Showing posts with label Alzheimer's. Show all posts
Showing posts with label Alzheimer's. Show all posts

Saturday, September 20, 2008

MEDICAL NEWS: New Pathways Between Memory Loss, Alzheimer's

(previously published here at www.thebulletin.us)

Mild cognitive impairment (MCI) is a stage between normal aging and Alzheimer's earliest stages. Understanding how it goes from mild thought problems to dementia could be key to figuring out how to prevent Alzheimer's. The following details of some of the latest research can give you an idea of the importance of aiming early.


Understanding Risk Factors

According to a Mayo Clinic report, the MCI rate increases with age and is higher in men, who are almost twice as likely to develop the condition than women. Although previous studies show women at higher risk of dementia and Alzheimer's, women generally outlive men, perhaps surviving long enough for their conditions to progress.

According to Dr. B. Brent Simmons, assistant professor and head of Temple University Hospital's Senior Care Specialists section of geriatrics, the higher rates of heart disease in men might also affect their chances of getting vascular dementia.

This study collected data from 1,786 people aged 70 to 89 and found that after a year, about 3.5 percent of 70- to 79-year-olds and 7.2 percent of 80- to 89-year-olds become afflicted with it. Overall, the growth rate of new MCI cases in the elderly population is at 5 percent per year - higher than anticipated.


Drug Development

In research by New York's Mt. Sinai School of Medicine, the brains of 124 diabetics taking medication (insulin and other glucose-lowering drugs) had up to 80 percent less beta-amyloid plaque compared to other diabetics and 124 non-diabetics. Beta-amyloid protein clumps in and around the brain, forming plaque that inhibits and destroys neurons necessary for daily functions and memory.

However, even if a combination of insulin and oral anti-diabetes medications may prevent Alzheimer's-related factors, they cannot be prescribed for non-diabetics. Hopefully, though, brain pathways such as insulin signaling could be used in developing new treatment methods.

Besides plaque, Alzheimer's indicators include unusual changes to a protein called tau. A yearlong trial at Duke University Medical Center tested a promising new drug - a nasal spray called AL-108 - on 144 patients with MCI, between ages 55 and 85, and saw a 62.4 percent improvement in memory ability.

Patients took several tests that measured memory ability before and after medication. The tests measured short-term visual, verbal and auditory working memory, functions that deteriorate throughout the progression of Alzheimer's.

Although this drug doesn't cure Alzheimer's, it showed that attacking the protein tangles does work, stabilizing some of the progress of dementia.


Getting It Before It Starts

Instead of just treating symptoms, researchers at the University of Pennsylvania School of Medicine are trying to stop it before it starts, by finding chemical and biological markers of these conditions.

Since Alzheimer's is a disease measured by analyzing symptoms, the goal of the first investigation was, according to its lead researcher, Dr. Leslie Shaw, "to determine if we could detect Alzheimer's disease pathology before a patient went on to have full blown dementia and memory disorders."

The research focused on measuring levels of cerebral spinal fluid (CSF) and establishing benchmark concentration levels of biological indicators for normal, mildly cognitively impaired, and Alzheimer's individuals.

The differences between the baseline levels of three Alzheimer's-associated proteins were significant enough to speed up drug development efforts of biological compounds that can fix these differences.

The second Penn study uses MRI scans to detect abnormal structural changes linked to MCI in the brains of healthy elderly. Radiology professor Christos Davatzikos, Ph.D. and his colleagues monitored these slight physical changes to the brain successfully might provide a way to alert patients and doctors to brain deterioration and memory decline early enough to prepare or begin treatment.

With around 18 percent of 400 patients converting to Alzheimer's a year, this study is ongoing, and doctors are able to "study the progression as it's happening ... at a rate large enough to make our tests reliable or not with sufficiently large number of study subjects," said Dr. Shaw, who is also the director of Penn's ADNI Biomarker Core Lab.

Collaboration is key for all involved, and as Dr. Shaw noted, "the earlier we can detect the disease reliably with confidence, the earlier we can institute and monitor treatment such as diet, exercise, adjusted sleep patterns and having a social life, along with doctor visits, to delay and stop the disease."

The MRI-based study used images from the Baltimore Longitudinal Study of Aging (BLSA) and the Alzheimer's Disease Neuroimaging Initiative (ADNI) and was funded by the National Institute on Aging and the Institute for the Study of Aging.

Dr. Shaw's research was funded by the Alzheimer's Disease Neuroimaging Initiative via the National Institutes of Health.


Heather J. Chin can be reached at hchin@thebulletin.us.

©The Evening Bulletin 2008

Friday, August 29, 2008

HEALTH: Alzheimer's Patients Resist 'Elderspeak'

(previously published here at www.thebulletin.us)

Most parents have experienced a child's resistant behavior at being lectured, then realized their tone often outweighs what they try to say. Now a study published in the American Journal of Alzheimer's Disorders and Other Dementias shows Alzheimer's patients often resist care, become upset and act out when caregivers talk to them like children.

University of Kansas School of Nursing researchers found the tendency of caregivers - whether by family or professional nursing staff - to use infantilizing speech dealing with elderly or infirm patients likely increases a patient's agitation and resistance to care.

The disruptiveness to nursing care contributes to an overall 30-percent increase in costs of such care. These findings were presented Monday at the International Conference on Alzheimer's Disease in Chicago.

Nursing experts describe "Elderspeak" as a type of speech involving an overly caring, yet controlling, tone of voice, shortened sentences, repetition and the use of inappropriately intimate terms of endearment such as "sweetie" or "dear."

"The style of communication that we use with people with Alzheimer's influences how they feel about themselves and how well they respond to those providing care," said Sam Fazio, Ph.D., director of medical and scientific relations at the Alzheimer's Institute.

"People who have dementia are trying to maintain their sense of being a person. And ... if someone is talking to them like they are an infant, that might be distressing," said lead researcher Kristine Williams, R.N., Ph.D., an associate professor at the University of Kansas.

In the study, researchers videotaped the nurses' and nursing assistants' daily interactions with 20 nursing home residents. Ranging between 69 and 97 years of age, the residents had moderate levels of dementia, requiring different levels of care.

A measure called the Resistiveness to Care Scale (RTCS) was used to gauge the type and degree of disruptive behaviors. Actions termed "resistive" included grabbing onto persons or objects; turning away; pulling the limbs tightly to the body; saying 'no' or crying out; and hitting or kicking.

When these behaviors occurred, the researchers rewound the tape seven seconds to see whether any particular type of communication led up to it.

"[We found] they were more likely to be resistive to care if the nurses were using the 'Elderspeak' communication compared to the normal adult-to-adult kind of talk," said Dr. Williams.

"They also tend to alter the pronouns, [perhaps saying] 'Are we ready for our bath?' ... instead of 'Are you ready for me to help you with your bath?'"

Combined, these alterations in communication and speech patterns have the effect of enforcing the sense the patient receiving treatment stands helpless or highly dependent on the caregiver. Furthermore, the caregiver tends to use "Elderspeak" more often according to how much infirmity they perceive in the patient.

"What, theoretically, we think is going on is that younger people have stereotypes of older adults as being less able to communicate, less competent in a lot of different areas," Dr. Williams said

For family members who witness "Elderspeak" in a nursing home or assisted-care environment, Dr. Williams does not recommend hostile criticisms. Instead, "try and tell them a little bit about your loved one, that they were a high-functioning adults. To get them thinking more of the person in terms of that competent adult framework."

"[Caregivers] really have to know who that person's been their whole life, and not just define them in terms of their disease or their symptoms," said Dr. Fazio, of the Alzheimer's Institute.

"People are always saying, 'Oh, I can't do that because it's going to take more time and I have too many people to take care of.' But this showed us that the other way of doing things was causing even more time and care."

The number of people with Alzheimer's likely will increase to over 106 million people worldwide by 2050.


Heather J. Chin can be reached at hchin@thebulletin.us

©The Evening Bulletin 2008

Tuesday, July 22, 2008

Alumnus Donates $1.5M In Grants To Two Penn Schools

(previously published here at www.thebulletin.us)

University of Pennsylvania alumnus Arthur Bilger and his wife, Dahlia, made two monetary gifts this week to his alma mater to be used to support research into interactive media business models and therapeutic drugs to treat Alzheimer's disease.

The Wharton School received a $1 million gift to create and support the Wharton Interactive Media Initiative (WIMI), a research program focusing on interactive media, its effect on global business and its influence on traditional media business models. This data-driven research will hopefully be applied to helping media companies do profitable business.

Of his family's donation to Wharton, Mr. Bilger said "Through the WIMI, Wharton will continue its tradition of cutting-edge scholarship with practical applications... to the world of business."

The Bilger Foundation's $500,000 donation to the School of Medicine will establish the Nathan Bilger Alzheimer Drug Discovery Initiative in memory and honor of Mr. Bilger's father. The monetary gift will be used by the Center for Neurodegenerative Disease Research (CNDR) to identify new methods and drug targets for the treatment of Alzheimer's disease that can hopefully be translated by their Marian S. Ware Alzheimer's Drug Discovery Center into new therapeutic drugs.

"The Bilger family gift will enable us to determine if an off-label drug used to treat organ rejection in transplant patients can be used to treat Alzheimer's disease," Dr. Virginia M.Y. Lee, CNDR director, said to the Almanac, a Penn-run publication.

Dr. John Q. Trojanowski, director of PennMed's Institute on Aging, explained that this is significant because early studies that are promising need a lot of money to evaluate them further as potential Alzheimer's therapies, and, "if successful, could put more drugs in the pipeline aimed at helping... patients by blocking... the disease process."

Mr. Bilger manages a private investment firm in California, is a member of Wharton's Board of Overseers, and along with his wife has supported the School of Arts and Sciences, Penn Medicine, and a scholarship for undergraduates.

Heather J. Chin can be reached at hchin@thebulletin.us

©The Evening Bulletin 2008

Saturday, June 28, 2008

An Alzheimer's Minibreakthrough

(previously published at www.thebulletin.us)


The dementia and loss of mental faculties resulting from Alzheimer's disease has long been recognized, but the exact cause has remained elusive, until perhaps now.

New research suggests that one form of beta-amyloid protein - which clumps around an afflicted brain's neurons and forms plaque that inhibits and destroys neurons needed for daily functions and memories - causes symptoms of Alzheimer's.

Previous research had been unable to determine whether the beta-amyloid plaque was a cause or a side effect of Alzheimer's disease.

In the new study, researchers caused Alzheimer's symptoms of impaired memory function in rats by injecting them with a two-molecule soluble form of beta-amyloid protein.

One-molecule and three-molecule forms of both soluble and insoluble proteins did not trigger illness in the rats, which researchers say may explain why some people with beta-amyloid plaque don't exhibit such symptoms.

Dr. Ganesh M. Shankar and Dr. Dennis J. Selkoe of Harvard Medical School published their findings in Sunday's online edition of the journal Nature Medicine. In the report, they noted that when studies were also conducted on mice, the brain cell density was reduced by 47 percent, and affected the synapses, or connections between cells that are necessary for cell communication.

Beta-amyloid extracts were taken from the brains of people who had donated their bodies to medical research.

This is the first time that research has showed the effect of a particular type of beta-amyloid in the brain, said Dr. Marcello Morrison-Bogorad, director of the division of neuroscience at the National Institute on Aging, to the Associated Press.

He added that the revelation that only one of three types of the proteins had a damaging effect on the brain is important because doctors have long wondered why they find some plaque-covered brains in autopsy that belong to a person who didn't have Alzheimer's.

"A lot of work needs to be done," stated Dr. Morrison-Bogorad, as to why one protein has a damaging effect and not others. "Nature keeps sending us down paths that look straight at the beginning, but there are a lot of curves before we get to the end."

The Harvard study was funded by the National Institute on Aging, Science Foundation Ireland, Wellcome Trust, the McKnight and Ellison foundations and the Lefler Small Grant Fund.

In a separate study out of the Feinstein Institute of Medical Research in New York, Dr. Yousef al-Abed, chief of medicinal chemistry, and his colleagues Michael Bacher and Richard Dodel of Marburg University in Germany created and tested an experimental drug that they say might neutralize or reduce the effects of the beta-amyloid plaques in the patient's brain.

Published in the Journal of Experimental Medicine, the study's results describe an experimental medicine, CNI-1493, already being tested as a medicine for the bowel affliction called Crohn's disease, that targets and transforms amyloid in the brain so that it does not clump and form plaque and also loses its toxicity.

Their results show a 70 to 85 percent reduction of amyloid buildup in the cortex and the hippocampus - the two areas of the brain most affected in Alzheimer's patients and which affect memory, attention, perceptual awareness, language, consciousness and the regulation of emotion.

Heather Chin can be reached at heather.jean.chin@gmail.com

©The Evening Bulletin 2008