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| Sniffing insulin may help memory lost to Alzheimer’s |
| Sunday, 25 July 2010 | |
Squirting insulin up the noses of patients with early forms of Alzheimer’s disease showed signs of improving their memory, US researchers say.
Patients who got the treatment for four months showed improvements in tests of memory recall that lasted for two months.
“We believe our results are very promising and they warrant future trials,” said Dr. Suzanne Craft of the VA Puget Sound Health Care System and the University of Washington in Seattle, who presented her findings at a meeting of the Alzheimer’s Association in Honolulu.
Alzheimer’s disease is a fatal and incurable deterioration of the brain that affects 26 million people globally. It is the most common form of dementia.
Several studies have suggested that people with Alzheimer’s have reduced levels of insulin in the brain, even in the earliest stages. Insulin is important for communication between brain cells and is needed for brain function.
Craft’s team wanted to see what would happen if they delivered insulin directly to the brain. They studied 109 non-diabetic patients with Alzheimer’s disease or a precursor condition called mild cognitive impairment.
A third of the patients got a placebo and the other two-thirds received different doses of insulin that had been loaded into a nebulizer and squirted up their nose twice daily for four months.
Patients who got the lower dose of insulin showed significant improvements on all primary measures of thinking and memory and in a test of their ability to do daily activities.
In 15 insulin-treated patients who agreed to a spinal tap, the team found a link between improved memory and improvements in measurements of key proteins linked with Alzheimer’s disease.
Craft said the treatment is a long way from being useful to patients, but the findings are strong enough to be studied in a large clinical trial.
Current Alzheimer’s drugs only treat symptoms, but so far no drugs have been shown to improve memory in patients with Alzheimer’s.
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| Depression May Nearly Double Risk of Dementia |
| Wednesday, 07 July 2010 | |
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A new study shows that having depression may nearly double your risk of developing dementia later in life. The research will be published in the July 6, 2010, issue of Neurology®, the medical journal of the American Academy of Neurology.
For the study, researchers examined research data on 949 people with an average age of 79 from the Framingham Heart Study. At the start of the study, participants were free of dementia and were tested for depressive symptoms based on questions about general depression, sleep complaints, social relationships and other factors. A total of 125 people, or 13 percent, were classified as having depression at the start of the study.
At the end of the study, 164 people had developed dementia with 136 specifically diagnosed with Alzheimer’s disease. Nearly 22 percent of people who were depressed at the start of the study developed dementia compared to about 17 percent of those who were not depressed, a 70 percent increased risk in those who were depressed. The 10-year absolute risk for dementia was 0.21 in people without depressive symptoms and 0.34 in people with depressive symptoms. The results were the same regardless of a person’s age, sex, education and whether they had the APOE gene that increases a person’s risk of Alzheimer’s disease.
“While it’s unclear if depression causes dementia, there are a number of ways depression might impact the risk of dementia,” said study author Jane Saczynski, PhD, with the University of Massachusetts Medical School in Worcester, MA. “Inflammation of brain tissue that occurs when a person is depressed might contribute to dementia. Certain proteins found in the brain that increase with depression may also increase the risk of developing dementia. In addition, several lifestyle factors related to long-term depression, such as diet and the amount of exercise and social time a person engages in, could also affect whether they develop dementia.”
Saczynski hopes the study, which is one of the largest and longest population based studies to date, helps clear up confusion over earlier studies that reported inconsistent results about the link between depression and dementia. The study was supported by the National Institute on Aging, the National Institute of Neurological Disorders and Stroke, and the National Heart Lung and Blood Institute and was made possible by the continued participation of the study participants.
The American Academy of Neurology, an association of more than 22,000 neurologists and neuroscience professionals, is dedicated to promoting the highest quality patient-centered neurologic care. A neurologist is a doctor with specialized training in diagnosing, treating and managing disorders of the brain and nervous system such as stroke, Alzheimer’s disease, epilepsy, Parkinson’s disease, and multiple sclerosis. For more information about the American Academy of Neurology, visit http://www.aan.com.
VIDEO: http://www.youtube.com/AANChannel |
| Healthy diet could slow or reverse early effects of Alzheimer’s Disease |
| Sunday, 13 June 2010 | |
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Patients in the early to moderate stages of Alzheimer’s Disease could have their cognitive impairment slowed or even reversed by switching to a healthier diet, according to researchers at Temple University.
In a previous study, researchers led by Domenico Praticò, an associate professor of pharmacology in Temple’s School of Medicine, demonstrated that a diet rich in methionine could increase the risk of developing Alzheimer’s Disease. Methionine is an amino acid typically found in red meats, fish, beans, eggs, garlic, lentils, onions, yogurt and seeds.
“The question we asked now as a follow-up is if, for whatever reason, you had made bad choices in your diet, is there a chance you can slow down or even reverse the disease or is it too late — that there is nothing you could do,” said Praticò.
As in the previous study, the researchers fed one group of mice a diet high in methionine and another group a regular, healthy diet. After five months, they split the group receiving the methionine-rich diet into two, with one group continuing the amino-heavy diet while the second switched to the healthy diet for an additional two months. “At the end of the study, when we looked at these mice, what we found — very surprisingly — was that switching to a more healthy diet reversed the cognitive impairment that had built up over the first three months of eating the methionine-rich diet,” said Praticò. “This improvement was associated with less amyloid plaques — another sign of the disease — in their brains.
Pratico said that the cognitive impairment that had been observed in the mice after three months on the methionine-rich diet was completely reversed after two months on the healthier diet, and they were now able to function normally.
Pratico stressed that this was not a drug therapy for curing MCI or Alzheimer’s, but that it did demonstrate that a lifestyle change such as diet can improve some of the impairments that have already occurred in the brain.
“What it tells us is that the brain has this plasticity to reverse a lot of the bad things that have occurred; the ability to recoup a lot of things such as memory that were apparently lost, but obviously not totally lost,” he said.
Pratico also emphasized that the researchers believe that in addition to switching to a healthy diet, patients diagnosed with MCI or Alzheimer’s also need a regiment of physical as well as mental exercises.
“This combination won’t cure you, but we believe, as we saw in this study, that it will be able to slow down or even possibly reverse the effects on the cognitive impairment,” he said.
The study, “Normalization of hyperhomocysteinemia improves cognitive deficits and ameliorates brain amyloidosis of a transgenic mouse model of Alzheimer’s disease,” is being published in the Journal of the Federation of American Societies for Experimental Biology . It was funded by a grant from the National Institutes of Health. Copies of this study are available to working journalists and may be obtained by contacting Preston M. Moretz in Temple’s Office of University Communications at This e-mail address is being protected from spam bots, you need JavaScript enabled to view it |
| Abdominal Fat at Middle Age Associated with Greater Risk of Dementia |
| Friday, 21 May 2010 | |
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Researchers from Boston University School of Medicine determined that excess abdominal fat places otherwise healthy, middle-aged people at risk for dementia later in life. Preliminary findings suggest a relationship between obesity and dementia that could lead to promising prevention strategies in the future. Results of this study are published early online in Annals of Neurology, a journal of the American Neurological Association.
A 2005 World Health Organization (WHO) report estimated that 24.3 million people have some form of dementia, with 4.6 million new cases annually. Individuals with dementia exhibit a decline in short-term and long-term memory, language processing, problem solving capabilities, and other cognitive function. Clinical diagnosis of dementia is made when two or more brain functions are significantly impaired. Symptoms of dementia can be attributed to irreversible causes such Alzheimer’s disease, vascular dementia, and Huntington’s disease, or caused by treatable conditions such as brain tumor, medication reaction, or metabolic issues.
For the current study, Sudha Seshadri, M.D. and colleagues recruited participants from the Framingham Heart Study Offspring Cohort. The sample included 733 community participants who had a mean age of 60 years with roughly 70% of the study group comprised of women. Researchers examined the association between Body Mass Index (BMI), waist circumference, waist to hip ratio, CT-based measures of abdominal fat, with MRI measures of total brain volume (TCBV), temporal horn volume (THV), white matter hyperintensity volume (WMHV) and brain infarcts in the middle-aged participants.
“Our results confirm the inverse association of increasing BMI with lower brain volumes in older adults and with younger, middle-aged adults and extends the findings to a much larger study sample,” noted Dr. Seshadri. Prior studies were conducted in cohorts with less than 300 participants and the current study includes over 700 individuals. “More importantly our data suggests a stronger connection between central obesity, particularly the visceral fat component of abdominal obesity, and risk of dementia and Alzheimer’s disease,” Dr. Seshadri added. The research showed the association between VAT and TCBV was most robust and was also independent of BMI and insulin resistance. Researchers did not observe a statistically significant correlation between CT-based abdominal fat measures and THV, WMHV or BI.
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