Saturday, February 28, 2009
Sides
Brian has always been wonderful to me. I didn’t know he had a temper when we were first married. He never showed it to me. He gets his temper from the Murphy side of the family. Must be the Irish in him. I first found out about his temper when he came home from work one day and ranted and raved about his day. He told me he wasn’t mad at me but at his job. This happened a few times and I finally told him that if he was mad at his job, get mad there, not at home. Again, he assured me he wasn’t mad at me. He rarely brought his temper home from work after that. Brian has rarely gotten mad at me during our marriage. Not that I didn’t deserve it but because when it comes to me, he is the sweetest person on earth. Alzheimer’s has a tendency to change people’s personalities early in the disease process. This hasn’t happened with Brian. If anything, he is even more sweeter! I have been having muscle problems and several times a day he comes over and gives me a neck and shoulder massage. Not a day goes by that he doesn’t tell me how great I am. Someone will come onto the TV and I will mention that she is pretty and Brian will agree, then say, “But not as pretty as you!” And then we laugh, and he says, “I still have it!”, meaning his ability to sweet talk me. Brian has lost his temper. I haven’t seen it for years now. Without the stress of working his temper has disappeared. Brian is usually in a good mood and even hums a lot. We laughingly recall an old friend, Drydee, who hummed all the time. Brian is the new Drydee. This is a side of Alzheimer’s that we do not mind.
Friday, February 20, 2009
New Hope
Hope
A study found that in a mouse model of Alzheimer’s, stimulating the innate immune system reduced the amyloid plaque in their brains and improved cognition. Alzheimer’s disease is characterized by the deposit of amyloid protein in the brain. Researchers think that clearing those deposits might prevent the cognitive effects of the disease. There appeared to be no toxic side effects. The animals were treated with DNA constructs called CpG oligodeoxynucleotides, a relatively new pharmacotherapeutic class currently being evaluated in cancer, viral infection, and asthma/allergy.
The constructs used in this study have already been shown to be safe in humans, suggesting that clinical trials in humans could occur relatively quickly. In cognitive tests at 17 months, the treated animals did significantly better than untreated mice at navigating a maze and were not significantly different from wild-type animals.
When the researchers examined the brains of the animals, they found the level of amyloid in the cortex of treated animals was 66% lower than in untreated mice.
For the first time, an experimental drug shows promise for halting the progression of Alzheimer’s disease by taking a new approach: breaking up the protein tangles that clog victims’ brains.
The encouraging results from the drug called Rember. The tangles are made of a protein called tau and develop inside nerve cells. Studies suggest that Rember can dissolve them.
For decades, scientists have focused on a different protein — beta-amyloid, which forms sticky clumps outside of the cells — but have yet to get a workable treatment.
The drug, Rember, is in the second of three stages of development, and scientists are paying special attention to potential treatments because of the enormity of the illness, which afflicts more than 26 million people worldwide and is mushrooming as the population ages.
In the study, 321 patients were given one of three doses of Rember or dummy capsules three times a day. The capsules containing the highest dose had a flaw in formulation that kept them from working, and the lowest dose was too weak to keep the disease from worsening.
However, the middle dose helped, as measured by a widely used score of mental performance.
“The people on placebo lost an average of 7 percent of their brain function over six months whereas those on treatment didn’t decline at all,” he said.
After about a year, the placebo group had continued to decline but those on the mid-level dose of Rember had not. At 19 months, the treated group still had not declined as Alzheimer’s patients have been known to do.
Two types of brain scans were available on about a third of participants, and they show the drug was active in brain areas most affected by tau tangles.
“The company is raising money now for another test of the drug to start this year.
The main chemical in Rember is available now in a different formulation in a prescription drug sometimes used since the 1930s for chronic bladder infections — methylene blue. However, it predates the federal Food and Drug Administration and was never fully studied for safety and effectiveness, and not in the form used in the Alzheimer’s study. Even if bigger, more rigorous studies show it works, Rember is still several years away from being available, and experts warned against overexuberance.
A study found that in a mouse model of Alzheimer’s, stimulating the innate immune system reduced the amyloid plaque in their brains and improved cognition. Alzheimer’s disease is characterized by the deposit of amyloid protein in the brain. Researchers think that clearing those deposits might prevent the cognitive effects of the disease. There appeared to be no toxic side effects. The animals were treated with DNA constructs called CpG oligodeoxynucleotides, a relatively new pharmacotherapeutic class currently being evaluated in cancer, viral infection, and asthma/allergy.
The constructs used in this study have already been shown to be safe in humans, suggesting that clinical trials in humans could occur relatively quickly. In cognitive tests at 17 months, the treated animals did significantly better than untreated mice at navigating a maze and were not significantly different from wild-type animals.
When the researchers examined the brains of the animals, they found the level of amyloid in the cortex of treated animals was 66% lower than in untreated mice.
For the first time, an experimental drug shows promise for halting the progression of Alzheimer’s disease by taking a new approach: breaking up the protein tangles that clog victims’ brains.
The encouraging results from the drug called Rember. The tangles are made of a protein called tau and develop inside nerve cells. Studies suggest that Rember can dissolve them.
For decades, scientists have focused on a different protein — beta-amyloid, which forms sticky clumps outside of the cells — but have yet to get a workable treatment.
The drug, Rember, is in the second of three stages of development, and scientists are paying special attention to potential treatments because of the enormity of the illness, which afflicts more than 26 million people worldwide and is mushrooming as the population ages.
In the study, 321 patients were given one of three doses of Rember or dummy capsules three times a day. The capsules containing the highest dose had a flaw in formulation that kept them from working, and the lowest dose was too weak to keep the disease from worsening.
However, the middle dose helped, as measured by a widely used score of mental performance.
“The people on placebo lost an average of 7 percent of their brain function over six months whereas those on treatment didn’t decline at all,” he said.
After about a year, the placebo group had continued to decline but those on the mid-level dose of Rember had not. At 19 months, the treated group still had not declined as Alzheimer’s patients have been known to do.
Two types of brain scans were available on about a third of participants, and they show the drug was active in brain areas most affected by tau tangles.
“The company is raising money now for another test of the drug to start this year.
The main chemical in Rember is available now in a different formulation in a prescription drug sometimes used since the 1930s for chronic bladder infections — methylene blue. However, it predates the federal Food and Drug Administration and was never fully studied for safety and effectiveness, and not in the form used in the Alzheimer’s study. Even if bigger, more rigorous studies show it works, Rember is still several years away from being available, and experts warned against overexuberance.
Friday, February 13, 2009
I have heart!
I saw my heart doctor last week as I have been having more trouble breathing and am retaining water. Retaining water means my heart isn’t pumping as well as we’d like. He had me get a chest xray and to go back on lasix ( a diuretic), for the water retention. Dr. Devendra said I was a class three/class four in symptom severity of pulmonary arterial hypertension. The classifications are:
Class I: Patients with pulmonary hypertension but without resulting limitation of physical activity. Ordinary physical activity does not cause undue dyspnea or fatigue, chest pain, or near syncope.
Class II: Patients with pulmonary hypertension resulting in slight limitation of physical activity. They are comfortable at rest. Ordinary physical activity causes undue dyspnea or fatigue, chest pain, or near syncope.
Class III: Patients with pulmonary hypertension resulting in marked limitation of physical activity. They are comfortable at rest. Less-than-ordinary physical activity causes undue dyspnea or fatigue, chest pain, or near syncope.
Class IV: Patients with pulmonary hypertension with inability to carry out any physical activity without symptoms. These patients manifest signs of right heart failure. Dyspnea and/or fatigue may even be present at rest. Discomfort is increased by any physical activity.
I agree. Just talking on the phone puts me out of breath, let alone walking to the phone. There aren’t many statistics regarding PAH and scleroderma. Unfortunately, what little that is known, shows that patients who have PAH with scleroderma have a much higher rate of death than those with PAH without connective tissue disease which has a mortality rate of about 2.5 years after diagnosis without treatment. I have a CAT scan scheduled for next month. If nothing new shows up on the xray, then my dose of Letaris will be changed from 5mg to 10mg next month. I have to see him again the end of March.
When on Letaris, the defining test to see if the drug is working is a six minute walk test. Because avascular necrosis has limited my walking ability, I can not do the walk test. Now, I am actually happy not to do the test since it seems like a 24 hour test rather than only 6 minutes. I will continue to have echocardiagrams to see if the hypertension goes up. It is not as definitive as a heart cath but is less evasive.
Heart failure often causes edema. A weak heart can't pump hard enough to keep up with this cycle. It receives more blood from your lungs than it can pump out into your body. The blood it can't handle backs up and seeps out of your blood vessels into other tissue, including your lungs. Cells get waterlogged. This causes swelling called edema. Edema usually - but not always - shows up first in your legs and ankles.
Why does it usually show up in your legs and ankles? Because good old gravity is pulling all that "loose" fluid straight down. Presto: your feet and ankles look like the Goodyear blimp.
PAH is a complication of systemic sclerosis and adversely affects survival.
The main disturbance resides in constriction of pulmonary arteries and thickening of the pulmonary arterial wall. As a consequence, the right ventricle that pumps blood into the lungs works against an abnormally high resistance. Initially, the right ventricle is able to compensate for the increased workload, but in time, it decompensates, and patients develop right heart failure.
Typically, patients with PAH have no complaints at rest. The main symptom is shortness of breath with activity. Shortness of breath develops initially with exercise, such as climbing up a few flights of stairs.
Later, patients feel limited during activities of daily living, such as bathing or dressing, and ultimately, they feel short of breath even getting out of bed. In advanced cases, chest pain, lightheadedness, or loss of consciousness may occur with exertion and leg swelling may become prominent especially at the end of the day. Lasix makes me pee A LOT and then drink a lot because of dry mouth (sjorgrens) and pee A LOT more.
Happy Note: With part of our rent paid, our landlord is not kicking us out! Even though it is raining, things aren’t as bleak as they may seem.
Class I: Patients with pulmonary hypertension but without resulting limitation of physical activity. Ordinary physical activity does not cause undue dyspnea or fatigue, chest pain, or near syncope.
Class II: Patients with pulmonary hypertension resulting in slight limitation of physical activity. They are comfortable at rest. Ordinary physical activity causes undue dyspnea or fatigue, chest pain, or near syncope.
Class III: Patients with pulmonary hypertension resulting in marked limitation of physical activity. They are comfortable at rest. Less-than-ordinary physical activity causes undue dyspnea or fatigue, chest pain, or near syncope.
Class IV: Patients with pulmonary hypertension with inability to carry out any physical activity without symptoms. These patients manifest signs of right heart failure. Dyspnea and/or fatigue may even be present at rest. Discomfort is increased by any physical activity.
I agree. Just talking on the phone puts me out of breath, let alone walking to the phone. There aren’t many statistics regarding PAH and scleroderma. Unfortunately, what little that is known, shows that patients who have PAH with scleroderma have a much higher rate of death than those with PAH without connective tissue disease which has a mortality rate of about 2.5 years after diagnosis without treatment. I have a CAT scan scheduled for next month. If nothing new shows up on the xray, then my dose of Letaris will be changed from 5mg to 10mg next month. I have to see him again the end of March.
When on Letaris, the defining test to see if the drug is working is a six minute walk test. Because avascular necrosis has limited my walking ability, I can not do the walk test. Now, I am actually happy not to do the test since it seems like a 24 hour test rather than only 6 minutes. I will continue to have echocardiagrams to see if the hypertension goes up. It is not as definitive as a heart cath but is less evasive.
Heart failure often causes edema. A weak heart can't pump hard enough to keep up with this cycle. It receives more blood from your lungs than it can pump out into your body. The blood it can't handle backs up and seeps out of your blood vessels into other tissue, including your lungs. Cells get waterlogged. This causes swelling called edema. Edema usually - but not always - shows up first in your legs and ankles.
Why does it usually show up in your legs and ankles? Because good old gravity is pulling all that "loose" fluid straight down. Presto: your feet and ankles look like the Goodyear blimp.
PAH is a complication of systemic sclerosis and adversely affects survival.
The main disturbance resides in constriction of pulmonary arteries and thickening of the pulmonary arterial wall. As a consequence, the right ventricle that pumps blood into the lungs works against an abnormally high resistance. Initially, the right ventricle is able to compensate for the increased workload, but in time, it decompensates, and patients develop right heart failure.
Typically, patients with PAH have no complaints at rest. The main symptom is shortness of breath with activity. Shortness of breath develops initially with exercise, such as climbing up a few flights of stairs.
Later, patients feel limited during activities of daily living, such as bathing or dressing, and ultimately, they feel short of breath even getting out of bed. In advanced cases, chest pain, lightheadedness, or loss of consciousness may occur with exertion and leg swelling may become prominent especially at the end of the day. Lasix makes me pee A LOT and then drink a lot because of dry mouth (sjorgrens) and pee A LOT more.
Happy Note: With part of our rent paid, our landlord is not kicking us out! Even though it is raining, things aren’t as bleak as they may seem.
Friday, February 6, 2009
Teachers
2009 has already started to be a very tough year. Everyone I talk to has been affected by the recession, either in job layoffs, cuts in benefits or salary, stock losses or other cuts. No one that I know has been exempt. Teachers and employees in the San Juan school district will all get pink slips this spring. A pink slip is a warning you may be out of a job in the fall. Though California public education may receive $15 billion over the next two years if the federal stimulus package passes, estimators put California’s educational shortfall at $9.7 billion over the next 18 months. With the recession and California’s financial crisis, districts don’t know what numbers they’ll be working with for next fall. In better financial years, most districts are able to bring back most of their pink-slipped workers before the fall session. This year, 2009 will be much different for most school districts across the nation. The unfortunate thing about this, I think, is that older teachers who have lost enthusiasm for teaching and may be mediocre teachers get to keep their jobs, while newer, fresher teachers who have enthusiasm and new ideas lose their jobs. It comes down to how many years you have done your job, not how well you do it. It is a shame we cannot kill two birds with one stone by keeping only the best teachers and improving the quality of education, and getting rid of the worst teachers while improving the bottom line.
Thursday, February 5, 2009
New Year, New Problems
The new year has started and so has my 2009 drug plan. Caring voices has given me a grant again for Letaris but all the paperwork, etc. still has to be completed. Meanwhile, since I am on Letaris, I cannot stop it until all the t’s are crossed and i’s are dotted. (I didn’t start the drug last year until all of this was done.) So I had to pay a portion of my co-payment now and will be reimbursed. I do not mind this, but it makes me short on our rent again, something our landlord has told us cannot happen again. We had problems with social security and getting our checks during a period last year and were late on our rent then. Even with letters from social security stating they were fixing the problem, our landlord was not understanding. He hasn’t been understanding about my need for a wheelchair and a wheelchair ramp to get onto the sidewalk to get to my apartment, even though our building is the only building without one. He has a $2000. deposit of ours that I hoped would help him understand our predicament now. But I think he would like to get rid of us because of the ADA concerns we may have in the future. It is such a shame because we love our place and Brian is very comfortable here. To move would be hard for him since familiarity is important to people with Alzheimer’s. We are neither one in good health to make a move and the packing that comes with it. It is so frustrating! We finally have our social security checks coming to us in a timely manner, and our finances stable. I don’t know how others with medical bills do it. We do have good health coverage with Kaiser and now can manage the day to day costs. By this time next year, when I will have to come up with part of the co-payment for letaris again for the new year, we should have a cushion saved up to cover it. But right now, we don’t. Any ideas or suggestions on how to cope with this would be appreciated.
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