Posted by WBHI on Apr 15, 2013 in Sooner Than You Think
by University of Florida News:
A new study from researchers at the University of Florida may have uncovered a critical factor that drives the relentless progression of Alzheimer’s disease ― a discovery that could eventually slow its progression.
For more than 15 years, scientists have known that two types of brain lesions form in patients with Alzheimer’s disease, one type of lesion forming only after the other. David R. Borchelt, a professor of neuroscience, and Guilian Xu, an assistant research scientist at the UF College of Medicine, have used a mouse model to find a potential explanation for how the first type of brain lesion may trigger the second. They report their findings in the current issue of the journal Human Molecular Genetics.
“Understanding how this sequence of events works is thought to be critical and could lead to new therapeutic approaches,” said Borchelt, director of the SantaFe HealthCare Alzheimer’s Disease Research Center at UF and the McKnight Brian Institute.
Posted by WBHI on Oct 19, 2012 in Think About It
by Anna Hodgekiss for Daily Mail:
Older people who eat a diet high in carbohydrates are four times more likely to develop mild cognitive impairment – a precursor to Alzheimer’s disease.
New research from the prestigious Mayo Clinic in America has found the risk is also higher with a diet high in sugar. On the other hand, proteins and fats appear to offer some protection – people who consumed plenty of them are less likely to suffer cognitive decline.
Not everyone with mild cognitive impairment (MCI) develops Alzheimer’s disease, but many do, said lead author Rosebud Roberts, a professor in the department of epidemiology at the Mayo Clinic.
MCI is defined as memory loss apparent to the individual and those around them, but with an absence of other dementia symptoms such as changes in personality and mood.
Posted by WBHI on Aug 1, 2012 in Think About It
by Lauretta Ihonor for News-Medical:
Amyloid beta (Aβ) protein accumulation without neocortical tau deposition is a common pathologic feature of Parkinson’s disease (PD) with dementia, according to study findings. By contrast, neocortical tau accumulation is a known defining feature of Alzheimer’s disease (AD), say the authors.
This, say Paul Kotzbauer (Washington University School of Medicine, St Louis, Missouri, USA) and team, suggests that the pathologic processes that occur in PD with dementia are distinct from those seen in AD.
They add: “Definition of subgroups based on individual pathologic protein deposits, as done in this study, may provide a less ambiguous classification scheme than the application of terms such as AD-like pathology.”
Posted by WBHI on May 17, 2012 in Sooner Than You Think
by Rob Muir for Reuters:
Scientists in Australia have discovered a molecule in the brain that may hold the key to preventing or even curing dementia. During exercise, the molecule stimulates the growth of new cells associated with memory and scientists believe that by harnessing it, a treatment for dementia could be developed.
It’s long been known that exercise is good for the brain. Now scientists know why. University of Queensland researchers have demonstrated that, in mice, there are molecular pathways that affect the brain’s ability to regenerate. Professor Perry Bartlett says it presents evidence that a cure for dementia might be possible.
According to Professor Perry Bartlett, Director, Queensland Brain Institute, “If we’re right, we think we can not only stop, but perhaps reverse some of the cognitive decline.”
Posted by WBHI on May 14, 2012 in Think Outside The Box
by Raquel Maurier for Medical XPress:
A medical research team at the University of Alberta has made two related discoveries that could shed more light on Alzheimer’s disease.
Faculty of Medicine & Dentistry researcher Elena Posse de Chaves and her team recently published their findings in The Journal of Neuroscience.
It has been known for decades that cholesterol plays an important role in Alzheimer’s disease. Posse de Chaves’ team discovered that, in brain cells that accumulate toxic levels of the normally occurring beta amyloid protein, “there is a significant inhibition” in the process that creates brain cholesterol.
Brain cholesterol is vital for normal brain function because it helps protect neurons and helps brain cells fire properly. What the discovery means is that the relationship between this naturally occurring protein and cholesterol is not just one-way. These findings have been suggested by other research teams as well.
by Denise Grady for The New York Times
“If there’s something to be done, I want to be in on the ground floor,” said Elizabeth, 67, a woman participating in studies of frontotemporal degeneration at the University of California, San Francisco.
She asked to be identified by only her middle name to protect her privacy. She is healthy, but she has tested positive for a rare gene that makes the brain disease virtually inevitable; her father, her grandmother, two of her three brothers and other relatives have been affected.
Scientists think that abnormal protein deposits inside brain cells cause frontotemporal degeneration. The proteins vary, but they do not include amyloid, the substance found in Alzheimer’s patients.
In about 40 percent of patients, the deposits are an abnormal form of a protein called tau, which normally gives structural support to brain cells. (Tau is also one of the proteins found in Alzheimer’s patients.)
Two other types of deposits are abnormal versions of proteins involved in other cell functions. In about half of all patients with frontotemporal dementia, the protein is one known as TDP-43, and in about 10 percent it is a substance called FUS.
Posted by WBHI on May 2, 2012 in Sooner Than You Think
by The Press Association
A highly-toxic protein described as the “real bad guy” behind Alzheimer’s disease has been identified by scientists.
The molecule recruits other less harmful proteins and makes them deadly to brain cells, according to research published in the online edition of the journal Nature. Knowing how it forms and behaves is expected to lead to more effective Alzheimer’s treatments. One experimental drug to emerge from the research has already completed early phase I clinical trials.
The protein is a special type of beta-amyloid, which was already known to play a key role in Alzheimer’s. Beta-amyloid clumps together in the brains of Alzheimer’s patients, forming deposits that result in the destruction of nerve cells.
“This form of beta-amyloid, called pyroglutamylated (or pyroglu) beta-amyloid, is a real bad guy in Alzheimer’s disease,” said lead scientist Professor George Bloom, from the University of Virginia in the United States.
Posted by WBHI on Apr 23, 2012 in Sooner Than You Think
by UC San Diego Health System
Without p-tau protein present, impact of amyloid is “not significantly different from zero”
According to a new study, the neuron-killing pathology of Alzheimer’s disease (AD), which begins before clinical symptoms appear, requires the presence of both amyloid-beta (a-beta) plaque deposits and elevated levels of an altered protein called p-tau.
Without both, progressive clinical decline associated with AD in cognitively healthy older individuals is “not significantly different from zero,” reports a team of scientists at the University of California, San Diego School of Medicine in the April 23 online issue of theArchives of Neurology.
“I think this is the biggest contribution of our work,” said Rahul S. Desikan, MD, PhD, research fellow and resident radiologist in the UC San Diego Department of Radiology and first author of the study. “A number of planned clinical trials – and the majority of Alzheimer’s studies – focus predominantly on a-beta. Our results highlight the importance of also looking at p-tau, particularly in trials investigating therapies to remove a-beta. Older, non-demented individuals who have elevated a-beta levels, but normal p-tau levels, may not progress to Alzheimer’s, while older individuals with elevated levels of both will likely develop the disease.”
Posted by WBHI on Apr 20, 2012 in Think It Over
by John Phillip for Natural News
Alzheimer’s disease is characterized by an initial loss of short term memory and the ability to form rational and permanent thoughts. Protein tangles known as tau aggregates strangle neural synapses, blocking the vital flow of neurotransmitter and electrical signals necessary to form memories and personality. Once considered a disease of the aging, this form of dementia is increasing at a startling rate in younger individuals, largely due to a processed and refined food diet, environmental factors and long-term chronic stress.
Researchers from the University of California, San Diego School of Medicine have published the result of a study in the Proceedings of the National Academy of Sciences, explaining the mechanism behind continual exposure to stressors so common in our rapid-paced lifestyle, and the unnatural accumulation of insoluble tau protein aggregates in brain tissue.
They explain that neurofibrillary tangles are one of the physical hallmark signs of Alzheimer’s disease, and have been shown to contribute to disease progression in people under chronic stress conditions during the course of past studies.
by Elizabeth Lopatto for Bloomberg
Scientists have glimpsed proteins turning into the distinctive clumps of Alzheimer’s disease, an action that takes a millisecond or less, providing researchers with clues on drugs to target the ailment.
This stage when amyloid beta clumps begin to form may be a crucial place to target preventive medicines, said Michele Vedruscolo, the study author and a biophysicist at the University of Cambridge in the U.K. Today’s finding, published in the journal Science, could lead to “a statin for neurodegenerative disease,” he said.
Cholesterol-lowering statins like Pfizer Inc. (PFE)’s Lipitor work to prevent heart attacks, which damage heart muscle in ways that can’t be repaired, Vedruscolo said. Similarly, in Alzheimer’s disease, a drug targeted at preventing the characteristic abnormal proteins of the disease may ward off brain cell death and resulting memory loss.
“It’s fair to say prevention is the key,” Vedruscolo said in a telephone interview. “After the disease has already exhibited symptoms, it’s far, far more difficult to intervene.”