how to make my own pee pee muscle stronger through a couple of simple exercises.
Our reader explained that his mother does sleep during the day. Maybe most of the day. At night, when it is time to sleep, he puts his mother in bed and then turns on the TV. He know she is up and watching TV all night because he hears her talking to the television via the baby monitor he installed in her room.
Baby monitor, excellent idea. TV on, bad idea. Awake at night hearing mother talk and the TV on, very bad.
I don't watch television in the bedroom. I believe it is a bad idea. The bed is for sleeping. If you use the bed for sleeping you are establishing the correct pattern of behavior. If you use the bed to watch TV you are diluting the correct pattern of behavior. I will interject another tidbit here, I believe television in the bedroom is a bad idea if you are married. You can decide that one for yourself. Bed equals sleep.
After our reader told the doctor that he would not give his mother antipsychotic drugs, the doctor came up with another solution -- valium. So it now appears our reader will try the combination of Ambien and Valium. Double yikes.
First off, if Ambien doesn't work from the get go then it doesn't work. If it doesn't work, jettison the drug. Get rid of it. All drugs are designed to accomplish a mission. Sometimes they work very well for a person. Sometimes they don't work at all for a person. This is a simple fact of life. You are wasting your time, money, and maybe even hurting yourself when you try kicking a dead horse. A dead horse is not going to get up and starting running. Put the bubble up above your head. Imagine yourself kicking a dead horse. Let me know.
For some reason I will never fully understand, I wonder why doctors are addicted to writing prescriptions? You would think an experienced doctor would be asking the same questions I am asking here. What is the pattern of behavior?
Wouldn't it make more sense to first change the pattern of behavior before working your way through the PDR? The Physicians Desk Reference contains all the FDA approved drugs, a description of the drugs, and a picture of the drugs. Rather than trying all the drugs, how about this? Try reading the PDR when you get in bed. Sleep is on the horizon, trust me.
I am confident that changing the pattern of behavior is the best potential solution. Is if fool proof? Will it work every time? No. But I know that it can work because I suggested it to some readers and they told me it did work.
My advice is simple and straight forward. Start doing things during the day that engage the person suffering from Alzheimer's disease. Keep them up and moving to the degree possible. Involve them in normal every day activities like going to the store. If they have trouble walking try what I did, I get my mother to drive around in the motorized cart with me in Walmart while we shop.
Try and remember, what did the person suffering from Alzheimer's like to do before Alzheimer's? Puzzles, crossword puzzles, read the comics, art, music, going to the mall for no good reason? Try to engage them in these activities during the day.
Key word here day -- get them into some bright light. Sun is good. A well lit store is good.
Here are some simple activities. Take them to McDonald's for a cup of coffee. Ask for the senior discount. Take them for a ride in the car. Library anyone? Let them sit over near the kids section. This works wonderfully well. If they are not a wanderer, my mother isn't, this really works well on several levels.
If you want a person to sleep at night, you can't let them sleep all day. Alzheimer's or not, you sleep all day, you won't sleep at night. Simple observation.
With Alzheimer's disease it is all about establishing patterns of behavior. Whether it is the pee pee war, poop war, or sleeping you have to get into a pattern. You have to establish a pattern of behavior that is conducive to accomplishing a mission.
Whether it is pee pee, poop, or sleep in won't happen in a New York minute. You have to work on it. It takes time to establish a pattern of behavior. Here is the good news. Once you establish a good pattern of behavior it will stick if you keep reinforcing the pattern.
If you fall into a bad pattern of behavior guess what? It will persist. It will persist until you decide to change the pattern. To change a pattern of behavior to have to be committed to change. You have to be goal oriented. You have to be working toward that goal each day.
Or, you can keep kicking a dead horse.
By Bob DeMarco, Alzheimer's Reading Room
Friday, February 26, 2010
Wednesday, February 24, 2010
Predicting progression of Alzheimer’s disease
There is considerable variability in progression rates among Alzheimer’s disease (AD) patients. Patients and families frequently ask clinicians to prognosticate regarding expected rates of cognitive and functional decline, and clinicians have little basis for making such predictions.
We have shown that it is possible to reliably estimate early AD symptom onset, and together with baseline MMSE score, to calculate a rate of progression at the initial assessment (the preprogression rate).
The use of a rate to estimate early progression gives information on severity, but also on how long it took for the patient to reach the current severity level, which reflects that individual’s disease characteristics better than a severity score alone. However, it is not clear whether patients maintain a similar rate of decline throughout the course of their disease or change trajectories over time, due to endogenous or exogenous factors (such as treatment).
Demonstrating the predictive value of the calculated pre-progression rate would be valuable for patient and family counseling, as well as for providing a research marker of phenotypic variability to validate biological markers of progression. Further, the ability to model group progression of AD patients is essential for designing disease-modification studies of new AD treatments, and pre-progression might be an important baseline variable to take into account in the analysis of clinical trial data
The Baylor Alzheimer’s Disease and Memory Disorders Center has followed a cohort of AD patients for up to 15 years, with detailed clinical and neuropsychological data obtained at baseline and at annual follow up visits which are maintained in an ongoing electronic data base.
We used these data to answer the following questions: 1) does a pre-progression rate calculated at the initial assessment predict subsequent performance in specific cognitive and functional domains during follow up, and 2) is the pre-progression rate associated with overall survival, after adjustment for relevant covariates?
This research study was published in BioMed Central's open access journal. Go here to read Predicting progression of Alzheimer's disease.
Rachelle S Doody, Valory Pavlik, Paul Massman, Susan D Rountree, Eveleen Darby, Wenyaw Chan
We have shown that it is possible to reliably estimate early AD symptom onset, and together with baseline MMSE score, to calculate a rate of progression at the initial assessment (the preprogression rate).
The use of a rate to estimate early progression gives information on severity, but also on how long it took for the patient to reach the current severity level, which reflects that individual’s disease characteristics better than a severity score alone. However, it is not clear whether patients maintain a similar rate of decline throughout the course of their disease or change trajectories over time, due to endogenous or exogenous factors (such as treatment).
Demonstrating the predictive value of the calculated pre-progression rate would be valuable for patient and family counseling, as well as for providing a research marker of phenotypic variability to validate biological markers of progression. Further, the ability to model group progression of AD patients is essential for designing disease-modification studies of new AD treatments, and pre-progression might be an important baseline variable to take into account in the analysis of clinical trial data
The Baylor Alzheimer’s Disease and Memory Disorders Center has followed a cohort of AD patients for up to 15 years, with detailed clinical and neuropsychological data obtained at baseline and at annual follow up visits which are maintained in an ongoing electronic data base.
We used these data to answer the following questions: 1) does a pre-progression rate calculated at the initial assessment predict subsequent performance in specific cognitive and functional domains during follow up, and 2) is the pre-progression rate associated with overall survival, after adjustment for relevant covariates?
This research study was published in BioMed Central's open access journal. Go here to read Predicting progression of Alzheimer's disease.
Rachelle S Doody, Valory Pavlik, Paul Massman, Susan D Rountree, Eveleen Darby, Wenyaw Chan
Friday, February 19, 2010
Exercise associated with preventing, improving Mild Cognitive Impairment
Moderate physical activity performed in midlife or later appears to be associated with a reduced risk of mild cognitive impairment, whereas a six-month high-intensity aerobic exercise program may improve cognitive function in individuals who already have the condition, according to two reports in the January issue of Archives of Neurology, one of the JAMA/Archives journals. Mild cognitive impairment is an intermediate state between the normal thinking, learning and memory changes that occur with age and dementia, according to background information in one of the articles. Each year, 10 percent to 15 percent of individuals with mild cognitive impairment will develop dementia, as compared with 1 percent to 2 percent of the general population. Previous studies in animals and humans have suggested that exercise may improve cognitive function.
In one article, Laura D. Baker, Ph.D., of the University of Washington School of Medicine and Veterans Affairs Puget Sound Health Care System, Seattle, and colleagues report the results of a randomized, controlled clinical trial involving 33 adults with mild cognitive impairment (17 women, average age 70). A group of 23 were randomly assigned to an aerobic exercise group and exercised at high intensity levels under the supervision of a trainer for 45 to 60 minutes per day, four days per week. The control group of 10 individuals performed supervised stretching exercises according to the same schedule but kept their heart rate low. Fitness testing, body fat analysis, blood tests of metabolic markers and cognitive functions were assessed before, during and after the six-month trial.
A total of 29 participants completed the study. Overall, the patients in the high-intensity aerobic exercise group experienced improved cognitive function compared with those in the control group. These effects were more pronounced in women than in men, despite similar increases in fitness. The sex differences may be related to the metabolic effects of exercise, as changes to the body's use and production of insulin, glucose and the stress hormone cortisol differed in men and women.
"Aerobic exercise is a cost-effective practice that is associated with numerous physical benefits. The results of this study suggest that exercise also provides a cognitive benefit for some adults with mild cognitive impairment," the authors conclude. "Six months of a behavioral intervention involving regular intervals of increased heart rate was sufficient to improve cognitive performance for an at-risk group without the cost and adverse effects associated with most pharmaceutical therapies."
In another report, Yonas E. Geda, M.D., M.Sc., and colleagues at Mayo Clinic, Rochester, Minn., studied 1,324 individuals without dementia who were part of the Mayo Clinic Study of Aging. Participants completed a physical exercise questionnaire between 2006 and 2008. They were then assessed by an expert consensus panel, who classified each as having normal cognition or mild cognitive impairment.
A total of 198 participants (median or midpoint age, 83 years) were determined to have mild cognitive impairment and 1,126 (median age 80) had normal cognition. Those who reported performing moderate exercise—such as brisk walking, aerobics, yoga, strength training or swimming—during midlife or late life were less likely to have mild cognitive impairment. Midlife moderate exercise was associated with 39 percent reduction in the odds of developing the condition, and moderate exercise in late life was associated with a 32 percent reduction. The findings were consistent among men and women.
Light exercise (such as bowling, slow dancing or golfing with a cart) or vigorous exercise (including jogging, skiing and racquetball) were not independently associated with reduced risk for mild cognitive impairment.
Physical exercise may protect against mild cognitive impairment via the production of nerve-protecting compounds, greater blood flow to the brain, improved development and survival of neurons and the decreased risk of heart and blood vessel diseases, the authors note. "A second possibility is that physical exercise may be a marker for a healthy lifestyle," they write. "A subject who engages in regular physical exercise may also show the same type of discipline in dietary habits, accident prevention, adherence to preventive intervention, compliance with medical care and similar health-promoting behaviors."
Future study is needed to confirm whether exercise is associated with the decreased risk of mild cognitive impairment and provide additional information on cause and effect relationships, they conclude.
By e! Science News
Source: JAMA and Archives Journals
In one article, Laura D. Baker, Ph.D., of the University of Washington School of Medicine and Veterans Affairs Puget Sound Health Care System, Seattle, and colleagues report the results of a randomized, controlled clinical trial involving 33 adults with mild cognitive impairment (17 women, average age 70). A group of 23 were randomly assigned to an aerobic exercise group and exercised at high intensity levels under the supervision of a trainer for 45 to 60 minutes per day, four days per week. The control group of 10 individuals performed supervised stretching exercises according to the same schedule but kept their heart rate low. Fitness testing, body fat analysis, blood tests of metabolic markers and cognitive functions were assessed before, during and after the six-month trial.
A total of 29 participants completed the study. Overall, the patients in the high-intensity aerobic exercise group experienced improved cognitive function compared with those in the control group. These effects were more pronounced in women than in men, despite similar increases in fitness. The sex differences may be related to the metabolic effects of exercise, as changes to the body's use and production of insulin, glucose and the stress hormone cortisol differed in men and women.
"Aerobic exercise is a cost-effective practice that is associated with numerous physical benefits. The results of this study suggest that exercise also provides a cognitive benefit for some adults with mild cognitive impairment," the authors conclude. "Six months of a behavioral intervention involving regular intervals of increased heart rate was sufficient to improve cognitive performance for an at-risk group without the cost and adverse effects associated with most pharmaceutical therapies."
In another report, Yonas E. Geda, M.D., M.Sc., and colleagues at Mayo Clinic, Rochester, Minn., studied 1,324 individuals without dementia who were part of the Mayo Clinic Study of Aging. Participants completed a physical exercise questionnaire between 2006 and 2008. They were then assessed by an expert consensus panel, who classified each as having normal cognition or mild cognitive impairment.
A total of 198 participants (median or midpoint age, 83 years) were determined to have mild cognitive impairment and 1,126 (median age 80) had normal cognition. Those who reported performing moderate exercise—such as brisk walking, aerobics, yoga, strength training or swimming—during midlife or late life were less likely to have mild cognitive impairment. Midlife moderate exercise was associated with 39 percent reduction in the odds of developing the condition, and moderate exercise in late life was associated with a 32 percent reduction. The findings were consistent among men and women.
Light exercise (such as bowling, slow dancing or golfing with a cart) or vigorous exercise (including jogging, skiing and racquetball) were not independently associated with reduced risk for mild cognitive impairment.
Physical exercise may protect against mild cognitive impairment via the production of nerve-protecting compounds, greater blood flow to the brain, improved development and survival of neurons and the decreased risk of heart and blood vessel diseases, the authors note. "A second possibility is that physical exercise may be a marker for a healthy lifestyle," they write. "A subject who engages in regular physical exercise may also show the same type of discipline in dietary habits, accident prevention, adherence to preventive intervention, compliance with medical care and similar health-promoting behaviors."
Future study is needed to confirm whether exercise is associated with the decreased risk of mild cognitive impairment and provide additional information on cause and effect relationships, they conclude.
By e! Science News
Source: JAMA and Archives Journals
Creative Expression: Is It the Key to Self-Actualization for an Alzheimer's Patient?
The quote above is one of the best I read in a long time. It is from an article in the Vancouver Sun by Dalia Gottlieb-Tanaka, a professor at the Centre for Population Health Promotion Research at the University of British Columbia.
Canada is facing the reality that by 2025 one out of four senior citizens over 80 will be living with dementia.
The author says,
“Those of us who carry their memories need to make every effort to include them in our world the way they are.” In other words, we need to meet the patient at their level and not expect the patient to match our preconceived notions.
The author cautions that, in addition to providing medical and physical care we need to provide “meaningful activities” and these “can be found in Creative Expression Programs that give people with dementia the opportunity for self-actualization.”
Again and again, caregivers, medical personnel, and researchers are finding that creative activities like puzzles, art, and music are the path to improving the lives of those with Alzheimer’s.
In the Vancouver Sun article, Gottlieb-Tanaka also discusses the phenomenon of Alzheimer’s patients always wanting to “go home.” She explains that a longing for going home may be a longing for what is familiar, important, and loved by the patient. It may tell us that the patient is feeling lonely or isolated.
I was particularly interested in the following two paragraphs, since they so clearly explain what Bob DeMarco is accomplishing when he “lends his mom his brain.”
“We become the vessel that carries vanishing memories of their past life, occupation, hobbies, achievements. We can then turn around and communicate this information in the present. Specific memories such as remembering dates and details of events are irrelevant, as long as the person with dementia recalls a familiar feeling, thought or wish; they may even adopt memories of somebody else sitting next to them.”
“As long as we engage them in a conversation based even on a few words that may be accompanied by facial expressions and body gestures, we are communicating. As long as we engage them in singing, dancing, reminiscing, storytelling, painting, gardening, caring for animals, or even writing poems, we have brightened their day. As long as we accept their present abilities, we dignify, acknowledge and validate their existence.”
The author tells us that according to Dr. Bruce Miller, a neurologist, some dementia patients may even develop new skills such as painting or composing music.
I was thinking that this is similar to a blind person having a heightened sense of hearing. That part of the brain that is still working becomes stronger from exercise. Not only does the Alzheimer’s patient have the portion of their brain that deals with creativity get affected last in their disease, but there is even a possibility of increasing the abilities of the remaining brain functions.
The author mentions that various programs in Canada that are working to include creative expression in the care of dementia patients. One is the Society for the Arts in Dementia Care. They came up with a “Creative-Expression Abilities tool”, to assess the effects of creative activities on dementia patients. The B.C. Medical Services Foundation is conducting a survey on the facial expressions of dementia patients when they are engaged in creativity.
The more I read articles like this one, the more pleased I am to be distributing puzzles for Alzheimer's patients though my non-profit charitable organization Puzzles to Remember.
How wonderful that I might even be able to help develop new abilities in these patients and not just help save previous abilities.
To read the article referenced go here.
By Max Wallack
Monday, February 8, 2010
Exercise Associated With Preventing, Improving Mild Cognitive Impairment
Moderate physical activity performed in midlife or later appears to be associated with a reduced risk of mild cognitive impairment, whereas a six-month high-intensity aerobic exercise program may improve cognitive function in individuals who already have the condition, according to two reports in the January issue of Archives of Neurology, one of the JAMA/Archives journals.
Mild cognitive impairment is an intermediate state between the normal thinking, learning and memory changes that occur with age and dementia, according to background information in one of the articles. Each year, 10 percent to 15 percent of individuals with mild cognitive impairment will develop dementia, as compared with 1 percent to 2 percent of the general population. Previous studies in animals and humans have suggested that exercise may improve cognitive function.
In one article, Laura D. Baker, Ph.D., of the University of Washington School of Medicine and Veterans Affairs Puget Sound Health Care System, Seattle, and colleagues report the results of a randomized, controlled clinical trial involving 33 adults with mild cognitive impairment (17 women, average age 70). A group of 23 were randomly assigned to an aerobic exercise group and exercised at high intensity levels under the supervision of a trainer for 45 to 60 minutes per day, four days per week. The control group of 10 individuals performed supervised stretching exercises according to the same schedule but kept their heart rate low. Fitness testing, body fat analysis, blood tests of metabolic markers and cognitive functions were assessed before, during and after the six-month trial.
A total of 29 participants completed the study. Overall, the patients in the high-intensity aerobic exercise group experienced improved cognitive function compared with those in the control group. These effects were more pronounced in women than in men, despite similar increases in fitness. The sex differences may be related to the metabolic effects of exercise, as changes to the body's use and production of insulin, glucose and the stress hormone cortisol differed in men and women.
"Aerobic exercise is a cost-effective practice that is associated with numerous physical benefits. The results of this study suggest that exercise also provides a cognitive benefit for some adults with mild cognitive impairment," the authors conclude. "Six months of a behavioral intervention involving regular intervals of increased heart rate was sufficient to improve cognitive performance for an at-risk group without the cost and adverse effects associated with most pharmaceutical therapies."
In another report, Yonas E. Geda, M.D., M.Sc., and colleagues at Mayo Clinic, Rochester, Minn., studied 1,324 individuals without dementia who were part of the Mayo Clinic Study of Aging. Participants completed a physical exercise questionnaire between 2006 and 2008. They were then assessed by an expert consensus panel, who classified each as having normal cognition or mild cognitive impairment.
A total of 198 participants (median or midpoint age, 83 years) were determined to have mild cognitive impairment and 1,126 (median age 80) had normal cognition. Those who reported performing moderate exercise -- such as brisk walking, aerobics, yoga, strength training or swimming -- during midlife or late life were less likely to have mild cognitive impairment. Midlife moderate exercise was associated with 39 percent reduction in the odds of developing the condition, and moderate exercise in late life was associated with a 32 percent reduction. The findings were consistent among men and women.
Light exercise (such as bowling, slow dancing or golfing with a cart) or vigorous exercise (including jogging, skiing and racquetball) were not independently associated with reduced risk for mild cognitive impairment.
Physical exercise may protect against mild cognitive impairment via the production of nerve-protecting compounds, greater blood flow to the brain, improved development and survival of neurons and the decreased risk of heart and blood vessel diseases, the authors note. "A second possibility is that physical exercise may be a marker for a healthy lifestyle," they write. "A subject who engages in regular physical exercise may also show the same type of discipline in dietary habits, accident prevention, adherence to preventive intervention, compliance with medical care and similar health-promoting behaviors."
Future study is needed to confirm whether exercise is associated with the decreased risk of mild cognitive impairment and provide additional information on cause and effect relationships, they conclude.
By ScienceDaily, Adapted from materials provided by JAMA and Archives Journals.
Mild cognitive impairment is an intermediate state between the normal thinking, learning and memory changes that occur with age and dementia, according to background information in one of the articles. Each year, 10 percent to 15 percent of individuals with mild cognitive impairment will develop dementia, as compared with 1 percent to 2 percent of the general population. Previous studies in animals and humans have suggested that exercise may improve cognitive function.
In one article, Laura D. Baker, Ph.D., of the University of Washington School of Medicine and Veterans Affairs Puget Sound Health Care System, Seattle, and colleagues report the results of a randomized, controlled clinical trial involving 33 adults with mild cognitive impairment (17 women, average age 70). A group of 23 were randomly assigned to an aerobic exercise group and exercised at high intensity levels under the supervision of a trainer for 45 to 60 minutes per day, four days per week. The control group of 10 individuals performed supervised stretching exercises according to the same schedule but kept their heart rate low. Fitness testing, body fat analysis, blood tests of metabolic markers and cognitive functions were assessed before, during and after the six-month trial.
A total of 29 participants completed the study. Overall, the patients in the high-intensity aerobic exercise group experienced improved cognitive function compared with those in the control group. These effects were more pronounced in women than in men, despite similar increases in fitness. The sex differences may be related to the metabolic effects of exercise, as changes to the body's use and production of insulin, glucose and the stress hormone cortisol differed in men and women.
"Aerobic exercise is a cost-effective practice that is associated with numerous physical benefits. The results of this study suggest that exercise also provides a cognitive benefit for some adults with mild cognitive impairment," the authors conclude. "Six months of a behavioral intervention involving regular intervals of increased heart rate was sufficient to improve cognitive performance for an at-risk group without the cost and adverse effects associated with most pharmaceutical therapies."
In another report, Yonas E. Geda, M.D., M.Sc., and colleagues at Mayo Clinic, Rochester, Minn., studied 1,324 individuals without dementia who were part of the Mayo Clinic Study of Aging. Participants completed a physical exercise questionnaire between 2006 and 2008. They were then assessed by an expert consensus panel, who classified each as having normal cognition or mild cognitive impairment.
A total of 198 participants (median or midpoint age, 83 years) were determined to have mild cognitive impairment and 1,126 (median age 80) had normal cognition. Those who reported performing moderate exercise -- such as brisk walking, aerobics, yoga, strength training or swimming -- during midlife or late life were less likely to have mild cognitive impairment. Midlife moderate exercise was associated with 39 percent reduction in the odds of developing the condition, and moderate exercise in late life was associated with a 32 percent reduction. The findings were consistent among men and women.
Light exercise (such as bowling, slow dancing or golfing with a cart) or vigorous exercise (including jogging, skiing and racquetball) were not independently associated with reduced risk for mild cognitive impairment.
Physical exercise may protect against mild cognitive impairment via the production of nerve-protecting compounds, greater blood flow to the brain, improved development and survival of neurons and the decreased risk of heart and blood vessel diseases, the authors note. "A second possibility is that physical exercise may be a marker for a healthy lifestyle," they write. "A subject who engages in regular physical exercise may also show the same type of discipline in dietary habits, accident prevention, adherence to preventive intervention, compliance with medical care and similar health-promoting behaviors."
Future study is needed to confirm whether exercise is associated with the decreased risk of mild cognitive impairment and provide additional information on cause and effect relationships, they conclude.
By ScienceDaily, Adapted from materials provided by JAMA and Archives Journals.
Psoriasis Linked to Vascular Disease
Patients with psoriasis are at increased risk for atherosclerosis and accompanying vascular diseases, researchers found.
Among predominantly male patients at a Veterans Affairs medical center, the skin disease was associated with a greater likelihood of ischemic heart disease, cerebrovascular disease, and peripheral arterial disease, as well as death, according to Robert Kirsner, M.D., Ph.D., of the University of Miami, and colleagues.
"This result is not surprising, given the systemic nature of atherosclerosis," the researchers wrote in the June issue of Archives of Dermatology.
They said the findings have "tremendous and far-reaching clinical implications, as all of these vascular conditions represent a major financial cost to the healthcare system, as well as a major cause of disability and death."
Because psoriasis has recently been shown to be a systemic inflammatory condition, researchers are interested in looking at its connection to cardiovascular risk factors and myocardial infarction, Dr. Kirsner and colleagues said.
To explore the issue, they identified 3,236 patients with psoriasis and 2,500 control patients without the condition who were treated at the Miami VA Medical Center.
The patients with psoriasis were slightly older (67.9 versus 65.1) and more likely to male (95.5% versus 88.2%, P<0.01 for both).
As expected, they were also more likely to be smokers and to have diabetes, hypertension, and dyslipidemia (P<0.01 for all).
After adjusting for these differences, patients with psoriasis were more likely to be diagnosed with the following conditions:
•Atherosclerosis (OR 2.18, 95% CI 1.59 to 3.01)
•Ischemic heart disease (OR 1.78, 95% CI 1.51 to 2.11)
•Cerebrovascular disease (OR 1.70, 95% CI 1.33 to 2.17)
•Peripheral arterial disease (OR 1.98, 95% CI 1.32 to 2.82)
Psoriasis was also independently predictive of death (OR 1.86, 95% CI 1.56 to 2.21).
Future studies are needed to determine whether aggressive treatment of psoriasis or traditional cardiovascular risk factors will improve the total atherosclerotic burden associated with the skin condition, the researchers said.
"In the meantime, we recommend that healthcare providers who are caring for patients with psoriasis be vigilant with respect to traditional risk factor screening," they said.
In addition, they continued, "it would be prudent for dermatologists to be familiar with suggested screening for cardiovascular risk factors and recommendations for aspirin use. If not, it is imperative that they work in collaboration with a primary care provider or another internal medicine specialist, who also needs to be aware of our findings."
They acknowledged some limitations of the study, including the possibility of inaccurate coding of diagnoses and the inability to assess temporal relationships between psoriasis and vascular disease because of the cross-sectional design.
By Todd Neale, Staff Writer, MedPage Today
Primary source: Archives of Dermatology
Among predominantly male patients at a Veterans Affairs medical center, the skin disease was associated with a greater likelihood of ischemic heart disease, cerebrovascular disease, and peripheral arterial disease, as well as death, according to Robert Kirsner, M.D., Ph.D., of the University of Miami, and colleagues.
"This result is not surprising, given the systemic nature of atherosclerosis," the researchers wrote in the June issue of Archives of Dermatology.
They said the findings have "tremendous and far-reaching clinical implications, as all of these vascular conditions represent a major financial cost to the healthcare system, as well as a major cause of disability and death."
Because psoriasis has recently been shown to be a systemic inflammatory condition, researchers are interested in looking at its connection to cardiovascular risk factors and myocardial infarction, Dr. Kirsner and colleagues said.
To explore the issue, they identified 3,236 patients with psoriasis and 2,500 control patients without the condition who were treated at the Miami VA Medical Center.
The patients with psoriasis were slightly older (67.9 versus 65.1) and more likely to male (95.5% versus 88.2%, P<0.01 for both).
As expected, they were also more likely to be smokers and to have diabetes, hypertension, and dyslipidemia (P<0.01 for all).
After adjusting for these differences, patients with psoriasis were more likely to be diagnosed with the following conditions:
•Atherosclerosis (OR 2.18, 95% CI 1.59 to 3.01)
•Ischemic heart disease (OR 1.78, 95% CI 1.51 to 2.11)
•Cerebrovascular disease (OR 1.70, 95% CI 1.33 to 2.17)
•Peripheral arterial disease (OR 1.98, 95% CI 1.32 to 2.82)
Psoriasis was also independently predictive of death (OR 1.86, 95% CI 1.56 to 2.21).
Future studies are needed to determine whether aggressive treatment of psoriasis or traditional cardiovascular risk factors will improve the total atherosclerotic burden associated with the skin condition, the researchers said.
"In the meantime, we recommend that healthcare providers who are caring for patients with psoriasis be vigilant with respect to traditional risk factor screening," they said.
In addition, they continued, "it would be prudent for dermatologists to be familiar with suggested screening for cardiovascular risk factors and recommendations for aspirin use. If not, it is imperative that they work in collaboration with a primary care provider or another internal medicine specialist, who also needs to be aware of our findings."
They acknowledged some limitations of the study, including the possibility of inaccurate coding of diagnoses and the inability to assess temporal relationships between psoriasis and vascular disease because of the cross-sectional design.
By Todd Neale, Staff Writer, MedPage Today
Primary source: Archives of Dermatology
Huntington's Disease: Discovery Of Mechanism In Brain Cell Injury Offers New Treatment Approaches
Scientists at the Brain Research Centre and Centre for Molecular Medicine and Therapeutics have uncovered a key cellular mechanism that alters brain cell function in Huntington's disease, and identified a possible treatment for the disease.
The results of the study were published online today and will appear in the January 28 edition of the journal Neuron.
Huntington's disease is an inherited degenerative brain disease that causes cognitive and motor impairment, and eventually death. One in 10,000 Canadians suffers from Huntington's disease.
The researchers found that, in mouse models, the genetic mutation that causes Huntington's disease results in an excessive number of NMDA receptors - special receptors found at the surface of brain cells - to accumulate and be active outside synapses, which are the connections between brain cells. In healthy conditions, there should be few NMDA receptors outside the synapse.
The researchers also found that the over-activation of the NMDA receptors outside the synapse leads to a reduction in brain cell survival signals and disruption in brain function.
"Previous work in cell cultures showed that NMDA receptors located within the synapse can have beneficial effects on brain cells, whereas NMDA receptors outside the synapse, called 'extra-synaptic NMDA receptors,' have a detrimental effect," says Dr. Lynn Raymond, a professor in the UBC Department of Psychiatry, a member of the Brain Research Centre at UBC Hospital, and co-director of the Huntington's Disease Medical Clinic.
"Our study shows an increase in the number of extrasynaptic NMDA receptors, shifting the balance between these opposing cellular mechanisms in animal models of early stages of Huntington's disease," Raymond says.
While further work still needs to be done to determine how the genetic mutation causes the excessive number and activity of NMDA receptors to localize outside the synapses, the researchers did find a way to mitigate damage and slow disease progression at early stages of the disease - using Memantine, a drug currently used to treat Alzheimer's disease.
"Memantine in low dose works by preferentially blocking the activity of NMDA receptors outside the synapse," says Dr. Michael Hayden, director of the Centre for Molecular Medicine and Therapeutics, professor in the UBC Department of Medical Genetics, and co-author on the study.
"It was previously shown to reverse deficits and damage in late stages of animal models of Huntington's disease, but we found it could improve learning and cell survival signaling even at early stages of the disease," says Hayden. "A small human clinical trial of Memantine for Huntington's disease has also recently shown positive effects. Larger, international clinical trials are now being planned."
"Memantine's beneficial effects appear to be dose-specific," Raymond adds. "Before it can be prescribed to treat Huntington's disease, we need to know how to determine appropriate dosing and whether it interferes with other essential cellular and brain functions."
This study was funded by the Canadian Institutes of Health Research, Cure Huntington Disease Initiative, Michael Smith Foundation for Health Research, Heart & Stroke Foundation of BC & Yukon, Huntington's Disease Society of America, and the Huntington Society of Canada.
Source: Melissa Ashman
University of British Columbia
The results of the study were published online today and will appear in the January 28 edition of the journal Neuron.
Huntington's disease is an inherited degenerative brain disease that causes cognitive and motor impairment, and eventually death. One in 10,000 Canadians suffers from Huntington's disease.
The researchers found that, in mouse models, the genetic mutation that causes Huntington's disease results in an excessive number of NMDA receptors - special receptors found at the surface of brain cells - to accumulate and be active outside synapses, which are the connections between brain cells. In healthy conditions, there should be few NMDA receptors outside the synapse.
The researchers also found that the over-activation of the NMDA receptors outside the synapse leads to a reduction in brain cell survival signals and disruption in brain function.
"Previous work in cell cultures showed that NMDA receptors located within the synapse can have beneficial effects on brain cells, whereas NMDA receptors outside the synapse, called 'extra-synaptic NMDA receptors,' have a detrimental effect," says Dr. Lynn Raymond, a professor in the UBC Department of Psychiatry, a member of the Brain Research Centre at UBC Hospital, and co-director of the Huntington's Disease Medical Clinic.
"Our study shows an increase in the number of extrasynaptic NMDA receptors, shifting the balance between these opposing cellular mechanisms in animal models of early stages of Huntington's disease," Raymond says.
While further work still needs to be done to determine how the genetic mutation causes the excessive number and activity of NMDA receptors to localize outside the synapses, the researchers did find a way to mitigate damage and slow disease progression at early stages of the disease - using Memantine, a drug currently used to treat Alzheimer's disease.
"Memantine in low dose works by preferentially blocking the activity of NMDA receptors outside the synapse," says Dr. Michael Hayden, director of the Centre for Molecular Medicine and Therapeutics, professor in the UBC Department of Medical Genetics, and co-author on the study.
"It was previously shown to reverse deficits and damage in late stages of animal models of Huntington's disease, but we found it could improve learning and cell survival signaling even at early stages of the disease," says Hayden. "A small human clinical trial of Memantine for Huntington's disease has also recently shown positive effects. Larger, international clinical trials are now being planned."
"Memantine's beneficial effects appear to be dose-specific," Raymond adds. "Before it can be prescribed to treat Huntington's disease, we need to know how to determine appropriate dosing and whether it interferes with other essential cellular and brain functions."
This study was funded by the Canadian Institutes of Health Research, Cure Huntington Disease Initiative, Michael Smith Foundation for Health Research, Heart & Stroke Foundation of BC & Yukon, Huntington's Disease Society of America, and the Huntington Society of Canada.
Source: Melissa Ashman
University of British Columbia
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