A new study indicates that patients with high blood pressure are at a higher risk of developing dementia. This research also shows (for the first time) that an MRI can be used to detect very early signatures of neurological damage in people with high blood pressure, before any symptoms of dementia occur.
With two of the last drug-makers abandoning their late stage trials, the familiar question comes up again: Why would you want to know if you have Alzheimer’s when there is no cure? The opinions are divided.
Researchers are looking for seniors of all backgrounds, including healthy adults, people with mild memory complaints and people who have been diagnosed with the disease, said Dr. Michael Weiner, an internationally-recognized Alzheimer’s expert.
UC San Diego and Scripps Research Institute scientists announced Wednesday they have identified a gene that prevents harmful protein deposits, or “aggregates,” associated with neurological disorders such as Alzheimer’s and Parkinson’s disease.
Researchers have reversed symptoms of Alzheimer’s disease in fruit flies by adjusting the production of certain enzymes. The finding may open doors to exploring epigenetics as a potential avenue for Alzheimer’s disease treatments
Have you ever looked at your dog or cat and wondered whether it can remember that you recently rewarded or scolded them — and when that happened?
Indiana University neuroscientists have discovered what they say is the first evidence nonhuman animals can replay a stream of past events from memory — and even the sequence in which those events occurred.
The discovery of this type of episodic memory in rodents may someday help advance the development of new drugs to treat Alzheimer’s disease, said Jonathon Crystal, a professor and director of the neurosciences program at IU-Bloomington
Numerous studies suggest being overweight during middle age increases the risk of developing Alzheimer’s. A new study by the National Institutes of Health found that people who are obese at age 50 may develop, or have a higher risk for, younger-onset Alzheimer’s disease.
“While spare change doesn’t seem like a lot, automatically rounding up one’s transaction adds up to about $50 per month on average,” Tokarsky said. “Just think about it. Does it really make sense for millions of people to wait around to die from a horrible disease, simply because one can’t make a profit developing a cure? Doesn’t it make more sense to invest our spare change, regardless if we make money or lose it, but so that we have a pretty decent chance for a cure in 5, 10 or 15 years?”
The study in the link for today paints a grim picture of the danger of how we live in our society. Switch off your internet at 9 pm, dim the lights at 10 and go sleep, the unpaid bills and unfinished projects will be waiting for you the next day.
A momentous scientific study focused on early detection of Alzheimer’s disease, and tracking it over time, seeks healthy volunteers without memory problems, as well as people who have mild memory problems and those who have been diagnosed with mild dementia due to Alzheimer’s disease.
Potential study volunteers can learn more by visiting www.ADNI3.org or by calling 1-888-2-ADNI-95 (1-888-223-6495).
In the next three minutes, three people will develop Alzheimer’s disease. Two of them will be women.
There are 5.7 million Alzheimer’s patients in the United States. By 2050, there will probably be as many as 14 million, and twice as many women as men will have the disease.
And yet research into “women’s health” remains largely focused on reproductive fitness and breast cancer. We need to be paying much more attention to the most important aspect of any woman’s future: her ability to think, to recall, to imagine — her brain.
In a first-of-its-kind study, researchers have found that in people middle-aged and older, a brain structure that is key to learning and memory is plumpest in those who spend the most time standing up and moving. At every age, prolonged sitters show less thickness in the medial temporal lobe and the subregions that make it up, the study found.
Scientists have recently made a major discovery that could lead to a breakthrough in the treatment of Alzheimer’s disease. A recent study published in Nature Medicine reports that researchers were able to identify the primary genetic risk factor the development of the disease, and they even figured out a potential way to neutralize the risk factor.
A new study has uncovered a biological clock circuit that may explain why people with Alzheimer’s disease or other forms of dementia can become more agitated or aggressive in the early evening.
People with Alzheimer’s can feel more agitated during the evening.
The researchers hope that their findings will lead to new treatments that help to calm the aggressiveness and agitation that individuals with Alzheimer’s and other neurodegenerative diseases commonly experience as part of a condition known as “sundowning.”
Government and other scientists are proposing a new way to define Alzheimer’s disease — basing it on biological signs, such as brain changes, rather than memory loss and other symptoms of dementia that are used today.
One of the more vexing problems bedeviling Alzheimer’s research is why so many treatments that are successful in mouse models fail in clinical trials with humans. In a paper published yesterday in Nature Medicine, a team of researchers at the Gladstone Institutes identified how a key genetic variant associated with the development of Alzheimer’s operates differently in mice and humans. They also showed that the problematic gene can be repaired.
A new study reports a newly discovered link between the loss of dopamine-firing cells in the brain and the brain’s ability to form new memories. It questions the implications of these findings regarding Alzheimer’s disease.
Research from the University of Texas at San Antonio suggests that the plaques that cause the symptoms of Alzheimer’s disease may be more complicated than previously believed, a finding that could significantly affect drug development for the disease.
Researchers found that in addition to the sticky proteins called amyloid beta, other neural and repair proteins also exist within the plaques, indicating new biomarkers for the disease that affects more than 5 million people in the United States.