Children and teens who took antipsychotic medicines in a study gained weight and developed increased blood-fat levels, possibly harming their future health, researchers in New York State said.
The subjects, taking the antipsychotic drugs for the first time, gained from 9.7 to 18.7 pounds (4.4 to 8.5 kilograms) after about 11 weeks of treatment, depending on which medicine they were given, the scientists said today in the Journal of the American Medical Association. Fifteen patients who didn’t stick with drugs or who declined to participate in the research gained less than half a pound on average.
The study was the largest to show how antipsychotic medicines affect the bodies of children taking the drugs for the first time, the researchers wrote. Many past studies of the drugs involved patients who had also used other treatments -- methodology that may have masked the extent of weight gain, according to an editorial published with the study.
“We were able to show all of these agents can cause quite a bit of body weight changes and body composition changes that are not beneficial to the health,” said Christoph Correll, the study’s lead author, in a telephone interview on Oct. 23.
“What we need to figure out is what are the long-term consequences in the lives of children,” Correll, who is a medical director at Zucker Hillside Hospital in New York City’s Queens borough and an associate professor of psychiatry at Yeshiva University’s Albert Einstein College of Medicine in the Bronx.
Metabolic Syndrome
Gaining weight and changes in blood sugars and fats can be precursors to metabolic syndrome, a group of risk factors linked to heart disease and diabetes, according to the research article. Weight gain, obesity and increases in cholesterol in children are linked to their adult risk of cardiovascular problems and cancer.
Patients in the study had been diagnosed with mood disorders, schizophrenia and disruptive or aggressive behavior. Their doctors had prescribed Abilify, made by New York-based Bristol-Myers Squibb Co.; Zyprexa, made by Indianapolis-based Eli Lilly & Co.; Seroquel, made by London-based AstraZeneca Plc, or Risperdal made by New Brunswick, New Jersey-based Johnson & Johnson.
Risperdal and Abilify are the only two antipsychotics approved for pediatric use. A panel of outside advisers to the U.S. Food and Drug Administration recommended in June that Seroquel, Zyprexa and New York-based Pfizer Inc.’s Geodon be cleared for pediatric use.
Impact in Children
The medicines, so-called atypical antipsychotics, were introduced for adults in the mid-1990s and marketed as having fewer neurological side effects than older drugs. The FDA has grappled with pediatric use for years because of concerns that weight gain, sleepiness and movement disorders reported as side effects in adults may be more pronounced in children.
U.S. sales of antipsychotic drugs reached $14.6 billion last year, the most for any class of medicines, according to IMS Health Inc. in Norwalk, Connecticut. Use of antipsychotic medicines by people younger than 20 years old has more than doubled since 2001, according to data compiled by Medco Health Solutions Inc. of Franklin Lakes, New Jersey.
The study reported today was conducted to determine if weight gain and other changes to the body were related to the start of a psychiatric illness or hospital admission, or to the medicines.
Prescribed for Behavior
Researchers at Zucker Hillside, and at the Feinstein Institute for Medical Research in Manhasset, New York, studied 272 people ages 4 to 19 who were prescribed the antipsychotic medicines for behavioral, mood or psychosis-related problems. The patients were followed for the first 12 weeks.
At about 11 weeks, those taking Zyprexa gained 18.7 pounds on average, compared with 13.4 for Seroquel, 11.7 for Risperdal and 9.7 for Abilify, the study showed.
“The extent and the rate of weight gain is remarkable,” said Christopher Varley, a professor in the psychiatry and behavioral sciences department at the University of Washington in Seattle, in a telephone interview on Oct. 23. “Realistically the kids were exposed to 11 or 12 weeks of medication. Some of them gained over 20 pounds.” Varley co-wrote the editorial in the journal that was published with the study.
Ten percent to 36 percent of the patients in the study became overweight or obese within 11 weeks of starting the medicine, the researchers said.
Cholesterol Increases
Those on Zyprexa had larger increases in cholesterol and blood sugars, according to the study. Those on Risperdal had rises in their levels of triglyceride, a type of fat found in the blood, without affecting their blood sugar, the researchers wrote. Those on Seroquel also had an increase in total cholesterol and triglycerides, and patients on Abilify didn’t have any significant worsening in their blood fats or blood sugars, according to the scientists.
Correll recommended that parents monitor their children’s weight and make sure the kids are eating healthy food and exercising.
Doctors in some cases should consider counseling and behavior therapy, as well as parental training, before prescribing the drugs, Correll said. Once the medicines are given to children and adolescents, doctors need to frequently monitor the weight gain and the patients’ blood sugars and blood fats, he said.
In the editorial accompanying the study, Varley wrote, “Given the risk for weight gain and long-term risk for cardiovascular and metabolic problems, the widespread and increasing use of atypical antipsychotic medications in children and adolescents should be reconsidered.”
The study was funded partly by the U.S. National Institutes of Health, based in Bethesda, Maryland.
Showing posts with label Mind and brain. Show all posts
Showing posts with label Mind and brain. Show all posts
Wednesday, October 28, 2009
Wednesday, August 26, 2009
UPDATE 1-Dainippon schizophrenia drug meets trial goals
apan's Dainippon Sumitomo Pharma Co Ltd (4506.T) said its experimental schizophrenia drug, lurasidone, was significantly better than placebo in a pivotal late-stage clinical trial, according to data released on Wednesday.
The company said it plans to submit its application seeking U.S. approval to sell the medicine early next year.
Dainippon Sumitomo will decide by autumn whether it will market the new drug, if approved, via its own sales network or a co-promotion deal with another firm or if it will acquire a U.S. company, a spokesman for the mid-sized drugmaker said.
Patients with acute schizophrenia in the 478-subject, six-week, Phase III trial received either 40 milligrams or 120 milligrams of lurasidone daily or a placebo.
Both doses of the drug proved to be statistically significantly better than placebo in the primary goal of the study, which was 30 percent or better improvement in the Positive and Negative Syndrome Scale, the company said.
Fifty-three percent of patients who received 40 mg of lurasidone and 47 percent of those on the 120 mg dose achieved the primary goal compared with 38 percent on placebo.
Both doses of lurasidone were also significantly more effective than placebo on a secondary measure used to test antipsychotic drugs called the Clinical Global Impressions Severity scale, the company said.
In previous trials, lurasidone was also tested at 80 mg and Dainippon Sumitomo said it would submit all three doses for FDA approval.
Lurasidone belongs to a class of drugs known as atypical antipsychotics and works by blocking serotonin receptors in the brain. If approved, it would join an already crowded field of such treatments.
"We're still searching for the right drug for many of these patients. There's no one size fits all," Dr Herbert Meltzer, one of the study's lead investigators and professor of psychiatry at Vanderbilt University School of Medicine, said in a telephone interview.
Patients in the trial had been diagnosed with schizophrenia on average for more than 13 years and most had been previously hospitalized prior to entering the study.
"If you look at the weight gain, the lipid changes, it's among the most benign of any antipsychotic drugs, clearly better than olanzapine, clozapine and Seroquel," Meltzer said.
Olanzapine is the chemical name for Eli Lilly and Co's (LLY.N) widely-used Zyprexa; clozapine in sold by Novartis AG (NOVN.VX) under the brand name Clozaril; and Seroquel is sold by AstraZeneca Plc (AZN.L).
Zyprexa and similar drugs can cause significant weight gain and have been linked to increased risk of diabetes.
But "this class of drugs as a whole is so superior to the first generation drugs," said Meltzer, who plans to present the data from the lurasidone trial at a major medical meeting in December.
Lurasidone was well tolerated with a discontinuation rate nearly identical to placebo -- 40 percent versus 39 percent -- and the adverse events were generally mild, such as restlessness and sleepiness.
"From the point of view of efficacy and side effect profile, once a day administration, the fact that the lower dose works as well as the higher dose, I think this is going to have a very good chance of major acceptance among my colleagues," Meltzer added. (Additional reporting by Yumiko Nishitani in Tokyo; Editing by Andre Grenon and Edwina Gibbs)
The company said it plans to submit its application seeking U.S. approval to sell the medicine early next year.
Dainippon Sumitomo will decide by autumn whether it will market the new drug, if approved, via its own sales network or a co-promotion deal with another firm or if it will acquire a U.S. company, a spokesman for the mid-sized drugmaker said.
Patients with acute schizophrenia in the 478-subject, six-week, Phase III trial received either 40 milligrams or 120 milligrams of lurasidone daily or a placebo.
Both doses of the drug proved to be statistically significantly better than placebo in the primary goal of the study, which was 30 percent or better improvement in the Positive and Negative Syndrome Scale, the company said.
Fifty-three percent of patients who received 40 mg of lurasidone and 47 percent of those on the 120 mg dose achieved the primary goal compared with 38 percent on placebo.
Both doses of lurasidone were also significantly more effective than placebo on a secondary measure used to test antipsychotic drugs called the Clinical Global Impressions Severity scale, the company said.
In previous trials, lurasidone was also tested at 80 mg and Dainippon Sumitomo said it would submit all three doses for FDA approval.
Lurasidone belongs to a class of drugs known as atypical antipsychotics and works by blocking serotonin receptors in the brain. If approved, it would join an already crowded field of such treatments.
"We're still searching for the right drug for many of these patients. There's no one size fits all," Dr Herbert Meltzer, one of the study's lead investigators and professor of psychiatry at Vanderbilt University School of Medicine, said in a telephone interview.
Patients in the trial had been diagnosed with schizophrenia on average for more than 13 years and most had been previously hospitalized prior to entering the study.
"If you look at the weight gain, the lipid changes, it's among the most benign of any antipsychotic drugs, clearly better than olanzapine, clozapine and Seroquel," Meltzer said.
Olanzapine is the chemical name for Eli Lilly and Co's (LLY.N) widely-used Zyprexa; clozapine in sold by Novartis AG (NOVN.VX) under the brand name Clozaril; and Seroquel is sold by AstraZeneca Plc (AZN.L).
Zyprexa and similar drugs can cause significant weight gain and have been linked to increased risk of diabetes.
But "this class of drugs as a whole is so superior to the first generation drugs," said Meltzer, who plans to present the data from the lurasidone trial at a major medical meeting in December.
Lurasidone was well tolerated with a discontinuation rate nearly identical to placebo -- 40 percent versus 39 percent -- and the adverse events were generally mild, such as restlessness and sleepiness.
"From the point of view of efficacy and side effect profile, once a day administration, the fact that the lower dose works as well as the higher dose, I think this is going to have a very good chance of major acceptance among my colleagues," Meltzer added. (Additional reporting by Yumiko Nishitani in Tokyo; Editing by Andre Grenon and Edwina Gibbs)
Tuesday, August 25, 2009
Foreclosures Make for Subprime Mental Health
t's official: The economy is bad for your health.
Researchers at the University of Pennsylvania School of Medicine questioned 250 homeowners going through foreclosure in Philadelphia and found that 47 percent showed symptoms of depression, with 37 percent exhibiting signs of major depression. The rate was especially high considering previous research showed that only about 12.8 percent of people living in poverty were depressed, the study found.
"Although the health status of homeowners has traditionally tended to be better than that of renters, the financial and emotional stress of foreclosure may undermine the potential benefits of homeownership," said the study, which will appear in the October edition of the American Journal of Public Health.
The researchers found deep attachment to homes. "There is a sense of hope when people buy their homes," said Craig Evan Pollack, an internist who recently completed a fellowship at Penn's medical school and is now an associate scientist at Rand Corp. "The difference between those dreams and hopes and [the] reality that people are finding themselves in may be part of the stress that people are feeling, and a sense of sadness as well."
Borrowers facing foreclosure were more likely to forgo filling prescriptions, and nearly 60 percent reported that they had skipped or delayed meals, according to the study. "We've barely begun to think about the health consequences of the foreclosure crisis," Pollack said.
And it's likely to get worse. Nearly 2 million homeowners are expected to lose their homes to foreclosure this year, according to some economists.
"It's surprising to me that the rates of depression aren't even higher," said John Taylor, president of the National Community Reinvestment Coalition, a nonprofit group. "All aspects of their life are just disrupted. They lose their center."
Researchers at the University of Pennsylvania School of Medicine questioned 250 homeowners going through foreclosure in Philadelphia and found that 47 percent showed symptoms of depression, with 37 percent exhibiting signs of major depression. The rate was especially high considering previous research showed that only about 12.8 percent of people living in poverty were depressed, the study found.
"Although the health status of homeowners has traditionally tended to be better than that of renters, the financial and emotional stress of foreclosure may undermine the potential benefits of homeownership," said the study, which will appear in the October edition of the American Journal of Public Health.
The researchers found deep attachment to homes. "There is a sense of hope when people buy their homes," said Craig Evan Pollack, an internist who recently completed a fellowship at Penn's medical school and is now an associate scientist at Rand Corp. "The difference between those dreams and hopes and [the] reality that people are finding themselves in may be part of the stress that people are feeling, and a sense of sadness as well."
Borrowers facing foreclosure were more likely to forgo filling prescriptions, and nearly 60 percent reported that they had skipped or delayed meals, according to the study. "We've barely begun to think about the health consequences of the foreclosure crisis," Pollack said.
And it's likely to get worse. Nearly 2 million homeowners are expected to lose their homes to foreclosure this year, according to some economists.
"It's surprising to me that the rates of depression aren't even higher," said John Taylor, president of the National Community Reinvestment Coalition, a nonprofit group. "All aspects of their life are just disrupted. They lose their center."
Friday, August 14, 2009
6 hours of sleep? It's not enough
Scientists have good and bad news for hard-driving people who boast they need only six hours of sleep a night.
The good news is a few may be right: Researchers at the University of California-San Francisco have identified a family with a genetic mutation that causes members to require only six hours sleep a night. The bad news? The gene is vanishingly rare in humans, found in less than 3% of people.
So almost everyone who says he needs only six hours' sleep is kidding himself. And the consequences of chronic sleep deprivation are serious, says Clete Kushida, president of the American Academy of Sleep Medicine and director of Stanford University's Sleep Medicine Center. Sleep deprivation has been linked to an increase in motor vehicle accidents, deficiencies in short-term memory, focus and attention. It's also tied to depressed mood and a decrease in the ability to control appetite.
The family members — a mother and daughter with the gene mutation — were discovered by researchers at UCSF studying circadian rhythms, the waxing and waning biochemical cycles that govern sleep, hunger and activity. Neither woman needed more than six to 6½ hours of sleep a night, and yet both were well-rested, healthy and energetic.
"One of them is over 70, always traveling internationally and extremely active. She dances three or four nights a week," says Ying-Hui Fu, a professor of neurology at UCSF.
When scientists examined the pair's DNA, they found a mutation in a gene called DEC2, which governs cell production and circadian rhythm.
The mutation seems to result in people who need much less than the normal eight to 8½ hours that most humans require for well-rested functioning, according to the paper, which is published in today's edition of the journal Science. The research by Fu and her colleagues determined that humans and mice that carry the mutation get more intense sleep, as measured by slow-wave electrical activity in the brain, and so they need less of it.
But Fu estimates that only about 3% of the population is likely to have this gene and cautions that most people who habitually get less than eight hours sleep a night are only building up a large, and dangerous, sleep debt.
Fu says her lab is investigating whether it might be possible to mimic the effects of the gene with therapeutic compounds, but she cautions the research is only at the very beginning. For now, the only real answer to true productivity is to sleep as much as your body needs, she says.
The good news is a few may be right: Researchers at the University of California-San Francisco have identified a family with a genetic mutation that causes members to require only six hours sleep a night. The bad news? The gene is vanishingly rare in humans, found in less than 3% of people.
So almost everyone who says he needs only six hours' sleep is kidding himself. And the consequences of chronic sleep deprivation are serious, says Clete Kushida, president of the American Academy of Sleep Medicine and director of Stanford University's Sleep Medicine Center. Sleep deprivation has been linked to an increase in motor vehicle accidents, deficiencies in short-term memory, focus and attention. It's also tied to depressed mood and a decrease in the ability to control appetite.
The family members — a mother and daughter with the gene mutation — were discovered by researchers at UCSF studying circadian rhythms, the waxing and waning biochemical cycles that govern sleep, hunger and activity. Neither woman needed more than six to 6½ hours of sleep a night, and yet both were well-rested, healthy and energetic.
"One of them is over 70, always traveling internationally and extremely active. She dances three or four nights a week," says Ying-Hui Fu, a professor of neurology at UCSF.
When scientists examined the pair's DNA, they found a mutation in a gene called DEC2, which governs cell production and circadian rhythm.
The mutation seems to result in people who need much less than the normal eight to 8½ hours that most humans require for well-rested functioning, according to the paper, which is published in today's edition of the journal Science. The research by Fu and her colleagues determined that humans and mice that carry the mutation get more intense sleep, as measured by slow-wave electrical activity in the brain, and so they need less of it.
But Fu estimates that only about 3% of the population is likely to have this gene and cautions that most people who habitually get less than eight hours sleep a night are only building up a large, and dangerous, sleep debt.
Fu says her lab is investigating whether it might be possible to mimic the effects of the gene with therapeutic compounds, but she cautions the research is only at the very beginning. For now, the only real answer to true productivity is to sleep as much as your body needs, she says.
Thursday, August 6, 2009
Alzheimer's: Where Art Thou?
Placing some sort of GPS tracking device on patients has proven incredibly useful for knowing the whereabouts of patients who are likely to go missing, escape, or wander off and not receive the care they require for their condition. The Alzheimer’s Association reports that in 2009:
* As many as 5.3 million people in the United States are living with Alzheimer’s.
* Alzheimer's and dementia triple healthcare costs for Americans age 65 and older.
* Every 70 seconds, someone develops Alzheimer’s.
* Alzheimer's is the seventh-leading cause of death.
* The direct and indirect costs of Alzheimer's and other dementias to Medicare, Medicaid and businesses amount to more than $148 billion each year.
There are many GPS devices marketed to both care givers and medical professionals. A higher degree of sophistication has led to more thoughtful ergonomic designs and a wider range of tracking and reporting capabilities. Both RFID and GPS have provided solutions, with GPS having a definite advantage in its ability to locate without regard to specialized receivers found in RFID systems.
Current emphasis on designs are for bracelet and belt devices, special placement in clothing, and newly introduced GPS-equipped shoes. The challenge for this disease is securing the device to be nonobtrusive and affixed to a patient without his or her ability to remove it. Digital Angel was an early pioneer in this space, with the more recent Columbia medical bracelet becoming available in the U.S. The Columba is monitored via Assisted GPS and has a GSM/GPRS transmitter/receiver with a SIM card for voice and data.
* As many as 5.3 million people in the United States are living with Alzheimer’s.
* Alzheimer's and dementia triple healthcare costs for Americans age 65 and older.
* Every 70 seconds, someone develops Alzheimer’s.
* Alzheimer's is the seventh-leading cause of death.
* The direct and indirect costs of Alzheimer's and other dementias to Medicare, Medicaid and businesses amount to more than $148 billion each year.
There are many GPS devices marketed to both care givers and medical professionals. A higher degree of sophistication has led to more thoughtful ergonomic designs and a wider range of tracking and reporting capabilities. Both RFID and GPS have provided solutions, with GPS having a definite advantage in its ability to locate without regard to specialized receivers found in RFID systems.
Current emphasis on designs are for bracelet and belt devices, special placement in clothing, and newly introduced GPS-equipped shoes. The challenge for this disease is securing the device to be nonobtrusive and affixed to a patient without his or her ability to remove it. Digital Angel was an early pioneer in this space, with the more recent Columbia medical bracelet becoming available in the U.S. The Columba is monitored via Assisted GPS and has a GSM/GPRS transmitter/receiver with a SIM card for voice and data.
Saturday, July 18, 2009
Weight gain during menopause tied to brain changes
Healthy women who put on weight between the premenopausal and postmenopausal years risk losing nerve cells in the brain, research suggests.
Gaining weight is a "highly modifiable" risk factor that may be targeted to prevent or slow the progression of potentially harmful age-related changes in the brain, the University of Pittsburgh-based study team suggests in the June issue of Psychosomatic Medicine.
Dr. Isabella Soreca and colleagues analyzed brain imaging data obtained from 48 healthy older women who were tracked over a 20-year period as part of the longitudinal epidemiological Pittsburgh Healthy Women Study.
They report in the journal Psychosomatic Medicine that an increase in body weight during the transition to menopause and beyond was "uniquely associated" with a lower volume of gray matter (the portion of the brain containing nerve cell bodies).
Soreca and colleagues say this finding is "particularly noteworthy" given that these were healthy older women who entered menopause naturally and had no history of cardiovascular disease or psychiatric disease and none were obese in mid-life or later on.
"Women may be particularly motivated to maintain a healthy weight in the postmenopausal years, should it be confirmed that weight gain causes alteration in brain function that is important to quality of life," Soreca and colleagues conclude.
Gaining weight is a "highly modifiable" risk factor that may be targeted to prevent or slow the progression of potentially harmful age-related changes in the brain, the University of Pittsburgh-based study team suggests in the June issue of Psychosomatic Medicine.
Dr. Isabella Soreca and colleagues analyzed brain imaging data obtained from 48 healthy older women who were tracked over a 20-year period as part of the longitudinal epidemiological Pittsburgh Healthy Women Study.
They report in the journal Psychosomatic Medicine that an increase in body weight during the transition to menopause and beyond was "uniquely associated" with a lower volume of gray matter (the portion of the brain containing nerve cell bodies).
Soreca and colleagues say this finding is "particularly noteworthy" given that these were healthy older women who entered menopause naturally and had no history of cardiovascular disease or psychiatric disease and none were obese in mid-life or later on.
"Women may be particularly motivated to maintain a healthy weight in the postmenopausal years, should it be confirmed that weight gain causes alteration in brain function that is important to quality of life," Soreca and colleagues conclude.
Wednesday, July 15, 2009
Promising Alzheimer's drug boosts toxic protein
Dimebon, Medivation Inc's (MDVN.O) promising experimental Alzheimer's drug, significantly raised levels of a toxic protein in the brains of mice, yet has been shown to delay thinking problems in human dementia patients, U.S. researchers said on Wednesday.
"This is an unexpected result," said Dr. Samuel Gandy, a researcher at Mount Sinai School of Medicine in New York, whose findings were presented at an Alzheimer's meeting in Vienna.
The study raises new questions about how the drug works and new worries about drugs meant to remove telltale clumps of a protein called beta amyloid from the brain as a way to reverse Alzheimer's disease.
Researchers are not sure whether amyloid is a cause or a symptom of Alzheimer's but, either way, getting rid of it had appeared to be a good thing.
"We think we want amyloid levels to go down," Gandy said in a telephone interview. "Here is this compound that is looking very promising clinically that is making amyloid levels go up."
Dimebon, first sold in Russia as an antihistamine, is being developed jointly with Pfizer Inc (PFE.N), maker of the Alzheimer's drug Aricept.
Researchers see Dimebon as the best hope for a new treatment for the incurable, mind-robbing disease that affects 26 million people globally.
Now in late-stage testing, Dimebon seems to delay thinking problems in people but it is not clear how.
"We wanted to know what Dimebon was doing to amyloid," Gandy said.
His team tested mice genetically engineered to have a human form of Alzheimer's. The drug increased amyloid outside nerve cells.
"This is an unexpected result," said Dr. Samuel Gandy, a researcher at Mount Sinai School of Medicine in New York, whose findings were presented at an Alzheimer's meeting in Vienna.
The study raises new questions about how the drug works and new worries about drugs meant to remove telltale clumps of a protein called beta amyloid from the brain as a way to reverse Alzheimer's disease.
Researchers are not sure whether amyloid is a cause or a symptom of Alzheimer's but, either way, getting rid of it had appeared to be a good thing.
"We think we want amyloid levels to go down," Gandy said in a telephone interview. "Here is this compound that is looking very promising clinically that is making amyloid levels go up."
Dimebon, first sold in Russia as an antihistamine, is being developed jointly with Pfizer Inc (PFE.N), maker of the Alzheimer's drug Aricept.
Researchers see Dimebon as the best hope for a new treatment for the incurable, mind-robbing disease that affects 26 million people globally.
Now in late-stage testing, Dimebon seems to delay thinking problems in people but it is not clear how.
"We wanted to know what Dimebon was doing to amyloid," Gandy said.
His team tested mice genetically engineered to have a human form of Alzheimer's. The drug increased amyloid outside nerve cells.
Monday, July 13, 2009
New Alzheimer's Disease Treatment Promising
Researchers at Mount Sinai School of Medicine have found that a compound called NIC5-15, might be a safe and effective treatment to stabilize cognitive performance in patients with mild to moderate Alzheimer's disease. The two investigators, Giulio Maria Pasinetti, M.D., Ph.D. , and Hillel Grossman, M.D., presented Phase IIA preliminary clinical findings at the Alzheimer's Association 2009 International Conference on Alzheimer's Disease (ICAD) in Vienna on July 12.
NIC5-15's potential to preserve cognitive performance will be further evaluated in a Phase IIB clinical trial. Early evidence suggests that NIC5-15 is a safe and tolerable natural compound that may reduce the progression of Alzheimer's disease-related dementia by preventing the formation of beta-amyloid plaque, a waxy substance that accumulates between brain cells and impacts cognitive function
"With Alzheimer's disease affecting 5.2 million Americans, another 5 million with early-state disease, and nearly a half million new cases reported annually, treatments like NIC5-15 would make a significant difference in the lives of many Alzheimer's patients," said Dr. Pasinetti, Professor of Psychiatry, Professor of Neuroscience and Professor of Geriatrics and Adult Development, in the Department of Psychiatry at Mount Sinai School of Medicine. "We are hopeful that the follow up clinical study will support this preliminary evidence."
"There are no FDA-approved Alzheimer's disease modifying drugs available today," said Dr. Hillel Grossman, Assistant Professor of Psychiatry, Co-Director of the Clinical Research Core of the Alzheimer's Disease Research Center, and Clinical Director of the Mount Sinai Memory and Aging Center. "Current drugs approved for use help maintain cognitive function, but only for a limited time. NIC5-15 is part of a new class of natural compound we found to have the potential of precluding the generation of β-amyloid and, eventually, attenuating cognitive deterioration in preclinical models of Alzheimer's disease."
The study was conducted at the Mount Sinai Alzheimer's Disease Research Center (ADRC). ADCR is a comprehensive research facility and clinical program dedicated to the study and treatment of both normal aging and Alzheimer's disease. The Center is supported by the National Institute on Aging, a branch of the National Institutes of Health. Humanetics Corporation, manufacturers of NIC5-15, sponsored the study. Phase IIB clinical trials on NIC5-15 are expected to begin later this year.
Disclosure: Dr. Pasinetti has a patent pending for the use of NIC5-15 in the treatment of Alzheimer's disease. The patent application was filed on his behalf by the Mount Sinai School of Medicine. Dr. Pasinetti and the School of Medicine could benefit financially from the results of this trial.
NIC5-15's potential to preserve cognitive performance will be further evaluated in a Phase IIB clinical trial. Early evidence suggests that NIC5-15 is a safe and tolerable natural compound that may reduce the progression of Alzheimer's disease-related dementia by preventing the formation of beta-amyloid plaque, a waxy substance that accumulates between brain cells and impacts cognitive function
"With Alzheimer's disease affecting 5.2 million Americans, another 5 million with early-state disease, and nearly a half million new cases reported annually, treatments like NIC5-15 would make a significant difference in the lives of many Alzheimer's patients," said Dr. Pasinetti, Professor of Psychiatry, Professor of Neuroscience and Professor of Geriatrics and Adult Development, in the Department of Psychiatry at Mount Sinai School of Medicine. "We are hopeful that the follow up clinical study will support this preliminary evidence."
"There are no FDA-approved Alzheimer's disease modifying drugs available today," said Dr. Hillel Grossman, Assistant Professor of Psychiatry, Co-Director of the Clinical Research Core of the Alzheimer's Disease Research Center, and Clinical Director of the Mount Sinai Memory and Aging Center. "Current drugs approved for use help maintain cognitive function, but only for a limited time. NIC5-15 is part of a new class of natural compound we found to have the potential of precluding the generation of β-amyloid and, eventually, attenuating cognitive deterioration in preclinical models of Alzheimer's disease."
The study was conducted at the Mount Sinai Alzheimer's Disease Research Center (ADRC). ADCR is a comprehensive research facility and clinical program dedicated to the study and treatment of both normal aging and Alzheimer's disease. The Center is supported by the National Institute on Aging, a branch of the National Institutes of Health. Humanetics Corporation, manufacturers of NIC5-15, sponsored the study. Phase IIB clinical trials on NIC5-15 are expected to begin later this year.
Disclosure: Dr. Pasinetti has a patent pending for the use of NIC5-15 in the treatment of Alzheimer's disease. The patent application was filed on his behalf by the Mount Sinai School of Medicine. Dr. Pasinetti and the School of Medicine could benefit financially from the results of this trial.
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