Immune System plays a role in preventing Alzheimer's disease

Caregivers, and healthcare professionals, here is some great information


Here is a great dementia resource for caregivers and healthcare professinals,


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The Dementia Caregiver's Little Book of Hope [Kindle Edition

Medical News Today

Researchers from the Peninsula College of Medicine and Dentistry at Exeter's University collaborated with a team from the National Institute on Aging in the USA and in Italy to screen expression levels of thousands of genes in blood samples from nearly 700 people. They discovered that the best marker associated with memory in people was a gene called CCR2, which showed immune system activity against beta-amyloid. Using the Mini mental State Examination, the team measured memory and other cognitive functions.

Earlier animal studies demonstrated that memory and function in mice susceptible to Alzheimer's improved when researchers augmented the CCR2-activated part of the immune system in the animals' blood.

Study leader, Professor David Melzer, declared:

"This is a very exciting result. It may be that CCR2-associated immunity could be strengthened in humans to slow Alzheimer's disease, but much more work will be needed to ensure that this approach is safe and effective".

Dr Lorna Harries, who co-authored the study, concluded:

"Identification of a key player in the interface between immune function and cognitive ability may help us to gain a better understanding of the disease processes involved in Alzheimer's disease and related disorders."

Written By Petra Rattue 

Dementia and cancer: Hard diseases to cure

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Via: MedicareSupplementalInsurance.com

Healthcare professionals, care givers and others, here is some information that you will find of interest.


Dementia and cancer have many things in common if you think about it. Dementia as with cancer is a hard disease to find a cure for.As with cancer, there are many different types.


As with cancer dementia survival rate is longer and better than it was in the past.
Great strides have been made in curing both sets of diseases, but cures are not absolute. In both cases earl  detection is key. Research will bring about even better survival to those who are unfortunate enough to get them.

Successful Alzheimer's vaccine trial

ANI


London: Scientists have found a new vaccine to be effective against Alzheimer’s disease.

The vaccine, CAD106, can prove a breakthrough in the search for a cure for this seriously debilitating dementia disease
Alzheimer’s disease is a complex neurological dementia disease that is the cause of much human suffering and a great cost to society.

According to the World Health Organisation, dementia is the fastest growing global health epidemic of our age. The prevailing hypothesis about its cause involves APP (amyloid precursor protein), a protein that resides in the outer membrane of nerve cells and that, instead of being broken down, form a harmful substance called beta-amyloid, which accumulates as plaques and kills brain cells.

There is currently no cure for Alzheimer’s disease, and the medicines in use can only mitigate the symptoms. In the hunt for a cure, scientists are following several avenues of attack, of which vaccination is currently the most popular.

The first human vaccination study, which was done almost a decade ago, revealed too many adverse reactions and was discontinued. The vaccine used in that study activated certain white blood cells (T cells), which started to attack the body’s own brain tissue.

The new treatment involves active immunisation, using a type of vaccine designed to trigger the body’s immune defence against beta-amyloid.

In this second clinical trial on humans, the vaccine was modified to affect only the harmful beta-amyloid.

The researchers found that 80 per cent of the patients involved in the trials developed their own protective antibodies against beta-amyloid without suffering any side effects over the three years of the study.

The researchers believe that this suggests that the CAD106 vaccine is a tolerable treatment for patients with mild to moderate Alzheimer’s. Larger trials must now be conducted to confirm the CAD106 vaccine’s efficacy.

The study, financed by Swiss pharmaceutical company Novartis, was carried out by Professor Bengt Winblad at Karolinska Institutet’s Alzheimer’s Disease Research Centre in Huddinge and leading neurologists in the Swedish Brain Power network: consultant Niels Andreasen from Karolinska University Hospital, Huddinge; Professor Lennart Minthon from the MAS University Hospital, Malmo; and Professor Kaj Blennow from the Sahlgrenska Academy, Gothenburg.
The study has been published in the distinguished scientific journal Lancet Neurology. 

Father's day suggestions for those with dementia

Caregivers, and healthcare professionals, here is some great information


Here is a great dementia resource for caregivers and healthcare professinals,


Your residents will love the Amazon Kindle Fire




Here is information on being the best caregiver you can be


Here is a way for nurses administrators, social workers and other health care  professionals to get an easyceu or two


Follow alzheimersideas on twitter

The Dementia Caregiver's Little Book of Hope [Kindle Edition

The man with dementia deserves a gift he will enjoy and will make him smile.


What is this gift for the person with dementia ?


It is a book called Adorable Photographs of Our Baby-Meaningful, Mind-Stimulating Activities and More for the Memory Challenged, Their Loved Ones, and Involved Professionals, a book for those with dementia and an excellent resource for caregivers and healthcare professionals.


Why this dementia book?


This book improves the dementia persons' day because:
*Baby pictures capture their attention and make them smile


*Focusing on one photograph at a time is not confusing.


*Large print statements are easy to read.


*Activity ideas hold their attention.


*Remembering the "good old days" is fun


*Creative thoughts boost their self esteem


*Focusing on feelings is effortless for them


*Singing familiar songs puts them in a good mood


*Laughter releases endorphins


*Unwanted behavior is lessened.


*Looking at the book independently improves their personal worth


*Visits from friends and family increase because of the visitor packet


Another way you can make those with dementia feel better is to be complimentary. In the early stages, these individuals often realize that something is wrong. Thus telling them good things about themselves and focusing on the abilities they still have rather than on what abilities they have lost.is important.


In addition to sharing the book, you must help the memory challenged person communicate. He may have trouble word finding. Fill in the blanks for him. At the same time, be complimentary and allow ample time for a response.


Also make sure you give out plenty of hugs. Please note that there are a few dementia folks that do not like to be touched.

Alzheimer's Association: The Longest Day

Caregivers, and healthcare professionals, here is some great information


Here is a great dementia resource for caregivers and healthcare professinals,


Your residents will love the Amazon Kindle Fire




Here is information on being the best caregiver you can be


Here is a way for nurses administrators, social workers and other health care  professionals to get an easyceu or two


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The Dementia Caregiver's Little Book of Hope [Kindle Edition]

For you, this challenge is one day. For people with Alzheimer’s, it’s every day. Run, walk, bike or challenge yourself to some other endurance activity to honor those facing Alzheimer’s. Form a team and raise funds for Alzheimer’s care, support and research.

Alzheimers Association

On June 20, 2012, the longest day of the year, participants across the northern hemisphere will push their limits in a sunrise-to-sunset relay to raise awareness and funds for the fight against Alzheimer’s. It’s one day to honor the passion, dedication and strength displayed by people with Alzheimer’s and their caregivers every day.


Join us for year one of this exciting and innovative event! The Longest Day allows you to participate with ultimate flexibility - you choose your activity, route and time of day to get active. The only rule is that someone on your team is in motion throughout the 16 hours of daylight on the longest day. The Alzheimer’s Association will provide fundraising support and connect you to a virtual community of other participants. We’ll also be cheering you on throughout The Longest Day!

Each team member pledges to raise a commitment fee and is asked to raise a minimum of $100/hour of activity (suggested minimum: $400). Participants will receive a virtual fundraising toolkit, an event day experience kit (including a T-shirt and awareness and celebration materials) and ongoing staff support to help plan a great day and reach fundraising goals. Through smartphone technology and social media, every participant will be able to showcase their efforts and share their stories as part of the global movement to fight against Alzheimer’s.


We’re in it until Alzheimer’s is finished. Show your support for the cause by donating to a team or participant in The Longest Day. Give to honor the more than 35 million people worldwide who are living with Alzheimer’s and the countless caregivers who face this disease so bravely every day.

make a donation

Treating astrocytes can help eliminate plaquer in Alzheimer's disease

Caregivers, and healthcare professionals, here is some great information


Here is a great dementia resource for caregivers and healthcare professinals,


Your residents will love the Amazon Kindle Fire




Here is information on being the best caregiver you can be


Here is a way for nurses administrators, social workers and other health care  professionals to get an easyceu or two


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The Dementia Caregiver's Little Book of Hope [Kindle Edition

Medical News Today


When brain cells start oozing too much of the amyloid protein that is the hallmark of Alzheimer's disease, the astrocytes that normally nourish and protect them deliver a suicide package instead, researchers report.


Amyloid is excreted by all neurons, but rates increase with aging and dramatically accelerate in Alzheimer's. Astrocytes, which deliver blood, oxygen and nutrients to neurons in addition to hauling off some of their garbage, get activated and inflamed by excessive amyloid.


Now researchers have shown another way astrocytes respond is by packaging the lipid ceramide with the protein PAR-4, which independently can do damage but together are a more "deadly duo," said Dr. Erhard Bieberich, biochemist at the Medical College of Georgia at Georgia Health Sciences University.


"If the neuron makes something toxic and dumps it at your door, what would you do?" said Bieberich, corresponding author of the study published in the Journal of Biological Chemistry. "You would probably do something to defend yourself."


The researchers hypothesize that this lipid-coated package ultimately kills them both, which could help explain the brain-cell death and shrinkage that occurs in Alzheimer's. "If the astrocytes die, the neurons die," Bieberich said, noting studies suggest that excess amyloid alone does not kill brain cells. "There must be a secondary process toxifying the amyloid; otherwise the neuron would self-intoxicate before it made a big plaque," he said. "The neuron would die first."


One of many avenues for future pursuit include whether a ceramide antibody could be a viable Alzheimer's treatment. In the researchers' studies of brain cells of humans with Alzheimer's as well as an animal model of the disease, antibodies to ceramide and Par-4 prevented astrocytes' amyloid-induced death.
apoxosomes
Ceramide and Par-4 get packaged in lipid-coated vesicles called exosomes; all cells secrete housands of these vesicles but scientists are only beginning to understand their normal function. When exosomes become deadly, they are called apoxosomes.


Ceramide and Par-4 are typically not in a vesicle, rather in two distinct parts of a cell. Ceramide appears to take the lead in bringing the two together when confronted with amyloid. Bieberich and colleagues at the University of Georgia reported in 2003 that the deadly duo helps eliminate duplicate brain cells that occur early in brain development when their survival could result in a malformed brain. They suspected then that the duo might also have a role in Alzheimer's.


Risk factors for Alzheimer's include aging, family history and genetics, according to the Alzheimer's Association. Increasing evidence suggests that Alzheimer's also shares many of the same risk factors for cardiovascular disease, such as high cholesterol, high blood pressure and inactivity.

Autoantibodies in Alzheimer’s disease

Caregivers, and healthcare professionals, here is some great information


Here is a great dementia resource for caregivers and healthcare professinals,


Your residents will love the Amazon Kindle Fire




Here is information on being the best caregiver you can be


Here is a way for nurses administrators, social workers and other health care  professionals to get an easyceu or two


Follow alzheimersideas on twitter

The Dementia Caregiver's Little Book of Hope [Kindle Edition]

ScienceDaily— New research by scientists at the University of Medicine and Dentistry of New Jersey-School of Osteopathic Medicine (UMDNJ-SOM) demonstrates how dying or damaged brain cells release debris into the bloodstream and give rise to specific autoantibodies that appear to be reliable biomarkers for early diagnosis of Alzheimer's and other neurodegenerative diseases. The researchers also identify a key mechanism in the development of Alzheimer's that mirrors a process that is common in such autoimmune disorders as rheumatoid arthritis

The study appears online in the Journal of Autoimmunity.

"Our earlier research showed that human blood contains perhaps thousands of autoantibodies for clearing cellular debris, and that some of these autoantibodies can potentially be used to accurately diagnose neurodegenerative diseases like Alzheimer's and Parkinson's," said Robert Nagele, PhD, a professor of medicine at the New Jersey Institute for Successful Aging at UMDNJ-SOM and the study's corresponding author. "Here, we found that the release of damaged proteins from dying neurons triggers the production of specific brain-reactive autoantibodies that are directed against this protein debris, a response similar to that seen in some autoimmune disorders."

The researchers focused on the role of enzymes, called PADs, in citrullination, a process that converts one type of amino acid into another (amino acids are the building blocks of proteins). After examining postmortem human brain tissue from individuals with Alzheimer's disease and healthy controls, the researchers found that neurons located in the area of the brain first affected by Alzheimer's disease accumulate both citrullinated proteins and a PAD enzyme. In addition, they demonstrated that a specific type of protein, PTCD2, which has been shown to be a potent biomarker for Alzheimer's, was present in citrullinated form in the neuron cells of the Alzheimer's disease brain samples.



Their results suggest that when neuron cells die, they release their contents into the fluid that surrounds the brain. The cellular remains then enter the bloodstream and their presence generates the production of specific autoantibodies that target this neuronal debris. This same protein citrullination process has been linked to the development of autoantibodies in rheumatoid arthritis, one of the most common forms of autoimmune disease.

"Our previous studies provided evidence that some of these autoantibodies may be able to return to the brain through breaches in the blood-brain barrier," said lead author Nimish Acharya of the UMDNJ-Graduate School of Biomedical Sciences and the New Jersey Institute for Successful Aging. "Once there, they selectively bind to the surfaces of neurons, disrupting the function of the brain cells and accelerating the accumulation of beta amyloid deposits. This chronic cycle of protein-debris-generating autoantibodies that can then seep through the blood-brain barrier helps explain the long-term, progressive degeneration that results from Alzheimer's disease."