Do incontinence drugs accelerate mental decline?


New York: Elderly people treated with drugs for dementia and bladder incontinence at the same time declined faster than those treated only for demenia, according to new research from the Wake Forest University School of Medicine in North Carolina.

Lead researcher Kaycee M Sink MD, MAS, Assistant Professor of Internal Medicine at the school commented: “It is likely that the oppositional effects of the drugs contributed to the accelerated decline.

“Over a year’s time, the decline we observed would represent a resident going from requiring only limited assistance in an activity to being completely dependent or from requiring only supervision to requiring extensive assistance in an activity.”

The combination of drugs affected older adults who started out with higher levels of function in activities of daily living such as dressing, personal hygiene, toileting, transferring, bed mobility, eating, and being able to get around the unit. The results which reveal a 50% greater decline are pubished in the Journal of the American Geriatrics Society.

The study looked at 395 nursing home residents in Indiana who were taking medications for both conditions and 3,141 who were taking only a dementia medication.

Residents included in the analysis were aged 65 years and older and had had at least two consecutive prescriptions for cholinesterase inhibitors, for example, donepezil (Aricept), galantamine (Razadyne), rivastigmine (Exelon), and tacrine (Cognex). These drugs are designed to increase levels of acetylcholine, a chemical that enhances communication between nerve cells in the brain.

About 10% of the residents were also taking either oxybutynin or tolterodine, the two most commonly prescribed drugs for urinary incontinence. These drugs are known as anticholinergic agents and are designed to block acetylcholine, a substance required by the brain for optimum function.

“The two drugs are pharmacological opposites, which led us to hypothesise that the simultaneous treatment of dementia and incontinence could lead to reduced effectiveness of one or both drugs,” said Dr. Sink.

She said the finding of the more rapid decline among residents taking both types of drugs represents a significant public health problem because an estimated 33% of people with dementia also take a drug for incontinence.

“Until now, the clinical dilemma for managing incontinence and dementia has been largely theoretical. This research suggests it may lead to worse outcomes, which is the opposite intention of therapy for dementia.”

The researchers also measured whether the residents taking both drugs experienced a decline in mental function as well, but there was no difference between the two groups, possibly because the test was not sensitive enough. Dr. Sink said that similar research should be extended to community-dwelling older adults with dementia and that more sensitive measures for cognition should be used. Previous studies have shown that the bladder medications are associated with cognitive decline and that people with dementia are especially sensitive to this side effect.

“The results suggest that clinicians should continue to try nondrug management strategies for incontinence before beginning therapy with one of these common drugs,” said Dr. Sink.

She noted that the study was conducted in 2003 and 2004, before newer incontinence medications were introduced that may have less effect on acetylcholine in the brain.

Scientists discover more about Alzheimer’s


Los Angeles: Scientists from UCLA have recently pinpointed a possible physical origin of Alzheimer’s disease. The amyloid-beta protein has long been known to clump in the brain and be involved in the progression of the disease. The UCLA team identified a loop in the protein that is likely to enable amyloid-beta’s adhesion process. This discovery suggests new ways to treat the disorder’s cause, rather than just the symptoms.

Alzheimer’s disease (AD) is the most common cause of late-life dementia. It is estimated to affect 24 million people worldwide, and half of the people over 85 may suffer from it. This fatal disorder is characterized by a decline in the individuals’ memory and in their ability to think and function independently. Current drugs treat the symptoms of Alzheimer’s but not the underlying cause of the disease.

A protein called the amyloid-beta protein (A-beta) is thought to be a key cause of AD. A-beta proteins apparently stick together to form toxic deposits in the brain. Self-associations of A-beta can form various clump structures called “amyloid plaques”. Recent studies suggest that these plaques have potent neurotoxic activities that may kill brain cells.

UCLA scientists, headed by David Teplow, Professor of Neurology at the David Geffen School of Medicine at UCLA, have recently identified a loop in the A-beta protein that is likely to be responsible for the adhesion process. The UCLA team employed an interdisciplinary research strategy. Among other methods, they have revealed morphologic, conformational, and aggregation features of synthetic A-beta in a tube (‘in vitro’), examined the effects of various A-beta assemblies on the physiology of cultured neuronal cell lines (‘in vivo’) and used computerized methods (‘in silico’) to produce models of A-beta structures and to study its conformational dynamics and assembly. The researchers thus discovered that gene mutations in A-beta increase the flexibility of the protein’s loop, enabling it to join easily with loops of other A-beta proteins to form clumps. The loop is also located in the region of the protein that regulates the formation of A-beta and its amount.

Understanding how the toxic A-beta clumps form in the brain could aid the design of new drugs that both block the production of A-beta and prevent it from clumping. Such drugs could be used to prevent or treat the disease. Furthermore, the A-beta assemblies are now known to share properties with other proteins linked to an increasing number of human diseases of aging. This revelation suggests the existence of a common pathogenetic pathway. Therefore, research conducted on AD is likely to advance efforts to understand and treat other disorders.

TFOT previously covered a couple of other AD related researches. One of them led to the discovery of a protein complex named Ab*56 (amyloid beta star 56), which is thought to be a dominant factor in the early development of AD, while the other one developed a method to decrease neuron loss rates.

Full details here:
Getting out of the Loop of Alzheimer’s Disease

Use your brain or loose it

Chicago: Brain exercises can help elderly people stay mentally fit for longer, says a new study.

It concluded that older people must “use-it-or-lose-it” . For people say aged 73 years all that was needed was ten sessions of hour-long classes and included exercises done on a computer.

Research has already shown that intellectual tasks such as crossword puzzles and reading can help keep the brain sharp as people grow old.

The $15m study which was sponsored by the National Institute on Aging, was published appeared in the Journal of the American Medical Association this month. It was led by Sherry Willis, a human-development professor at Penn State University.

Age-related mental decline is expected to affect 84 million people worldwide by 2040, according to statistics in the report.

Nearly 3,000 men and women in six cities – Baltimore, Birmingham, Ala.; Boston; Detroit; Indianapolis; and State College, Pa. took part in the study.

They were randomly assigned to six-week training sessions in either memory, reasoning or speedy mental processing, and were tested before and after. A comparison group received no training but was also tested.

About 700 of the 1,877 people who completed all five years also got short refresher sessions one year and three years after their initial training.

The memory training included organizing a 15-item grocery list into categories like dairy, vegetables and meat to make it easier to remember and locate items.

The reasoning training taught participants how to see patterns in everyday tasks such as bus schedules and taking medicines at different doses and times.

The speed training had participants quickly identify flashing objects on a computer screen. Those are some of the same reaction skills used while driving.

Nearly 90 percent of the speed training group, 74 percent of the reasoning group and 26 percent of the memory group showed almost immediate improvements in scores on tests of the mental functions they were trained in. The improvements in most cases lasted throughout the five years of the study and were most notable in people who got refresher sessions.

The comparison group participants also showed some improvement – perhaps just from the stimulation of being tested – but it was not as great.

After five years, the participants assessed their ability to perform everyday tasks such as shopping, driving and managing their finances. And the researchers rated the participants in their everyday functioning.

Only the group that received reasoning training reported substantially less decline than the comparison group. And only one group actually performed better, in the researchers’ opinion – those who got refresher sessions in speed training.

See also: JAMA: