Dimebon News and Information

A new PET scan neuroimaging technique measured drug-related reductions in the size of brain plaques thought to be responsible for the progression of Alzheimer’s disease, a new study found.

The technique, known as ¹¹C-PiB PET, showed that the drug bapineuzumab reduced the amyloid-β deposits in the brains of patients with mild-to-moderate Alzheimer’s disease by about 25% compared with placebo (mean difference in ¹¹C-PiB retention ratio change from baseline =–0.24; 95% CI –0.39 to –0.09; P=0.003).

The results were reported online in the March 1 issue of The Lancet Neurology. The study did not evaluate whether reduction in plaque size resulted in clinical improvement in patients’ condition.

“This trial has potential implications for interventional studies seeking to prevent or alter the clinical course of Alzheimer’s disease,” Juha O. Rinne, of the University of Turku, Finland, and colleagues wrote.

“Monitoring of the effects of antiamyloid-β drugs on amyloid-β deposition might be possible with radiotracers that bind to amyloid β in patients with Alzheimer’s disease or in those at risk before the onset of clinical decline,” they continued.

“This technique offers the opportunity to test more directly the amyloid-β hypothesis by confirming the ability of a particular drug to reduce or prevent amyloid-β accumulation and to assess the effect this has on clinical outcomes.”

Previous research has suggested that build-up of amyloid-β plaques in the brain is central to the development of Alzheimer’s disease, but until recently autopsy was the only method for confirming the presence of the plaques.

Recently, researchers have developed a method for measuring amyloid-β plaques with PET scans and the radiotracer ¹¹C-PiB, which binds to amyloid-β plaques and indicates their size and position.

In their study, Rinne and colleagues used the imaging technique to evaluate the plaque reducing ability of bapineuzumab, a humanized monoclonal antibody to the plaques.

The researchers assigned 28 patients with mild-to-moderate Alzheimer’s disease to receive one of three doses of bapineuzumab (0.5, 1.0, 2.0 mg/kg) or placebo by intravenous infusion every 13 weeks for up to six treatments between August 2005 and January 2009.

The PET scans were conducted at the beginning of the study and at weeks 20, 45, and 78. The trial was conducted in two centers in the U.K. and another in Finland.

Two patients in the 2.0 mg/kg bapineuzumab group had transient cerebral vasogenic edema, but the adverse events experienced by the participants were typically mild to moderate in severity and temporary, according to the report.

“Treatment with bapineuzumab for 78 weeks reduced cortical ¹¹C-PiB retention compared with both baseline and placebo,” the authors concluded. They added that “¹¹C-PiB PET seems to be useful in assessing the effects of potential Alzheimer’s disease treatments on cortical fibrillar amyloid-β load in vivo.”

The authors cautioned that the sequential recruitment of small groups of patients to increasingly large doses of bapineuzumab may have limited their ability to assess potential dose-response effects.

They also noted that baseline measurements of the plaques were different for the patients who received bapineuzumab and those in the control group, but added that they had adjusted for these in their analysis.

In an accompanying editorial, Sam Gandy, MD, PhD, of Mount Sinai School of Medicine, wrote that Rinne and colleagues had produced “something of a breakthrough” by showing that it is possible to test in live patients whether amyloid plaques in the brain are in fact central to sporadic Alzheimer’s disease.

While the clinical effectiveness remains unproven for bapineuzumab and latrepirdine (also known as Dimebon, an antihistamine developed in Russia), recent studies suggested that these drugs hold potential for treating Alzheimer’s, he wrote.

“Although it is premature to say that we have effective, disease-modifying drugs available, these emerging data concerning both bapineuzumab and latrepirdine move us closer to the goal of understanding, treating, and, eventually, preventing major neurodegenerative diseases such as Alzheimer’s disease,” he concluded.

Source: MedWire News

Postmenopausal women who consume high amounts of fat, in particular trans fat, have an increased risk for ischemic stroke, report US researchers.

“We found positive associations between total fat intake and ischemic stroke incidence and between trans fat intake and ischemic stroke incidence,” said study author Sirin Yaemsiri from the University of North Carolina in Chapel Hill who presented the results at the 2010 International Stroke Conference in San Antonio, Texas, USA.

They assessed links between dietary fat consumption, measured using a food-frequency questionnaire administered at baseline, and incidence of ischemic stroke over a 7.6-year follow-up period, in 87,230 postmenopausal women from the Women’s Health Initiative observational study aged 50–79 years.

Over the follow-up period, 1049 cases of ischemic stroke were recorded; these included 101 atherosclerotic, 269 lacunar, 234 cardioembolic, and 445 unclassified ischemic strokes.

Following adjustment for confounders such as age, ethnicity, smoking status, and physical activity, the researchers found that women in the highest quartile of total fat intake (average intake 86 g/day) had a significant 40% increased risk for ischemic stroke compared with women in the lowest quartile (average intake 26 g/day).

In addition, women in the highest quartile for trans fat consumption (average intake 7 g/day) had a significant 30% increase in risk for ischemic stroke compared with those in the lowest quartile (average intake 1 g/day). No significant associations between ischemic stroke and intake of other fat subtypes were seen, however.

“I think our findings support the American Heart Association recommendations for keeping trans fat intake at less than 1 percent of energy,” said co-investigator Ka He from UNC Gillings School of Global Public Health in Chapel Hill, North Carolina.

They also lend support to schemes such as the New York City trans fat restriction and attempts to replace trans fat with healthier alternatives, as reported by MedWire News.

Those with Huntington’s disease may be given a helping hand from a pill designed to fight the effects of Alzheimer’s disease, it is believed.

A pill being developed for Alzheimer’s disease has been found to help people with Huntington’s disease in improving their train of thought, learning skills and memory abilities, according to US researchers this month.

Dimebon, which is created by Medivation and produced under the generic name latrepirdine (formerly dimebolin), appears to be safe for Huntington’s disease patients and has minimal side-effects, according to the journal Archives of Neurology.

Dr Karl Kieburtz of the University of Rochester in New York spoke to Reuters about the treatment, noting that those taking Dimebon showed improvement in average scores on tests concerning cognitive function while average scores of people taking placebos remained much steadier.

He explained: “In diseases like Huntington’s disease where there is degeneration of the brain, one thing we look for is compounds that might favourably influence that and sometimes those compounds come out of things that can slow natural ageing.”

Huntington’s disease, which is regularly referred to as HD, is a hereditary disorder of the central nervous system and was previously known as Huntington’s Chorea.

MedPage Today (2/8, Gever) noted that 91 patients “receiving three months of treatment with latrepirdine (Dimebon), formerly known as dimebolin, showed a mean increase of 0.86 points (SD 0.31) on the Mini-Mental State Exam (MMSE), compared to an average decline of 0.12 points (SD 0.31, P=0.03) in a placebo group.”

Bloomberg News (2/9, Pettypiece) adds that the study in the Archives of Neurology released Monday is “encouraging because there are no treatments for the psychological effects of Huntington’s.” Reuters (2/9, Allen) also covered the story.

Source: Smart Money

Who’s responsible for the investment decisions of someone with dementia or other forms of diminished mental capacity—the investor, family members, a broker? The law isn’t always clear. Here’s where things stand now.

The law

Financial advisers are “fiduciaries” and legally have to put their clients’ financial interests above their own. Brokers, while not fiduciaries, must give clients a balanced picture of risks, costs and benefits in recommending products. Brokers must also make reasonable efforts to obtain information about a client’s finances, tax status and other factors to inform “reasonable” recommendations. All brokers have to do a “suitability analysis,” says Mary Shapiro, chief executive of the Financial Industry Regulatory Authority.

The gray area

Neither brokers nor other financial advisers are required to figure out if their clients are suffering from dementia or other maladies. Brokers are required to sell only “suitable” investments, but arguments over what is suitable for an aged client have led to lawsuits and arbitration cases.

Protecting yourself and loved ones

Follow the 70-40 rule. When an investor turns 70 or a child turns 40, discuss options such as holding joint accounts with children or assigning power of attorney, says financial adviser Jeff Broadhurst. Consider joining your older relatives at broker meetings, or draft a document that sets out specific investing goals. Some advisers also recommend hiring a money manager to ensure bills are in order.

Almost 16,000 people in Northern Ireland live with a diagnosis of dementia. That number is expected to treble by 2050.

BBC NI Spotlight reporter Declan Lawn talks to dementia sufferers and the people who care for them. He asks what health care plans will be in place for the future.

As he travelled around the UK for his job as a commercial salesman, Ian Travers never suspected that there was anything wrong with his memory.

But when he returned from his frequent trips, his wife Mary began to worry that something was not right.

“He would have come home on a Thursday night and I would pick him up at the airport and invariably he would have forgotten something coming back,” she said.

“One week, he came without his suitcase - he had left it behind.”

For months, Ian’s family put his new-found absent-mindedness down to stress at work.

His daughter Sarah, who as a BBC Newsline presenter is a well-known face in Northern Ireland, noticed that not only was her father’s memory deteriorating, but his behaviour was changing too.

The crisis came in the summer of 2008. Ian and Mary took a holiday to Spain, and whilst they were away, Sarah received a phone call from her mother that would change her family’s life forever.

“I just couldn’t believe it when she said: ‘We are going to have to leave Spain, there is something very wrong with your dad. He doesn’t seem to know who I am…’”

Within weeks, Ian was diagnosed with Alzheimer’s disease. He was just 62.

Today, two years later, family life has changed completely - yet Ian feels lucky. He has responded well to drugs which inhibit the symptoms of Alzheimer’s and still plays sport and goes out walking.

His advice to other people worried about serious memory lapses or behavioural changes is to go to their GP sooner than he did, and talk to close family and friends about what they might have noticed.

“I was daft enough not to think there was anything wrong,” he tells the BBC’s Spotlight programme.

“When Alzheimer’s arrived at our door, it changed our family and changed our lives. But it has brought us closer together and we are just so keen and eager to support dad and help him through what is going to be a difficult future,” Sarah says.

There are almost 16,000 people in Northern Ireland living with a diagnosis of dementia. It’s predicted that number will treble by 2050.

Tuesday night’s Spotlight programme hears directly from dementia sufferers and the people who care for them about how they are coping. It also looks at the state of dementia care in Northern Ireland

As Health Minister Michael McGimpsey prepares to launch a new draft strategy to deal with dementia, do we have the resources and understanding to deal with massive increases in the number of people with dementia in Northern Ireland?

That is what is worrying Professor Peter Passmore - one of the world’s foremost experts on dementia and Alzheimer’s who is based at Queen’s University in Belfast.

“I think that people maybe have not been taking this as seriously as they should and they are thinking ‘mañana’ - so tomorrow, tomorrow, tomorrow. This is not round the corner. This is very much upon us,” he said.

Alzheimer’s is a dreaded disease. It is fatal, and it affects millions in the United States. The Alzheimer’s Association describes the disease as follows: “It destroys brain cells, causing memory loss, and problems with thinking and behavior severe enough to affect work, lifelong hobbies, or social life. Alzheimer’s gets worse over time, and it is fatal. Today, it is the seventh leading cause of death in the United States.”

The Alzheimer’s Association estimates that 5.3 million people are living in the United States with the disease. Despite it being associated as a disease for older persons, Alzheimer’s affects the lives of many students. People you know and love may be struggling with the disease, and it is painful to see someone you love struggle with memory loss due to an incurable disease.

In some cases, Alzheimer’s resembles a genetic pattern, and students may be concerned about their parents’ or their own well being if a grandparent or other relative was diagnosed with the disease. Wondering if you could inherit Alzheimer’s adds worry to a person’s life, and sometimes, they would rather not know. However, the earlier Alzheimer’s is caught, the better, because once the brain damage begins, it is more difficult to treat.

The Telegraph reports that a team of British scientists have discovered an earlier means of discovering the disease. They believe that there is a positive correlation between some types of retina damage in the eye and nerve cell damage in the brain, and by assessing the retina, you can understand more about the brain. Their testing method, supposedly quick and cheap, leads to early detection of Alzheimer’s, even before the disease has taken physical effect.

Through this early detection, patients can treat the disease early and work to stop the damage. The damage can be prevented even before Alzheimer’s has taken effect, and by treating it in this early stage, patients stand a much better chance in living longer and more comfortably. If successful, this would mark a significant step in the fight against Alzheimer’s Disease through saving millions of lives through preventative means.

Regarding this scientific breakthrough, the Daily Mail reports that the eye test could become a routine test for middle-aged persons when they visit the opticians for their annual check-up. Diagnosis could even occur twenty years before the disease takes effect. Although most LSU students are too young to find this test necessary as an annual check-up, it may be beneficial to friends and family.