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Fundraising for dementia research: a million for a million

When you think about companies giving to charity, you wouldn’t think of a budget airline company as being among the generous, right? Wrong! easyJet, one of Europe’s budget carrier has just announced its pledge of raising one million pounds for charity. The beneficiary of this corporate generosity is no other than the Alzheimer’s Society of the UK. The fund raising drive is called “a million for a million”, a million pounds for a million people who will suffer from some form of dementia in the next ten years.

According to Andy Harrison, CEO of easyJet

‘I was shocked to learn that one million people will develop dementia in the next 10 years. That’s why we have committed to raising a million for a million - one million pounds to help the million people who will be facing dementia.

Dementia is not a natural part of ageing but it is often still viewed in these terms, meaning it doesn’t get the attention it deserves. The government only invests 2% of its medical research budget on dementia. We call on the government to boost research funding and make this condition a priority.’

Hre’s how the fundraising will work: Passengers on board all easyJet flights will be asked to donate their spare or excess foreign currency to dementia research. A collection bag will probably be given out to each passenger and collected just before landing. In addition, the Alzheimer’s Society will receive a percentage of the sales of scratch cards sold on easyJet flights. Collection starts this summer.

I think this is a splendid idea to raise money for charity. Those of you who are travelling international would know the hassle of different currencies and all those small change that clutters your purse. This is a great way of getting rid of them. And if you have more to spare, you can give more, too.

Neil Hunt, CEO of Azheimer’s Society UK says

‘easyJet has set a fantastic example by boosting funding for dementia. Charities, companies and the government can all work towards the goal of defeating dementia. We look forward to the forthcoming Dementia Research Summit and hope to see the development of an ambitious plan that drives real change.’

Thank you and happy landings.

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Pain relievers: do they or do they not prevent Alzheimers?

Previous studies have reported that pain relievers such as the anti-inflammatory drugs (NSAIDs) may prevent the onset of Alzheimer’s disease. This study by American researchers, however, shows a different story.

The researchers looked at 2,736 members of Group Health, an integrated healthcare delivery system, who did not have any form of dementia when they were enrolled in the study. The average age of the study group was 75 years. The researchers then tracked these patient for 12 years, monitored their use of NSAIDs, both as prescription and over-the-counter (OTC) drugs, and their likelihood of developing dementia especially Alzheimer’s disease.

In the study group, 351 participants had a history of heavy NSAID use at the start of the study. Over the follow up period, another 107 participants became heavy NSAID users. “Heavy use was defined as having prescriptions for NSAIDs at least 68 percent of the time in two years.”

The results of the monitoring for dementia gave the following results:

• 476 participants developed Alzheimer’s disease or dementia during the study period.
• Heavy NSAID users were 66% more likely to develop dementia compared to those who use little or no NSAID.

According to study author Dr. Eric B. Larson, executive director of Group Health Center for Health Studies.

“Although we hoped to find a protective effect, there was none. Thus, for this age group, there’s no basis for taking NSAIDs to prevent Alzheimer’s disease. Our study in this quite elderly population showed more risk of dementia with NSAIDs, especially when used heavily.”

The study results indicate a need to re-evaluate earlier research findings that suggested that NSAID use can delay or even prevent onset of Alzheimer’s disease.

There were, of course, key differences between previous studies and this study. For one thing, the study participants in this study are on average older. This could have a big influence on the results considering that dementia and Alzheimer’s disease are basically an elderly disease, even though there are cases of early onset.

NSAIDs such as Ibuprofen are available over-the-counter are popularly used as anti-fever drugs and pain relievers. In the older population, NSAIDs, marketed in the US as Advil, Motrin and Aleve, are used as pain relievers especially among those who suffer from arthritis. Recently, the US FDA has issued new labelling requirements for OTC drugs including NSAIDs, which should provide warnings about safety, including interaction between NSAIDs and alcohol.

 

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Your brain needs good cholesterol, too!

It is well-known that high blood cholesterol levels are not good for the heart. Is is also quite known that high levels of low-density lipoproteins (LDL) - the bad type of cholesterol - can build up and block arteries and adversely affect cardiovascular health.

What is not so well-known is the fact that low levels of high-density lipoproteins (HDL) - the good type of cholesterol - is linked to memory loss and increased risk for dementia. This is according to a study by European researchers.

It seems that cholesterol levels are important not only for heart health but for brain health as well.

The study followed up 3,673 people as part of the long-term Whitehall II study involving British civil servants. The results showed that low levels of HDL cholesterol are associated with diminished memory by age 60. No link was found between memory loss and levels of total cholesterol and triglycerides. The use of statins to manage cholesterol levels did not seem to have an effect.

According to lead author Dr. Archana Singh-Manoux of the French National Institute for Health and Medical Research (INSERM, France) and the University College London (UK)

“Memory problems are key in the diagnosis of dementia. We found that a low level of HDL may be a risk factor for memory loss in late midlife. This suggests that low HDL cholesterol might also be a risk factor for dementia.”

The mechanism behind this link between HDL cholesterol and dementia risk is not so clear but the following hypotheses are proposed:

• HDL cholesterol blocks the formation of beta-amyloid.
• HDL cholesterol may affect memory in relation to its role in maintaining vascular health.
• HDL cholesterol could influence memory through its -inflammatory and antioxidant.

HDL cholesterol… serves several vital biological functions. It helps clear excess cholesterol from the blood; assists nerve-cell synapses to mature; and helps control the formation of beta-amyloid, the major component of the protein plaques found in the brains of Alzheimer’s patients.

Dementia usually occurs in people 65 years or older. Alzheimer’s disease is the most common form of dementia. In the developed world where a large proportion of the population are elderly, dementia is becoming a major - and costly - health concern. The monitoring of HDL cholesterol (and not only LDL cholesterol!) should therefore be encouraged - for the heart as well as for the brain.

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Keeping a “cool head” not good for Alzheimers patients

I remember a food ad a long, long time ago which went like this: Keep cool but don’t freeze. In fact, keeping your cool is very important in our present day stressful society. But this isn’t seem to be the case in some people. In fact, a literarily cool head may actually be detrimental to your health especially if you have Alzheimer’s disease.

A research study published in the Federation of American Societies for Experimental Biology (FASEB) Journal shows that the “tau” proteins which forms the characteristic clumps in an Alzheimer brain actually multiply much faster when the temperatures are low. In addition, the same bad proteins also builds up faster when a patient in under anesthesia.

The researchers performe dhre study in laboratory mice genetically designed to produce tau proteins. One group of mice was anesthesized and the other group not. The amount of protein accumulated in the brain were compared before anesthesia and one week after.

The anesthetized group had more of these clumps than the group that was not anesthetized. Furthermore, in mice showing advanced signs of the disease, the build up of tau proteins occurred faster than in those in the early stages.

The results of the  study has some clinical implications, namely:

• Care should be taken when putting a patient with Alzheimer’s disease under anesthesia during medical interventions. However, even local anesthesia during dental surgery needs also to be reexamined.
• Care should also be taken that Alzheimer’s patients are not exposed to extreme cold temperature as hypothermia can hasten the damage to the brain. This is especially important considering that Alzheimer’s patients tend to be disoriented and may not be capable of taking care of themselves, including putting on protective clothing in the wintertime.

According to Dr. Gerald Weissmann, Editor-in-Chief of journal

“Every patient wants a surgeon with a cool headbut surgeons might not want the same for their patients. People are anesthetized for all kinds of reasons, even dental work, but this study really should make patients and doctors reconsider whether it’s really necessary.”

               

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The brain activity of the AD gene carrier

It’s in the genes. And the gene variant is called APOE-4. I am referring to the neurodegenerative disease Alzheimer’s disease (AD), the most common cause of dementia.

And even in early adulthood, this gene variant can already cause some structural and functional changes in the brain that is visible to the experts long before the symptoms become evident.

Researchers from the University of Oxford and Imperial College London have observed changes in the brain activity of healthy people carrying the APOE-4 gene variant. The variant is found in about 1 in every 4 people. Not every carrier will develop AD but those who have inherited one copy from their parents have 4 times higher risk for AD. Those who have inherited 2 copies have 10 times higher risk for AD compared to non-carriers.

Using the functional Magnetic Resonance Imaging (fMRI) technique, the researchers were able to distinguish difference patterns of brain activity between carriers and non-carriers. Specifically, the part of the brain involved in memory, the hippocampus, is shown to be hyperactive in APOE-4 carriers.

According to researcher Dr Christian Beckmann

“Our brains are always active - our minds wander even when we’re not carrying out specific tasks. We were surprised to see that even when the volunteers carrying APOE4 weren’t being asked to do anything, you could see the memory part of the brain working harder than it was in the other volunteers. Not all APOE4 carriers go on to develop Alzheimer’s, but it would make sense if in some people, the memory part of the brain effectively becomes exhausted from overwork and this contributes to the disease. This theory is supported by studies that have found the opposite pattern in people who have developed Alzheimer’s, with these people showing less activity than normal in the memory part of the brain.”

Similar findings have been reported by researchers at the Medical College of Wisconsin. Again using fMRI, the American researchers investigated the function of the hippocampus and the posterior cingulated cortex. These two brain structures are important for memory processing, especially information acquisition, filtering and sorting.

Offsprings of AD patients who are symptomless but nevertheless carry the APOE-4 gene variant exhibited significantly reduced (35% less) functional brain connectivity between the two previously mentioned brain structures.

The genetics behind AD is slowly becoming clear. So is the link between the gene variant and brain functioning. However, what still needs to be clarified is why some APOE-4 carriers develop full blown AD and some don’t. Surely it cannot be ruled out that environmental factors (e.g. lifestyle) may play a role.

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The link between Alzheimer’s and mad cow disease

Could there be a link between Alzheimer’s disease and mad cow disease? Most likely, according to researchers at Yale University. And the link seems to be in the proteins called prions that are associated with mad cow disease (bovine spongiform encephalopathy or BSE in medical speak) and its human equivalent Creutzfeldt-Jakob disease. BSE is a neurodegenerative disease in cattle that has caused fatalities in Europe, especially in the UK. Furthermore, it is feared that those who consume the brain of the infected animals may also develop the disease in the form of Creutzfeldt-Jakob disease (CJD).

Alzheimer’s disease (AD) is characterized by amyloid aggregrates or plaques that accumulate in the brain. These aggregates are formed by a misfolded protein β-amyloid (Aβ)

However, the mechanism with which Aβ triggers neuron damage and death in AD patients has always been a mystery.

According to Stephen Strittmatter, professor of neurology at Yale School of Medicine and lead study researcher

“The mechanism by which the production of Aβ makes neurons sick has been a black box. In this study we set out to understand how a certain form of Aβ associated with disease, the oligomeric form, can interact with neurons and trigger the toxic cascade of the disease process. We identified PrP [prion protein] as the surface protein needed for Aβ to disrupt functions of neurons in a dish.”

The prion protein (PrP) is the protein that forms aggregates in mad cow disease and CJD. The Yale researchers have also identified it to be one of the main cellular receptors for Aβ. The study findings suggest that these two proteins PrP and Aβ activate a neurodegenerative disease signaling pathway that is common to both AD and CJD. The results have been published in the journal Nature. Many researchers in the field of neurodegenerative disorders are surprised by the findings because PrP has never been linked to memory function and dysfunction before.

The Yale researchers made their observations on the behavior of the said proteins in vitro, e.g. in cell cultures in the lab. The study has opened new avenues in AD research. The next step would be to check whether the Aβ-PrP link has any functional significance in vivo. It is expected that more studies will now focus on the exploring this protein connections in animal models.

In addition, the study findings also suggest the possibility of a new therapeutic angle for AD. Monoclonal antibodies (mAbs) that target PrP, for example, could potentially be useful in treating AD. PrP antibodies which have been developed by veterinary diagnostics companies for animal use may also be explored for potential therapeutic use in the treatment of AD.

               

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In the making: blood test for Alzheimer’s disease

Diagnosing Alzheimer’s disease is often a problematic process. Over the years, the field of biotechnology has tried to come up with screening and testing methods that can help identify this disease. While diagnostic biomarkers for many diseases can be identified in a blood sample, this has so far proved elusive for Alzheimer’s. However, there is a lot of promise in biomarkers found in the cerebrospinal fluid (CSF), which makes a lot of sense - considering the CSF’s proximity to the brain. CSF is a colorless liquid found in the central nervous system (brain and spinal cord).

Taking CSF samples however is a bit controversial since it entails a procedure called a lumbar puncture or spinal tap, which is basically done inserting a needle in the lower part of the spine to collect the fluid. A spinal tap is performed to diagnose diseases affecting the nervous system.

Many experts feel that a lumbar puncture can be painful and presents some risks, complicated by the type of patients - elderly and disoriented - one is dealing with. Others claim that a lumbar puncture is essentially safe and straightforward. This controversy in relation to the CSF has led many researchers to explore further the possible of developing a blood test for Alzheimer’s.

And it seems that their efforts are bearing fruit.

American researchers “have revealed a direct relationship between two specific antibodies and the severity of Alzheimer’s disease symptoms, raising hopes that a diagnostic blood test for the devastating disorder is within reach.”

The researchers focused on antibodies that the body produces in response to two Alzheimer-associated proteins. One of these proteins is the well-known amyloid-beta which is responsible for the formation of plaques in the brains of Alzheimer’s patients. The other protein is the less known RAGE which is involved in the normal human aging process. However, it has been observed the RAGE is expressed at higher levels in the brains of people with Alzheimer’s.

The researchers found that anti-amyloid beta and anti-RAGE antibodies are significantly higher in the group with Alzheimer’s compared to a control group without Alzheimer’s. Furthermore, the concentrations of the two antibodies in the blood seem to be significantly associated with the severity of the disease.

According researcher Shyamala Mruthint

“Alzheimer’s is an inflammatory disease of the brain, and these two antibodies give us a way to measure that inflammation. Using them as an early diagnostic marker may allow us to start drug treatment early, when it’s most effective, to increase the patient’s quality of life.”

               

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Physical activity helps reduce memory decline

This study by psychologists at the University of Illinois at Pittsburg is not directly related to Alzheimers and dementia but it does tell us about how to keep our spatial memory functioning even at an advanced age.

The hippocampus is a curved structure deep inside the medial temporal lobe of the brain, is essential to memory formation. And for this part of the brain, size does matter. The bigger your hippocampus is, the better is your ability to store new experiences and the better is your spatial memory skills. A damage hippocampus however, prevents an individual to form new memories, as in the well-known case of Henry Gustav Molaison (also known as HM or Henry Right Now) who suffered from retrograde amnesia.

Certain activities make the size of the hippocampus bigger in some people and smaller in others.

For example, a study of London taxi drivers found that the posterior portion of the hippocampus was larger in experienced taxi drivers than in other subjects. And a study of German medical students found that the same region of the hippocampus increased in size as they studied for their final exams.

The size of the hippocampus, however, decreases with age, and with it certain brain functioning. The deterioration of spatial and relational memory in the elderly is one of the major causes of loss of independence and disorientation.

The shrinkage of the hippocampus, however, varies from one individual to another and the researchers found that one way of keeping the hippocampus- and thus memory skills fit is through physical exercise.

This has been observed before in laboratory studies using rodents. The University of Illinois researchers looked at 165 adults aged 59 to 81 years old. 65% of the participants were females. The researchers measured the cardiorespiratory fitness of the participants and conducted a volumetric analysis of the subjects’ left and right hippocampi using magnetic resonance imaging (MRI). The participants’ spatial reasoning was also tested.

The study results revealed that there is a significant link between an individual’s physical fitness and his or her performance in spatial memory tests as well as the size of his or her hippocampus. The size of the hippocampus in physically fit adults accounts for about 40% of their advantage in spatial memory.

According to lead researcher Kirk Erickson

“This is really a clinically significant finding because it supports the notion that your lifestyle choices and behaviors may influence brain shrinkage in old age. Basically, if you stay fit, you retain key regions of your brain involved in learning and memory.”

We all the benefits of exercise to our cardiovascular health. This study gives me another reason to leave my desk and go for a run in the early spring rain.

 

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Hope and Help For the Holidays — Involve Your Loved One

The holidays, for Alzheimer’s caregivers, are filled with a myriad of emotions. Hope and gratitude that another year has passed and our loved one is still with us. We have Fear and anxiety regarding the future, and a strange mixture of joy and sadness for the present. We look into our loved one’s eyes and realize that mom’s body is there, but SHE is long gone. We remember the good times when dad used to climb into the attic or descend the basement stairs to get the holiday accouterments. Grandma and pops used to host the Christmas Eve dinner and now he doesn’t even know that it’s Christmas.

On some levels it’s a bit challenging. On other levels, it feels impossible. How can we possibly balance the festivities of the holidays with the uncertainty of caring for a person with Alzheimer’s disease?

Today, I’ll give you a few suggestions as to how you and your family can enjoy the holidays, while caregiving. This post will specifically address how to include your loved one in as many activities as possible and practical.

• Think smaller instead of larger – Instead of having a huge, sell-out crowd over, consider having a smaller group
• Think participation – Allow your loved one to help and participate. From setting the table, to folding napkins, to knitting or even helping with the decorations; anything your loved one can do to feel loved, appreciated and helpful will bring more joy than the most well thought out gift. I used to ask my mom to fold laundry. Although it wasn’t a holiday-specfic task, she felt needed (and it kept her occupied and out of trouble, at least for a little while).
• Think personal – Take your loved one out for a nice dinner or prepare an intimate dinner. Enjoy a special worship service or other activity together.
• Think help – If you do plan to host a big holiday dinner. Get a family member, friend or even a paid caregiver to help out with your loved one. Having one person who is dedicated to making sure your loved one is taken care of makes a world of difference. A few years ago, my husband and I hosted the family Thanksgiving dinner. There were about 50 guests. My brother designated himself the caregiver for the day and stuck close to mom for the entire day. It took a major load off of me and helped to keep her grounded.
• Think Consistency - As much as possible, keep your loved one’s routine in tact. Major changes in schedule can cause problems in the present and for days or weeks long after the company is gone.

Finally, and maybe most importantly, breathe. Take time to enjoy your family, your loved one and this special time of year.

               

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Hope and Help for the Holidays — General Tips and Information

The holidays can be stressful for anyone. If you add sickness, dementia and Alzheimer’s disease to the mix, you can really have a recipe for disaster as you attempt to navigate the holidays. It’s natural to get a little down during the holidays and caring for a loved one with Alzheimer’s can really complicate what is to be a joyous occassion.

In the meantime, here are a few tips and tricks to make your holidays easier:

1) Move your furniture as little as possible. It may be your custom to change your home into a winter wonderland during the holidays, but that change can throw your loved one into a real tissy.

2) Consider the crowd factor. One year, we took my mom to Virgina to my in-laws. It was a major disaster. A combination of the different atmosphere, the noise level and the crowd really took its toll on my mother. Before the evening was over, she was literally crawling on the floor, under the piano looking for the stairs because she wanted to go to the basement. There was no basement in the house we were in, but of course, she would not hear of it. That was a l-o-n-g day and night. We didn’t get to bed until 3:00 am because we ended up taking mom for a long drive and then coming in through a different door hoping that she would then accept that we were now in a different place.

3) Be aware of safety considerations.
a. Your loved one could easily take to eating brightly colored decorations
b. Keep all extension cords tucked away
c. Secure all throw rugs
d. Keep your eye on the candy jar. I read a story once of a man who ate an entire jar of his favorite candy in one sitting. Although, we tend to splurge during the holidays, an entire jar of candy isn’t good for anyone.

4) Secure your Christmas tree or other standing decorations if you have them. The lights and decorations can be alluring to someone with Alzheimer’s disease. On the other hand, they can be scary. I heard of a man who attempted to pick up the entire Christmas tree and remove it because it was, “in the way.”

5) Check out the Mayo Clinic’s suggestions for balancing the holiday’s and caregiving for a loved one with Alzheimer’s disease.

Finally, do what you can do to jog your loved one’s positive memories. Pull out picutres, bake a favorite cake or dessert, tell favorite stories. Try to include your loved one, as appropriate, in festivities, even if it means that you have to listen to the same story over and over again.

Next time, I’ll give you some specific ideas for including your loved one as you make the most of the holidays while you battle Alzheimer’s disease.

               

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