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Nov. 30, 2005 -- Alzheimer's disease may be a new, third type of diabetes that shares common features of type 1 and type 2 diabetes, according to a new study.
Researchers found that insulin and the cells that process it in the brain drop sharply in the early stages of Alzheimer's disease. They also found that insulin levels continue to decline as the disease progresses and becomes more severe.
"Insulin disappears early and dramatically in Alzheimer's disease. And many of the unexplained features of Alzheimer's, such as cell death and tangles in the brain, appear to be linked to abnormalities in insulin signaling. This demonstrates that the disease is most likely a neuroendocrine disorder, or another type of diabetes," says researcher Suzanne M. de la Monte, professor of pathology at Brown Medical School, in a news release.
Alzheimer's Disease Linked to Diabetes
In the study, researchers examined insulin and insulin receptor function in an area of the brain affected by Alzheimer's disease in brain tissue samples from people who died at various stages of the disease. They compared them to those with normal aging.
The results, published in the Journal of Alzheimer's Disease, showed that insulin levels decreased as the disease progressed.
In addition, researchers found levels of insulin receptors in the brain decreased with increasing severity of the disease. Low levels of insulin receptors impair the brain's ability to respond to insulin.
At the most advanced stage of Alzheimer's, the study showed insulin receptors were 80% lower than in a normal brain.
Researchers say insulin also plays a role in the production of the brain enzyme acetylcholine. Acetylcholine deficiency is associated with dementia and Alzheimer's disease.
"This has important implications for treatment," says de la Monte. "If you could target the disease early, you could prevent the further loss of neurons. But you would have to target not just the loss of insulin but the resistance of its receptors in the brain."
Couple of press releases on breakthroughs in the understanding of Alzheimers:
From Science Daily:
Quote:
Two Pathways Found That Lead To Alzheimer's Disease
Mild cognitive impairment (MCI), a transitional stage between normal cognition and Alzheimer's disease, exists in two different forms, according to a study published today by researchers from the University of Pittsburgh School of Medicine and the University of California, Los Angeles in the Archives of Neurology.
Using a new imaging procedure that creates 3-D maps of the brain, researchers determined specific areas that had degenerated in people with MCI. Depending on the person's symptoms, more tissue was lost in the hippocampus, a brain area critical for memory and one of the earliest to change in Alzheimer's disease, indicating two different paths of progression to Alzheimer's disease. The finding could lead to better diagnosis and treatment of patients with MCI, perhaps delaying or preventing the onset of dementia.
MCI is categorized into two sub-types -- currently distinguished based solely on symptoms. Those with MCI, amnesic subtype (MCI-A) have memory impairments only, while those with MCI, multiple cognitive domain subtype (MCI-MCD) have other types of mild impairments, such as in judgment or language, but also have either mild or no memory loss. Both sub-types progress to Alzheimer's disease at the same rate. Until now it was not known if the pathologies of the two types of MCI were different, or if MCI-MCD was just a more advanced form of MCI-A.
Researchers found that the hippocampus of the patients with MCI-A was 14 percent smaller than that of the healthy subjects, nearly as great as the 23 percent shrinkage seen in Alzheimer's disease. But, the hippocampus of those with MCI-MCD most resembled that of the controls, showing only 5 percent shrinkage.
Using highly accurate Magnetic Resonance Imaging (MRI) data from six patients with MCI-A, 20 with MCI-MCD and 20 with Alzheimer's disease who were seen at the University of Pittsburgh's Alzheimer Disease Research Center and 20 healthy controls, researchers created 3-D mesh reconstructions of each participant's hippocampus that allowed them to see where the hippocampus had deteriorated. This study is the first to use such modeling technology to visualize changes in the brains of people with MCI. Prior studies have only been able to measure the volume of the hippocampus and estimate atrophy through noticeable volume loss.
"These vibrant images produced by 3-D modeling have proven what we suspected -- there are at least two transitional states that lead to Alzheimer's disease," said James T. Becker, Ph.D., a neuropsychologist and professor of psychiatry, neurology and psychology, at the University of Pittsburgh School of Medicine and lead author of the study. "Now we can investigate these pathways and develop treatments that, we hope, may slow or stop the progression of Alzheimer's."
Alzheimer's disease affects as many as 10 percent of people older than 65, and delaying or preventing the onset of dementia is an important medical priority. "We can now see the pattern of brain damage in people with MCI and we can use these new types of images to monitor how different therapies may be working," said Paul M. Thompson, Ph.D., associate professor of neurology, at the University of California, Los Angeles. "By imaging the brain like this, we can explore the progression of diseases, and see if therapies are protecting the brain."
TUESDAY, Jan. 17 (HealthDay News) -- The genetic underpinnings of Alzheimer's may just have gotten a little clearer.
An international research team led by investigators at Washington University School of Medicine in St. Louis say they've identified a region of DNA lying on chromosome 10 that's strongly associated with Alzheimer's disease.
The finding narrows the search for a gene in that area that causes Alzheimer's. The study appears in the January issue of the American Journal of Human Genetics.
"There are a few genes that have been implicated in the development of early-onset Alzheimer's disease, but other than APOE, no genes have been found that increase risk for the more common, late-onset form of the disease," principal investigator Alison M. Goate, a professor of genetics in psychiatry at Washington University, said in a prepared statement.
"The region of DNA identified in our study showed evidence of replication in four independent series of experiments. I haven't seen a putative risk factor show such consistent results since the e4 variant of the APOE gene was identified as a risk factor for late-onset Alzheimer's disease more than 10 years ago," Goate said.
The region of chromosome 10 pinpointed by Goate and her team contains six genes.
"We don't know which of those genes is most likely to harbor this particular risk factor for Alzheimer's disease, but we're getting closer. We're now trying to nail down which one of these six genes is the most likely to be involved," Goate said.
She expects that a total of five to 10 genes eventually will be identified as possible risk factors for late-onset Alzheimer's. It's possible that chromosome 10 contains more than one of those genes.
ScienceDaily are reporting: Diabetes Drug Shows Promise In Treating Alzheimer's
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Treatment of high blood sugar may have a scientific connection to memory loss that could, one day, benefit millions of people with Alzheimer's Disease, which affects up to 4.5 million older Americans, bringing with it impaired thinking and memory.
New research at the University of Virginia Health System and Case Western Reserve University shows that a drug approved by the Food and Drug Administration to treat type 2 diabetes may hold promise in treating Alzheimer's as well, without serious side effects. "We believe that the drug may reduce the body's inflammatory reaction to one of the toxic components that builds up in Alzheimer's, called amyloid plaque, " said Dr. David Geldmacher, an associate professor of neurology at UVa.
The drug, called pioglitazone HCl, was tested in a placebo-controlled trial involving 25 people with mild to moderate Alzheimer's. The study assessed the safety of the drug and, although the treatment appeared to reduce Alzheimer's progression, the study was too small for investigators to be sure of the effects on memory and everyday abilities. However, the findings are promising enough, researchers say, to carry out larger studies of pioglitazone.
The research was presented July 16 to the world's largest Alzheimer's conference, ICAD 2006, in Madrid, Spain. It was selected by ICAD organizers to be highlighted because of a growing sense of the relationship between diabetes and Alzheimer's.
"We don't know exactly how pioglitazone works in Alzheimer's, but there are two possibilities," Geldmacher said. "It could be that the drug reduces the body's response to the amyloid protein found in Alzheimer's. Or, it could be that this drug helps brain cells function. The real advantage is that it's a completely novel approach to treating the disease."
In the next few years, Geldmacher and his colleagues hope to study the effectiveness of pioglitazone in a group of 200 to 300 Alzheimer's patients nationwide. "If it works, this treatment might allow people to better hold on to memory and brain function over a period of time, despite having Alzheimer's," Geldmacher said. "It could also complement other treatments and become part of a multi-pronged approach to Alzheimer's treatment." Right now, there are 5 drugs approved by the FDA to treat Alzheimer's, Geldmacher said, but pioglitazone is unrelated to any of the others. The trial of pioglitazone at UVa and Case Western Reserve was supported by the National Institutes of Health and Takeda Pharmaceuticals North America, Inc., which manufactures the drug.
CTV are also reporting: Diabetes may be linked to Alzheimer's: studies
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New studies suggest some links between Alzheimer's and Type 2 diabetes, raising questions whether the two are actually different forms of the same disease.
Research indicates the damage Type 2 diabetes causes to the pancreas follows a similar pattern to how Alzheimer's affects the brain.
The studies were shown Saturday during the International Conference on Alzheimer's Disease and Related Disorders in Madrid, Spain.
Scientists have found that Alzheimer's patients show a build up of amyloid plaque in their brains. In Type 2 diabetics, amyloid is found in the pancreas, and possibly kills insulin-producing cells.
"This is another similarity between these two conditions," Dr. Patrick McGeer, of the University of British Columbia, told CTV News.
Meanwhile, those suffering from diabetes have an estimated 70 per cent increased risk of developing memory and attention problems -- symptoms of Alzheimer's. Doctors point to toxins produced by diabetes that may negatively affect the brain's ability to use sugar.
Scientists meeting in Madrid are reviewing several studies that suggest controlling Type 2 diabetes can lower the risk of developing Alzheimer's.
In fact, the same drugs used to control blood sugar levels may also slow, or even prevent, the dementia risk.
The apparent connections between Alzheimer's and Type 2 diabetes is causing concern among health officials, because as more Canadians become obese, their risk of developing diabetes also increases.
Obesity is passing smoking as the leading cause of preventable death, and almost one-quarter of Canada's population is obese, according to The Canadian Press.
"With more and more people developing Type 2 diabetes, largely because of too much food and not enough exercise, doctors worry this will lead to thousands more cases of Alzheimer's disease if more isn't done to control and prevent diabetes," reported CTV's Avis Favaro.
The link is also a major concern for Canada's aging baby-boom population.
"As the baby-boomers age into the period of risk for both diseases, we're talking about a large segment of the population, so this is a major public health concern," Dr. Ron Petersen from the Alzheimer's Association told Canada AM Monday.
"It's a common disorder, and if we can nail down the cause and develop an effective treatment, that would be a big medical advance," said McGeer.
A little red wine every day could be exactly what the doctor ordered. A new study reveals moderate consumption of Cabernet Sauvignon actually prevents an Alzheimer's-like disease in mice.
Researchers at Mount Sinai School of Medicine in New York wanted to know if the FDA's recommended servings of red wine per day, approximately one glass for women and two glasses for men, would have the same effect on health previous studies and surveys of populations have shown in the past.
"We wanted to get as close as possible to the human condition," says researcher Giulio Maria Pasinetti, M.D., director of the Neuroinflammation Research Center at Mount Sinai School of Medicine. He and his colleagues gave mice that mimic Alzheimer's disease the equivalent of once glass of Cabernet Sauvignon a day.
What the researchers discovered was that one glass of red wine a day was all the mice needed to get significant brain-protecting benefits. "Moderation is the key word, otherwise you lose all the benefit," says Dr. Pasinetti.
Researchers also report that they now have a better idea of what in the wine is so good for us. It's all thanks to the effects the chemicals in wine have on amyloid precursor protein, which is the stuff that hardens into plaques in the brain, causing Alzheimer's. The red wine chemicals seem to keep that from happening.
Press Release: MayoClinic Highlights Possible Diabetes And Alzheimer's Connection
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An article on MayoClinic.com sheds light on the possible connection between diabetes and Alzheimer's disease and offers advice on how to reduce the risk of getting both conditions.
Alzheimer's disease is the most common form of dementia, a general term for a group of conditions that gradually destroy brain cells and lead to progressive decline in mental function. More than 5 million people in the United States have Alzheimer's disease.
Researchers have identified several ways in which the abnormal insulin and blood sugar levels in diabetes could promote the brain damage that causes dementia. They include:
-- Inflammation and blood vessel damage related to high blood sugar
-- Less insulin in the brain, which results in less glucose to nourish brain cells
-- Increased production of certain proteins that clump in the brain
Reducing the risk:
Weight loss and exercise can help prevent type 2 diabetes. In fact, people who have pre-diabetes -- a precursor to type 2 diabetes -- can cut the risk of developing type 2 diabetes in half by losing 5 percent of their body weight and exercising 30 minutes a day. In addition to reducing the risk of diabetes and Alzheimer's, these lifestyle changes also offer some protection from heart attacks and strokes.
Another new report on this: Could Alzheimer’s be a Form of Diabetes? (Ivanhoe Newswire) -- Could a new form of diabetes be to blame for the memory loss of Alzheimer’s disease?
Quote:
Recent research has revealed levels of brain insulin are lower in patients with the Alzheimer’s and of a third form of diabetes may cause the disease, which results in loss of memory and, ultimately, death.
Now, researchers at Northwestern University in Chicago have discovered why brain insulin signaling -- crucial for memory formation -- would stop working in Alzheimer’s patients. The scientists report a toxic protein in the brains of Alzheimer’s patients removes insulin receptors from nerve cells, making those neurons insulin resistant. The protein, called ADDL, is known to attack memory-forming synapses. The findings support a theory that ADDL builds up at the beginning of Alzheimer’s disease and blocks memory function by a process thought to be reversible.
“We think this is a major factor in the memory deficiencies caused by ADDLs in Alzheimer’s brains,” lead author William Klein, Ph.D., was quoted as saying. “We’re dealing with a fundamental new connection between two fields, diabetes and Alzheimer’s disease, and the implication is for therapeutics. We want to find ways to make those insulin receptors themselves resistant to the impact of ADDLs. And that might not be so difficult.”
The findings may help determine which parts of existing diabetes drugs may protect neurons from ADDL and improve insulin signaling in patients with Alzheimer’s disease. Researchers report drugs for type-2 diabetes could translate into much better Alzheimer’s treatments than what is currently available.
Excess drinking of sugary beverages like soda may increase the risk of Alzheimer's disease, suggests new research in mice. Although the exact mechanisms aren't known, obesity and diabetes are both associated with higher incidences of Alzheimer's.
ScienceDaily are reporting: Diabetes Link To Alzheimer's Disease Explained
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Diabetic individuals have a significantly higher risk of developing Alzheimer's disease but the molecular connection between the two remains unexplained. Now, researchers at the Salk Institute for Biological Studies identified the probable molecular basis for the diabetes -- Alzheimer's interaction.
In a study published online in Neurobiology of Aging, investigators led by David R. Schubert, Ph.D., professor in the Cellular Neurobiology Laboratory, report that the blood vessels in the brain of young diabetic mice are damaged by the interaction of elevated blood glucose levels characteristic of diabetes and low levels of beta amyloid, a peptide that clumps to form the senile plaques that riddle the brains of Alzheimer's patients....
The pathological interaction between diabetes and presymptomatic Alzheimer's diseaseNeurobiology of Aging; Available online 26 March 2008
Joseph R. Burdo, Qi Chen, Nigel A. Calcutt, David Schubert
Quote:
Semantic dementia (SD) is a syndrome of progressive impairment in semantic memory. Fifty-eight brain regions were measured in seven post mortem SD cases, ten normal controls and two disease controls (diagnosis frontotemporal dementia and motor neuron disease, FTD–MND). Manual segmentation of the whole brain has not previously been undertaken in a series of SD cases, either post mortem or during life. Widespread volume loss relative to controls was found in SD, with anterior temporal lobe regions bearing the brunt (>60% atrophy of temporopolar and perirhinal cortices bilaterally). Comparison of regional volumes in SD and FTD–MND found greater atrophy in SD only in temporopolar and perirhinal volumes. The sole region showing atrophy relative to controls in FTD–MND but not SD was motor cortex. Posterior temporal and frontal regions were not consistently affected and no significant asymmetry of atrophy was found. In summary, whole-brain regional evaluation in SD, in comparison with normal controls and FTD–MND, found anterior temporal atrophy encompassing the perirhinal cortex with relative sparing of adjacent posterior temporal regions.
Science Daily are reporting:
Insulin Is A Possible New Treatment For Alzheimer's
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ScienceDaily (Feb. 3, 2009) — A Northwestern University-led research team reports that insulin, by shielding memory-forming synapses from harm, may slow or prevent the damage and memory loss caused by toxic proteins in Alzheimer's disease.
The findings, which provide additional new evidence that Alzheimer's could be due to a novel third form of diabetes, will be published online the week of Feb. 2 by the Proceedings of the National Academy of Sciences (PNAS).
In a study of neurons taken from the hippocampus, one of the brain's crucial memory centers, the scientists treated cells with insulin and the insulin-sensitizing drug rosiglitazone, which has been used to treat type 2 diabetes. (Isolated hippocampal cells are used by scientists to study memory chemistry; the cells are susceptible to damage caused by ADDLs, toxic proteins that build up in persons with Alzheimer's disease.)
The researchers discovered that damage to neurons exposed to ADDLs was blocked by insulin, which kept ADDLs from attaching to the cells. They also found that protection by low levels of insulin was enhanced by rosiglitazone.
ADDLs (short for "amyloid beta-derived diffusible ligands") are known to attack memory-forming synapses. After ADDL binding, synapses lose their capacity to respond to incoming information, resulting in memory loss.
The protective mechanism of insulin works through a series of steps by ultimately reducing the actual number of ADDL binding sites, which in turn results in a marked reduction of ADDL attachment to synapses, the researchers report.
"Therapeutics designed to increase insulin sensitivity in the brain could provide new avenues for treating Alzheimer's disease," said senior author William L. Klein, a professor of neurobiology and physiology in the Weinberg College of Arts and Sciences and a researcher in Northwestern's Cognitive Neurology and Alzheimer's Disease Center. "Sensitivity to insulin can decline with aging, which presents a novel risk factor for Alzheimer's disease. Our results demonstrate that bolstering insulin signaling can protect neurons from harm."...
Is Alzheimer's a New Form of Diabetes?
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