Posts tagged alzheimer disease
Articles and news from the latest research reports.
Researchers Identify Possible Treatment Window for Memory Problems
Researchers have identified a possible treatment window for plaques in the brain that are thought to cause memory loss in diseases such as Alzheimer’s, according to a new study published in the February 27, 2013, online issue of Neurology®, the medical journal of the American Academy of Neurology.
“Our study suggests that plaques in the brain that are linked to a decline in memory and thinking abilities, called beta amyloid, take about 15 years to build up and then plateau,” said Clifford R. Jack, Jr., MD, with the Mayo Clinic in Rochester, Minn.
For the study, 260 people between the ages of 70 and 92 underwent two or more brain scans over an average of 1.3 years that measured plaque buildup in the brain. Of the participants, 78 percent did not have impaired thinking abilities or memory at the start of the study.
The study found that the rate of buildup accelerates initially, then slows down before plateauing at high levels. For example, lower rates of plaque buildup were found in both people who had low and high levels of the plaques at the start of the study while the rate of plaque accumulation was highest in participants with mid-range levels at the start of the study.
The study also found that the rate of buildup of plaques was more closely tied to the total amount of amyloid plaques in the brain than other risk factors, such as the level of cognitive impairment, age and the presence of the APOE gene, a gene linked to Alzheimer’s disease.
“Our results suggest that there is a long treatment window where medications may be able to help slow buildup of the amyloid plaques that are linked to cognitive decline,” said Jack. “On the other hand, trying to treat the plaque buildup after the amyloid plaque load has plateaued may not do much good.”
UGA discovery sheds light on Alzheimer’s mystery
In 1906, when Alois Alzheimer discovered the neurodegenerative disease that would later be named for him, he saw amyloid-beta plaques and neurofibrillary tangles inside the brain. Several decades later, abnormal protein structures called Hirano bodies also were frequently observed in patients with neurodegenerative diseases.
A hundred years and many millions of suffering patients and families later, scientists still don’t know what these structures do. They do know, thanks to new research from the University of Georgia, that Hirano bodies may have a protective role in the brain of Alzheimer’s patients.
Matthew Furgerson, a doctoral candidate in the UGA Franklin College of Arts and Sciences department of biochemistry and molecular biology, used cell culture models to study the role of Hirano bodies in cell death induced by AICD, or a fragment of AICD called c31, that are released inside the cell during cleavage of the amyloid precursor protein. This cleavage also produces amyloid-beta, which forms extracellular plaques.
Furgerson found mixtures of amyloid precursor protein, c31 and tau-the protein that forms the intracellular neurofibrillary tangles-or of AICD and tau cause synergistic cell death that is significantly higher than cell death from amyloid precursor protein, c31, AICD or tau alone.
"This synergistic cell death is very exciting," Furgerson said. "Other groups have shown synergy between extracellular amyloid beta or amyloid precursor protein with tau, but these new results show that there may be an important interaction that occurs inside the cells."
The results of this study were published in the September issue of PLoS One. Ruth Furukawa, associate research scientist, and Marcus Fechheimer, University Professor in cellular biology, are co-authors on the paper.
Furgerson also found cell death is significantly reduced in cells that contain Hirano bodies compared to cells without Hirano bodies. The protective effect of Hirano bodies was observed in cell cultures in both the presence and absence of tau. The findings reveal that Hirano bodies may have a protective role during the progression of Alzheimer’s disease.
While this research offers no cure for the disease, it does offer some understanding about how the disease operates. The lab has been a leader of Hirano body research for more than a decade due to their development of cell culture and mouse model systems.
Before the development of model systems, the only way to study these abnormal structures was in post-mortem brain tissue. The recently developed Hirano body mouse model is currently being used with an Alzheimer’s model mouse to investigate whether cell culture results can translate to a complex animal.
"I feel privileged to lead a team that might be able to contribute knowledge to help us understand Alzheimer’s disease processes," Fechheimer said. "Other groups have focused on plaques and tangles, and we don’t know as much about Hirano bodies. Results from the cell culture studies are exciting and reveal the protective role of Hirano bodies. Our ongoing studies with mouse models are essential to defining the role of Hirano bodies in Alzheimer’s disease progression in a whole animal."
(Source: news.uga.edu)
A team of neuroscientists and chemists from the U.S. and China September 24 publish research suggesting that a class of currently used anti-cancer drugs as well as several previously untested synthetic compounds show effectiveness in reversing memory loss in two animal models of Alzheimer’s disease.
CSHL Professor Yi Zhong, Ph.D., who led the research conducted in fruit flies and mice, says he and his colleagues were surprised with their results, which, he stressed, used two independent experimental approaches “the results of which clearly converged.”
Specifically, the research converged on what Zhong’s team suggests is a “preferred target” for treating memory loss associated with the amyloid-beta (Aβ) plaques seen in advanced Alzheimer’s patients. That target is the epidermal growth factor receptor, often called by its acronym, EGFR.
Overexpression of the EGFR is a characteristic feature of certain cancers, notably a subset of lung cancers. Two targeted treatments, erlotinib (Tarceva) and gefitinib (Iressa), can dramatically, albeit transiently, reverse EGFR-positive cancers, by blocking the EGF receptor and thus preventing its activation.
The newly published research by Zhong’s team suggests that the signaling within cells that is induced by EGFR activation also plays a role in the pathology – still poorly understood – involved in Aβ-associated memory loss seen in Alzheimer’s patients.
Alzheimer’s triggered by “type three diabetes”
An unhealthy diet could lead to Alzheimer’s disease by triggering a form of insulin resistance dubbed “type three diabetes”, scientists claim.
Photo: Getty Images/Peter Macdiarmid
High levels of the hormone insulin, brought on by a bad diet, may harm the brain in the same way that the muscle, liver and fat cells are affected by type two diabetes. Exposing the brain to too much insulin could cause it to stop responding to the hormone, hampering our ability to think and create new memories and ultimately leading to permanent damage, researchers said.
A diet high in fat and sugar has long been linked to a higher risk of Alzheimer’s, while studies of health among large populations have shown that a healthy Mediterranean diet may offer some protection. In type two diabetes, eating too much fatty and sugary food raises our insulin levels to such a consistently high degree that our muscles, fat and liver cells are no longer affected by the hormone.
This means that the amount of glucose and fat in our blood is allowed to increase unchecked, forcing the pancreas to produce even more insulin to try to cope. Ultimately it becomes exhausted and production drops to very low levels.
A small-scale trial on human patients at Washington University found that those who were given a nasal spray containing insulin were better at remembering details of stories, had longer attention spans and were more independent. A further trial on 240 volunteers showing early signs of dementia will provide further clues as to whether the spray can protect memory and learning ability and keep track of brain changes in patients.
A study on rats by experts from Brown University suggest that a similar process could affect the brain, which relies on insulin to regulate nerve signals related to memory and learning and to produce energy from glucose. Researchers found that blocking insulin from rats’ brains made them disorientated and unable to find their way out of a maze because they could not remember where they were.
Examination of their brains showed the same pattern of deterioration seen in Alzheimer’s patients, including increased levels of the amyloid plaque which is a key hallmark of the condition. If the theory is correct, it means eating more healthy foods and exercising more could reduce the risk of Alzheimer’s, and potentially reverse or slow down the memory loss in patients with the condition.
Dr Suzanne de la Monte, who led the study, told New Scientist magazine: “[The rats] were demented. They couldn’t learn or remember. “I believe [Alzheimer’s] starts with insulin resistance. If you can avoid brain diabetes you’ll be fine. But once it gets going you are going to need to attack on multiple fronts.”
(Source: telegraph.co.uk)
Simple eye test could diagnose Alzheimer’s
The researchers from Lancaster University have found that those with the degenerative brain disease have difficulty with one particular test. They also found that the inability to carry out the tests in those who had already been diagnosed with Alzheimer’s was linked to lower memory function.
Photo: ALAMY
Dr Trevor Crawford said the latest results were potentially exciting. They showed, for the first time, a physical connection with the memory impairment that so often is the first noticeable symptom in Alzheimer’s.
Dr Crawford, of the department of Psychology and the Centre for Ageing Research, Lancaster University, said: “The diagnosis of Alzheimer’s disease is currently heavily dependent on the results of a series of lengthy neuropsychological tests.
"However, patients with a dementia often find that these tests are difficult to complete due to a lack of clear understanding and lapse in their attention or motivation.
"Over the last 10 years, researchers in laboratories around the world have been working on an alternative approach based on the brain’s control of the movements of the eye as a tool for investigating cognitive abilities, such as attention, cognitive inhibition and memory."
During the study, 18 patients with Alzheimer’s disease, 25 patients with Parkinson’s disease, 17 healthy young people and 18 healthy older people were asked to follow the movements of light on a computer monitor. In some instances they were asked to look away from the light. Detailed eye–tracking measurements showed stark contrasts in results.
Patients with Alzheimer’s made errors on the task when they were asked to look away from the light. They were unable correct those errors, despite being able to respond normally when they were asked to look towards the light.
These uncorrected errors were 10 times more frequent in the Alzheimers’ patients than the control groups. Researchers also measured memory function among those Alzheimer’s patients who found the test difficult and were able to show a clear correlation with lower memory function. Dr Crawford added: “The light tracking test could play a vital role in the diagnosis of Alzheimer’s.”
(Source: telegraph.co.uk)