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| Sniffing insulin may help memory lost to Alzheimer’s |
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| 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 |
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| 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 |
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| 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 |
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| 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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| Sunrise Senior Living Becomes an Authorized Validation Organization |
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| Sunday, 09 May 2010 | |
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Sunrise Senior Living Becomes an Authorized Validation Organization to Greatly Enhance Memory Care for More Than 10,000 Residents New Training Will Significantly Expand Validation Method Expertise in the United States MCLEAN, Va., May 6, 2010 /PRNewswire via COMTEX/ --Sunrise Senior Living (NYSE: SRZ) announced today that it has become an Authorized Validation Organization with the Validation Training Institute, a not-for-profit organization offering training and certification in the Validation Method used to care for individuals with Alzheimer's disease and other forms of dementia. Over the next few months, Sunrise professional caregivers will begin certification training in the Validation Method to be used in the Company's more than 360 communities. Sunrise's recognition as a training center will greatly expand the number of trained caregivers using the Validation Method in the United States.
In 2009, Sunrise created a new position in each community called a "Life Enrichment Manager." The sole responsibility of these trained professionals is to work with memory care residents and their families to create activities that enrich residents' lives and keep their cognitive functions active.
About Sunrise Senior Living Sunrise Senior Living, a McLean, Va.-based company, employs approximately 40,000 people. As of March 31, 2010, Sunrise operated 365 communities in the United States, Canada, Germany and the United Kingdom, with a combined unit capacity of approximately 36,600 units. Sunrise offers a full range of personalized senior living services, including independent living, assisted living, care for individuals with Alzheimer's and other forms of memory loss, as well as nursing and rehabilitative services. Sunrise's senior living services are delivered by staff trained to encourage the independence, preserve the dignity, enable freedom of choice and protect the privacy of residents. To learn more about Sunrise, please visit http://www.sunriseseniorliving.com. |
| Study Identifies Food Combination Associated With Reduced Alzheimer's Disease Risk |
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| Sunday, 18 April 2010 | |
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CHICAGO—Individuals whose diet includes more salad dressing, nuts, fish, poultry and certain fruits and vegetables and fewer high-fat dairy products, red meats, organ meats and butter appear less likely to develop Alzheimer's disease, according to a report posted online today that will appear in the June print issue of Archives of Neurology, one of the JAMA/Archives journals. "Epidemiological evidence linking diet, one of the most important modifiable environmental factors, and risk of Alzheimer's disease is rapidly increasing," the authors write as background information in the article. "However, current literature regarding the impact of individual nutrients or food items on Alzheimer's disease risk is inconsistent, partly because humans eat meals with complex combinations of nutrients or food items that are likely to be synergistic." Yian Gu, Ph.D., of Columbia University Medical Center, New York, and colleagues studied 2,148 older adults (age 65 and older) without dementia living in New York. Participants provided information about their diets and were assessed for the development of dementia every 1.5 years for an average of four years. Several dietary patterns were identified with varying levels of seven nutrients previously shown to be associated with Alzheimer's disease risk: saturated fatty acids, monounsaturated fatty acids, omega-3 fatty acids, omega-6 fatty acids, vitamin E, vitamin B12 and folate. During the follow-up, 253 individuals developed Alzheimer's disease. One dietary pattern was significantly associated with a reduced risk of the disease. This pattern involved high intakes of salad dressing, nuts, fish, tomatoes, poultry, fruits and cruciferous and dark and green leafy vegetables and low intakes of high-fat dairy, red meat, organ meat and butter. The combination of nutrients in the low-risk dietary pattern reflect multiple pathways in the development of Alzheimer's disease, the authors note. "For example, vitamin B12 and folate are homocysteine-related vitamins that may have an impact on Alzheimer's disease via their ability of reducing circulating homocysteine levels, vitamin E might prevent Alzheimer's disease via its strong antioxidant effect and fatty acids may be related to dementia and cognitive function through atherosclerosis, thrombosis or inflammation via an effect on brain development and membrane functioning or via accumulation of beta-amyloid," they write. "Our findings provide support for further exploration of food combination-based dietary behavior for the prevention of this important public health problem," they conclude. (Arch Neurol. 2010;67[6]:(doi:10.1001/archneurol.2010.84). Editor's Note: This work was supported by federal National Institute on Aging grants. Please see the article for additional information, including other authors, author contributions and affiliations, financial disclosures, funding and support, etc. For more information, contact JAMA/Archives media relations at 312/464-JAMA (5262) or e-mail This e-mail address is being protected from spam bots, you need JavaScript enabled to view it . |
| Rapamycin rescues learning, memory in Alzheimer’s mouse model |
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| Sunday, 04 April 2010 | |
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SAN ANTONIO — Rapamycin, a drug that keeps the immune system from attacking transplanted organs, may have another exciting use: fighting Alzheimer’s disease. Rapamycin rescued learning and memory deficits in a mouse model of Alzheimer’s, a team from The University of Texas Health Science Center at San Antonio reported Tuesday (Feb. 23). The study, in the Journal of Biological Chemistry, offers the first evidence that the drug is able to reverse Alzheimer’s-like deficits in an animal model, said the senior author, Salvatore Oddo, Ph.D., assistant professor in the Department of Physiology of the UT Health Science Center San Antonio. Rapamycin also reduced lesions in the brains of the mice, the team found. The lesions are similar to those seen in the brains of people who died with Alzheimer’s. “Our findings may have a profound clinical implication,” said Dr. Oddo, who is a member of the university’s Barshop Institute for Longevity and Aging Studies. “Because rapamycin is a U.S. Food and Drug Administration-approved drug, a clinical trial using it as an anti-Alzheimer’s disease therapy could be started fairly quickly.” Last year three institutions, including the Barshop Institute, announced that rapamycin extended the life span of aged research mice at each of the sites. It was the first pharmacologic intervention shown to extend life in an animal model of aging. For 10 weeks the mice that model Alzheimer’s disease were fed chow containing rapamycin. At the start of treatment the mice were 6 months old, roughly the age of young adults, but already exhibited indications of learning and memory deficits and brain lesions. At the end of the 10 weeks, the mice were tested in a contraption called the Morris water maze, sort of a miniature swimming pool used to assess learning and memory in rodents. At the end of the behavioral tests, the brains of the mice were analyzed to determine the effects of rapamycin on the lesions that indicate Alzheimer’s. Rapamycin, a bacterial product first isolated in soil from the island Rapa Nui in the South Pacific, also is being tested in cancer research studies. Rapa Nui is commonly known as Easter Island and is distinguished by ancient monoliths with faces. “While it remains to be determined whether our results obtained in mice could be translated in people, we are very excited as these findings may lead to a new therapeutic intervention to treat Alzheimer’s,” Dr. Oddo said. Co-authors, all from the UT Health Science Center San Antonio, are Antonella Caccamo, M.S.; Smita Majumder, M.S.; Arlan Richardson, Ph.D.; and Randy Strong, Ph.D. Dr. Richardson, professor of cellular and structural biology, is director of the Barshop Institute. Dr. Strong, professor of pharmacology, and Dr. Richardson are senior research career scientists with the South Texas Veterans Health Care System. ### The University of Texas Health Science Center at San Antonio, one of the country’s leading health sciences universities, ranks in the top 2 percent of all U.S. institutions receiving federal funding. Research and other sponsored program activity totaled a record $259 million in fiscal year 2009. The university’s schools of medicine, nursing, dentistry, health professions and graduate biomedical sciences have produced 27,000 graduates. The $753 million operating budget supports six campuses in San Antonio, Laredo, Harlingen and Edinburg. For more information on the many ways “We make lives better®,” visitwww.uthscsa.edu. |
| Memory May Decline Rapidly Even in Stage Before Alzheimer’s Disease |
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| Wednesday, 24 March 2010 | |
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ST. PAUL, Minn. – Memory and thinking skills may decline rapidly for people who have mild cognitive impairment, which is the stage before Alzheimer’s disease when people have mild memory problems but no dementia symptoms, and even more rapidly when dementia begins, which is when Alzheimer’s disease is usually diagnosed. The research is published in the March 23, 2010, print issue of Neurology®, the medical journal of the American Academy of Neurology.
“These results show that we need to pay attention to this time before Alzheimer’s disease is diagnosed, when people are just starting to have problems forgetting things,” said study author Robert S. Wilson, PhD, of Rush University Medical Center in Chicago.
The study involved 1,158 people living in Chicago with an average age of 79. A total of 149 of the participants had Alzheimer’s disease, 395 had mild cognitive impairment, and 614 had no thinking or memory problems.
Memory and thinking skills tests were given to the participants at the beginning of the study and again every three years. People took part in the study for an average of 5.5 years, and up to 11 years. The thinking skills of those with mild cognitive impairment declined twice as fast each year as those who had no cognitive problems, while the skills of those with Alzheimer’s disease declined four times as fast as those with no cognitive problems.
At the beginning of the study, scores on a global cognition test ranged from an average of 0.5 for people with no thinking problems to 0.2 for people with mild cognitive impairment to -0.5 for people with Alzheimer’s disease. Scores declined by 0.04 per year for those with no thinking problems, by 0.09 for those with mild cognitive impairment, and by 0.17 for those with Alzheimer’s.
“The changes in rate of decline occur as the brain atrophies due to the disease, first mainly in the hippocampus during the initial symptomatic stage, referred to as mild cognitive impairment, then in the temporal, parietal and frontal cortex during the dementing illness phase of Alzheimer’s disease,” said David S. Knopman, MD, of the Mayo Clinic in Rochester, Minn., and Fellow of the American Academy of Neurology, who wrote an editorial accompanying the article. The study was supported by the National Institute on Aging and the National Institute of Environmental Health Sciences. 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 multiple sclerosis, restless legs syndrome, Alzheimer’s disease, narcolepsy and stroke. For more information about the American Academy of Neurology, visit http://www.aan.com. |
| New Alzheimer’s Test Offers Better Opportunities for Early Detection |
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| Sunday, 14 March 2010 | |
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KNOXVILLE – Early detection is key to more effective treatment for Alzheimer’s disease and other forms of cognitive impairment, and new research shows that a test developed at the University of Tennessee is more than 95 percent effective in detecting cognitive abnormalities associated with these diseases.
Rex Cannon, an adjunct research assistant professor of psychology at UT Knoxville, and Dr. John Dougherty, an associate professor in the UT Graduate School of Medicine, worked with a team of researchers to develop CST. The impetus for the test came from data showing that 60 percent of Alzheimer’s cases are not diagnosed in the primary care setting, and that those delays lead to missed treatment opportunities.
“Early detection is at the forefront of the clinical effort in Alzheimer’s research, and application of instruments like CST in the primary care setting is of extreme importance,” said Cannon.
The CST is a brief, interactive online test that works to asses various impairments in functional cognitive domains – in essence, it’s a “fitness test” of sorts for the basic functions of thinking and processing information that are affected by Alzheimer’s and milder forms of cognitive impairment.
Cannon and Dougherty’s research, published in the April issue of the Journal of Alzheimer’s Disease and in an early online edition of the journal, showed that the CST was substantially more effective and more accurate in detecting the presence of Alzheimer’s and other forms of cognitive impairment in patients than other existing tests. The CST had a 96 percent accuracy rate compared to 71 percent and 69 percent for the tests that are currently in use.
Part of the goal in developing the test, according to Cannon, was to ensure that the test is useful in the primary care setting, where physicians may not have detailed training in recognizing cognitive impairments, but where an early diagnosis may do the most good for patients.
“Computerized testing is a developing and exciting area for research,” said Cannon, who noted that the test can provide an objective way to determine what diseases may affect the patient and provide information to begin treatments that can blunt the effects of Alzheimer’s.
Cannon and Dougherty, who also are affiliated with the Cole Neuroscience Center at the UT Medical Center, collaborated with Medical Interactive Education in developing the CST over the past two years. The journal article is titled “The Computerized Self Test (CST): An Interactive, Internet Accessible Cognitive Screening Test For Dementia” and can be found at http://iospress.metapress.com/content/a1242×878323454x/fulltext.pdf. |
| Damaged Protein Identified as Early Diagnostic Biomarker for Alzheimer's Disease in Health Adults |
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| Thursday, 25 February 2010 | |
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Researchers at NYU School of Medicine have found that elevated cerebrospinal fluid levels of phosphorylated tau231 (P-tau231), a damaged tau protein found in patients with Alzheimer’s disease, may be an early diagnostic biomarker for Alzheimer’s disease in healthy adults.
The study, published this month online by Neurobiology of Aging, shows that high levels of P-tau231 predict future memory decline and loss of brain gray matter in the medial temporal lobe—a key memory center. Prior studies found the medial temporal lobe to be the most vulnerable brain region in the early stages of Alzheimer’s disease, accumulating damaged tau proteins in the form of neurofibrillary tangles. Tangles are one of the signature indicators of Alzheimer’s disease, in addition to beta amyloid plaques.
“Our research results show for the first time that elevated levels of P-tau 231 in normal individuals can predict memory decline and accompanying brain atrophy,” said lead author Lidia Glodzik MD, PhD, assistant research professor, Department of Psychiatry at the Center for Brain Health and Center of Excellence on Brain Aging at NYU School of Medicine. “Our findings suggest that P-tau231 has the potential to be an important diagnostic tool in the pre-symptomatic stages of Alzheimer’s disease.”
Researchers evaluated 57 cognitively healthy older adults and studied the relationships between baseline cerebrospinal fluid biomarkers, longitudinal memory performance and longitudinal measures of the medial temporal lobe gray matter using magnetic resonance imaging, or MRI. Two years later, researchers found that 20 out of 57 healthy adults showed decreased memory performance. The group with worsened memory had higher baseline levels of P-tau231 and more atrophy in the medial temporal lobe. The higher P-tau231 levels were associated with reductions in medial temporal lobe gray matter. Authors concluded that elevated P-tau231 predicts both memory decline and medial temporal lobe atrophy.
“Indentifying people at risk for Alzheimer’s disease is the necessary first step in developing preventive therapies,” said co-author Mony de Leon, EdD, professor, Department of Psychiatry, and director of the Center for Brain Health at the Center of Excellence on Brain Aging at NYU School of Medicine and research scientist at the Nathan S. Kline Institute for Psychiatric Research. “This study shows that Alzheimer’s disease pathology may be recognized in the normal stages of cognition. This observation may be of value in future studies investigating mechanisms that cause or accelerate dementia.”
This study was done in collaboration with the Nathan S. Kline Institute for Psychiatric Research (NY), Applied NeuroSolutions, Inc. (IL), QiLu Hospital of Shandong University (China), The Sahlgrenska Academy at University of Gothenburg and Sahlgrenska University Hospital (Sweden) and the Institute for Basic Research (NY). Funding for this study was provided by the National Institutes of Health (NIH) in Bethesda, Maryland. |
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