Facebook Light for Dementia Patients

According to Medical News Today, there is a version of Facebook called Facebook Light being developed by SINTEF, the largest research organization in Scandinavia. This will enable the elderly and those with dementia to maintain important social contact. This will enable them to maintain their level of functioning longer, according to research and experience.

According to Tone Oderud, a research scientist at SINTEF, the elderly are being excluded from social media today. The user interface is too advanced for many of them. Oderud is working in a multidisciplinary research team to develop a web-based communications application which is simple enough to enable even people with dementia to use it. The goal is to create a simpler and more secure everyday life for elderly and senile people, their relatives and personnel in the community care services.

Furthermore, research scientists believe that contact through social media can improve the quality of health and life for the great numbers of elderly and those with dementia in our society. At the same time, this can ease the burden on therapists and caregivers.

Testing of other web-based communications systems have already been started. They include a “digital diary” and “scrapbook” with personal photos, newspaper cuttings, and other online information. Oderud says that both of these improved communication between both relatives and the community care services in an informal but valuable way.

The article states that the tests showed that constant, simple contact between relatives and the support services improved everybody’s security and at the same time it reduced the time the caregivers needed to follow up concerned relatives. This holds great potential in all fields of caregiving.

A prototype is currently being tested in the city of Drammen in southern Norway.

Alzheimer’s Action Day

Today is Alzheimer’s Action Day and September is World Alzheimer’s Month. Let’s all wear purple and show our support.

You’ve seen the staggering figures. There are already more than 5 million Americans diagnosed with Alzheimer’s disease and by 2050 as many as 16 million Americans will have the disease. Will you be counted in that figure? Let’s do all we can to take care of ourselves and to support the Alzheimer’s Association to eliminate this awful disease.


 

According to the 2010 World Alzheimer Report as produced by the Alzheimer’s Disease International, there are approximately 35.6 million dementia cases in the world. In the 2011 Facts & Figures of the Alzheimer’s Association, there are more than 5 million Americans who have Alzheimer’s disease (AD). A new mathematical model created by scientists (for mid-life hypertension, diabetes, smoking, mid-life obesity, depression, physical inactivity and low educational attainment) allowed them to estimate the entire number of Alzheimer’s disease risk attributable to lifestyle risk factors both in the world and US combined.

The researchers reported at the Alzheimer’s Association International Conference (AAIC) 2011 that the proportion of worldwide and United States (US) Alzheimer’s cases could be attributed to seven key risk factors:

Risk Factor World US
Physical Inactivity 13% 21%
Depression 11% 15%
Smoking 14% 11%
Mid-life Hypertension 5% 8%
Mid-life Obesity 2% 7%
Low Education 19% 7%
Diabetes 2% 3%

Altogether, the seven possible modifiable risk factors contributed to 50% of cases of Alzheimer’s worldwide while in the US, the number is 54%. Researchers were similarly surprised that factors such as smoking and physical inactivity contribute to a large quantity of cases compared to cardiovascular disease. However, this also suggests that simple changes in lifestyle such as regular physical activity and stopping smoking could have a drastic impact on the cases of Alzheimer’s disease over time.

According to calculations, a 10% decrease in all the risk factors could halt 1.1 million cases of Alzheimer’s worldwide as well as 184,000 cases in America. Take note that a reduction of 25% in all the risk factors could halt more than three million cases of Alzheimer’s in the world and 492,000 cases in America.

In the study conducted by Deborah Barnes,  Associate Professor of Psychiatry at the University of California – San Francisco and  San Francisco and Mental Health Research PI at the Veterans Affair Medical Center at San Francisco, she reports that what mattered was the common risk factors in the population. She adds that the study’s focus was how the risk factors were common within the population. In the US alone, a third of the population leads a sedentary lifestyle. A large quantity of cases could be attributed to physical inactivity. Smoking similarly contributed to a large number of cases.

According to Barnes, the estimates offer a valuable assumption – that there is a direct relationship between the studied risk factors as well as Alzheimer’s disease. The next step is to do an intervention to discover if changing such risk factors will decrease the risk of Alzheimer’s. The results of the study are to be published on the Lancet Neurology online.

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A brand new global mathematical model of Alzheimer’s disease risk shows that decreasing the pervasiveness of popular chronic diseases which are lifestyle-based risk factors by as much as 25% could possibly halt 3 million Alzheimer’s disease worldwide as based on the new research shown at the AAIC 2011 (Alzheimer’s Association International Conference) in Paris.

Previous research has seen a slew of potential changeable risk factors for the disease such as physical activity levels, diet and mental stimulation. However, it is unclear if changing such a lifestyle-based risk factors could result in lesser Alzheimer’s disease risk.

Scientists utilized mathematical modeling in order to compute the percentage of the disease that might be attributed to mid-life hypertension, diabetes, smoking, mid-life obesity, low educational attainment, depression as well as physical inactivity. According to researchers, such estimates provide a critical assumption that is yet to be proven (that there is a direct relationship between the examined risk factors as well as Alzheimer’s disease and that changing the risk factors could decrease the risk of Alzheimer’s).

In a study presented at 2011 AAIC, researchers are looking at the characteristics of old adults who kept their cognitive normal function in order to build a “cognitive resilient aging” index. Their objective is to know a group of factors which predict one’s cognitive stability later in life to be used in research trials and clinical practice.

William Thies, PhD, is the Chief Medical and Scientific Officer of the Alzheimer’s Association. According to him, Alzheimer’s disease and lifestyle is a worldwide emergency. We need to increase the discovery of ways to prevent and detect it as soon as possible. He adds that estimated costs of worldwide dementia is US$604 billion. In the US alone, the cost is US$183 billion.

Deaths related to Alzheimer’s disease are increasing. Meanwhile, those from other types of disease are decreasing. Take note that Alzheimer’s is in the top 10 causes of death in the US which could not be cured, prevented or be slowed down.

In the 2010 World Alzheimer Report produced by Alzheimer’s Disease International, dementia is significantly affecting the world’s social care and health system. Plus, dementia costs are about to soar. According to Thies, the Alzheimer’s Association – in behalf of those who are suffering with such a devastating disease as well as their families including the tons of researchers present in the conference – is calling for an unprecedented worldwide collaboration to further understand, treat and diagnose the disease with the objective of eliminating this global epidemic.

Meanwhile, Associate Professor of Psychiatry at San Francisco’s University of California, San Francisco and Mental Health Research PI at the Veterans Affair Medical Center at San Francisco, Deborah Barnes, PhD, MPH, as well as colleagues, utilized mathematical models to compute PARs or “population attributable risks” for possibly modifiable risk factors for Alzheimer’s disease to show the possible impact of risk factor decrease on the prevalence of Alzheimer’s in the US and the world.

PARs are utilized to estimate the number of cases of a specific disease which are possibly attributable to or necessitated by numerous risk factors. PARs usually consider the strength of the connection between the risk factors of the disease as well as the commonality of the risk factors.

They discovered that almost half of Alzheimer’s disease risks are attributed to changeable risk factors. Altogether, seven risk factors (to be discussed in the next post) are seen to contribute to as many as 17 million cases of Alzheimer’s disease and lifestyle worldwide and almost 3 million cases in America.

 

ICAD 2011

Last month the Alzheimer’s Association International Conference (AAIC) — there has been a name change from the International Conference on Alzheimer’s Disease (ICAD) — had their annual meeting in Paris, France with more than 5,000 scientists in attendance. Each year we look forward to hearing about the latest advances in detection and cure for Alzheimer’s disease. The good news is that there’s progress toward earlier detection, but as one of the leading causes of death, the bad news is that there is still no cure.

In my next two posts, I will present a study that caught my interest because it has to do with lifestyle changes that we can make to potentially lower our risk for Alzheimer’s disease. In the United States, the researchers found that there are seven potentially modifiable risk factors:

  1. Physical inactivity
  2. Depression
  3. Smoking
  4. Mid-life hypertension
  5. Mid-life obesity
  6. Low education
  7. Diabetes

To view a summary of the Alzheimer’s disease research presented, click here.

Next year the conference will be held in Vancouver, British Columbia, Canada, July 14 -19, 2012.

 

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Caregivers of Alzheimer’s disease patients have one of the toughest jobs in the world and yet sometimes one of the most rewarding. Stephanie Jewett, RN, MBA, in an article in ezinearticles.com, offers the following tips for caregivers in a home setting.

  • Find something they love to do and keep that favorite thing going everyday, i.e. take a walk in the park, watch their favorite television show or read articles in a magazine. Go to the Internet and learn more about their favorite subject.
  • Keep life simple; follow a schedule everyday. Eat at particular times, keep hair appointments to one specific day a week, and enjoy a meal out once a week, on the same day.
  • Get lots of rest – take a nap if one feels tired, but don’t sleep the day away. Get up at the same time each day, bathe and then have a nutritious breakfast each and every day!
  • Go through scrapbooks and old pictures, reminding them of family members — their names, ages, etc.
  • Get a dog or a cat so that the patient has some responsibility and company in the home. Pet therapy is one of the best methods known to keep a person happy and healthy.

As a caregiver, your top priority is to take care of yourself so that you will have the strength and stamina to take care of your loved one. So the tips for your Alzheimer’s disease patient apply to you as well. Take good care!

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Scientists are looking at a biomaker that may possibly aid in the identification of individuals with mild memory problems who will eventually develop Alzheimer’s disease. The finding, which was published in the online version of Neurology, the journal of the American Academy of Neurology. It is believed that the new biomarker may prove to be more accurate compared to already established biomarkers.

According to the study author Robert Perneczky, MD, of the Technical University Munich in Germany, identifying individuals who will have Alzheimer’s disease earlier will be an important development. Once treatments that can be used for the prevention of the disease are available, it will become easier to treat and even prevent memory loss.

Fifty eight people with mild cognitive impairment (MCI) participated in the study. It is estimated that as many as 15% of the people who have MCI will develop Alzheimer’s every year.

Cerebrospinal fluid was taken from each participant and tested for certain proteins. Participants were then studied for about three years. Of the participants, 21 developed Alzheimer’s, 27 remained with MCI while 8 people regained normal cognitive skills. Researchers discovered that participants who later developed Alzheimer’s had significantly high levels of sAPPβ or soluble amyloid precursor protein beta in their cerebrospinal fluid.

Based on their findings, the researchers discovered that the person’s age, a protein called tau, and sAPPβ were excellent predictors of future cases of Alzheimer’s. Using these factors as a basis, it was easier to predict if an individual ran the risk of developing the disease. The accuracy for this prediction is pegged at about 80%.

A protein amyloid known as Aβ1-42 or amyloid beta1-42 was once considered one of the biomarkers significant to Alzheimer’s disease. However, it was not used as one of the predictive factors in the study.

The results, Perneczky said, suggest that sAPPβ could be useful as a biomarker and that it may even be better than Aβ1-42 for use in diagnosing Alzheimer’s earlier. The reason for this may be that Aβ1-42 can only indicate events at a later stage – events that already point to the accumulation of amyloid plaques in the brain. Since sAPPβ can be used as a critical initial step in determining if the disease will develop, it is likely to provide a more accurate indication on important pathological events.

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Possible New Drug for Alzheimer’s Disease

Taken orally, E64d, a type of cysteine pro-tease inhibitor, has shown to reduce the buildup of β-amyloid (Aβ) present in animal model brains used in Alzheimer’s disease studies. This action resulted in significant improvement in memory loss. The findings were discovered by a group of researchers from the American Life Science Pharmaceuticals-San Diego, University of California-San Diego and the Medical University of South Carolina. Their findings will be published in the Journal of Alzheimer’s Disease in the September issue.

Dr. Vivian Y.H. Hook praises the discovery since according to her, E64d has been proven safe for human consumption and that the results of the research has excellent potential for use in the treatment of Alzheimer’s disease.

It is known that there is a co-relation in the increase in the levels of Aβ peptides, amyloid plaques and the onset of loss of memory. Aβ peptides are separated from the APP or amyloid precursor protein by the β-secretase. The peptides later develop plaques in the regions of the brain associated with memory.

E64d reduces the level of Aβ by blocking the β-secretase from taking apart the amyloid precursor chain. However, researchers also discovered that it also increases BACE1 activity, a protease known as the principal β-secretase. E64d seems to decrease Aβ in the lower brain by blocking the β-secretase activities of Cathepsin B, another protease.

According to Hook, the study shows that Cathepsin B may be used for the inhibition of the production of Aβ and the resulting improvement of memory function. The finding is important since inhibition of β-secretase and Cathepsin-B is possible without the inhibition of BACE1.

The research involved the use of young and old mice with transgenic Alzheimer’s. Young mice fed with E64d avoided memory loss while old mice showed improved memory.

The study is not new — it actually used a previous work where Cathepsin B was also utilized for memory enhancement. In that study published in 2008, though, Cathepsin B inhibitors were directly administered into brains of mice with AD. The recent study shows that oral administration was effective and could pave the way for future human clinical trials.

The study is co-authored by Dr. Gregory Hook of San Diego’s American Life Science Pharmaceuticals and Dr. Mark Kindy of the Medical University of South Carolina, the Ralph H. Johnson VA Medical Center, and Applied Neurotechnology, Inc. in Charleston, SD. The recent study also received some support from the National Institutes of Health and the Alzheimer’s Drug Development Foundation’s National Institute on Aging.

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One of the distinguishing characteristics of Alzheimer’s disease (AD) is the destruction of brain cells that lead to diminished brain function. Scientists from the University of California at Santa Barbara have discovered what actually happens to these cells in patients with Alzheimer’s and other types of dementia. The findings of the study have been published in The Journal of Biological Chemistry online version.

According to senior author Stuart Feinstein, Ph.D, co-director of UCSB’s Neuroscience Research Institute, brain cells (also known as neurons) stop working properly. Neurons are essential for an individual to perform cognitive skills. The loss of neuronal capacity signals the onset of dementia.

Feinstein, a Molecular, Cellular and Developmental Biology professor, had spent 30 years studying the ‘tau’ protein utilizing cultured cells and test tube bio-chemistry models. Tau is present in long axons which are responsible for connecting neurons and their specific targets. Tau proteins also stabilize microtubules, a component of the cells’ cytoskeleton which is critical to the function and structure of neuronal cells.

For years, it was known that amyloid beta, a type of peptide, can cause the death of neuronal cells and lead to Alzheimer’s disease. The only problem is that it has never been understood how the mechanism that triggers it works. Recent research has shown that amyloid beta requires tau in order to destroy neurons. What is not clear is how it does the action. Most researchers believe that it triggers the excessive chemical modification of tau proteins. For Feinstein, the important goal was to discover the exact details involved in the process of abnormal phosphorylation. By determining what exactly happens, drug companies would have sufficient clues to make the right decisions and pharmaceutical solutions for the problem.

But there is a glitch. The initial hypothesis regarding the effect of amyloid beta on tau phosphorylation was incorrect. What the team discovered was that taking neuronal cells and adding amyloid beta did not result in massively phosphorylated tau proteins. Instead, it resulted in the fragmentation of the proteins within one to two hours and the death of the cells within 24 hours.

According to Feinstein, tau performs multiple jobs, the most widely understood of which is the regulation of cellular cytoskeleton. Cell skeletons, unlike human skeletons, do not undergo abrupt change in its shape. Cell skeletons constantly move, grow and shorten to allow the cell to perform its many functions. The length of cytoskeleton is essential to neurons due to its length.

After the findings, Feinstein’s argument is that the death of neurons that occur in Alzheimer’s is due to a malfunctioning cytoskeleton and that destroying tau proteins can lead to cell death. Feinstein hypothesized the same action that destroys the cytoskeleton in cells treated with cancer drugs could be the same action that was triggered in the neuronal cells.

Prolonged stress does ugly things and now, possibly lead to Alzheimer’s disease (AD). Researchers at the Munich-based University of Minho in Braga, Portugal, have shown that stress, and the hormones released during stress, can accelerate the development of Alzheimer disease-like biochemical and behavioral pathology. Protein deposits in nerve cells are a typical feature of Alzheimer’s disease: the excessive alteration of the tau protein through the addition of phosphate groups — a process known as hyperphosphorylation — causes the protein in the cells to aggregate into clumps. Nerve cells die as a result and those in the hippocampus and the prefrontal cortex are important for learning, memory, and higher cognitive functions.

In this study, rats subjected to stress such as overcrowding and placement on a vibrating platform for one hour daily for one month showed increased hyperphosphorylation of tau protein in the hippocampus and prefrontal cortex. The animals that showed these changes in tau had deficient memories showing problems in the hippocampus area and impaired behavioral flexibility showing deficiency in the prefrontal cortex.

Less than 10 percent of Alzheimer cases are genetic. Previous studies have shown that stress leads to the formation of beta-amyloid, another protein implicated in Alzheimer’s disease. According to Osborne Almeida from the Max Planck Institute of Psychiatry, their findings indicate that stress hormones and stress can cause changes in the tau protein like those that arise in Alzheimer’s disease. The next step will be to see if results obtained in animals are applicable to the development of non-familial forms of Alzheimer’s disease.

Related Article: Stress Significantly Hastens Progression of Alzheimer’s Disease

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