Physical exercise is a fantastic way to stimulate our brain function. It has been shown in numerous studies to boost our cognitive skills of memory and learning. Children who exercise are known to perform better academically. Older adults can also boost their memory and thinking skills by undertaking regular exercise of thirty minutes of aerobic activity (enough to get the heart rate up).

Whilst it is known that exercising leads to more oxygen and nutrients getting to the brain, how the brain uses fuel during the actual process of exercise, hasn’t been understood until fairly recently.

Our neurons don’t store fuel themselves and their primary energy source is glucose. Our brain uses 20% of all the energy we put into our body as fuel, despite only accounting for 2% of our actual body weight. Hence the need to supply our greedy brain with a regular amount of food.

Another discovery a few years back, was that our other brain cells or astrocytes, which act as support agents for our neurons, can store fuel in the form of glycogen. It is this glycogen that is important for the normal function of all of the cells in our brain.

In 2011 scientists from the University of Tsukuba in Japan undertook a study on astrocyte glycogen in rat brains. They suspected that this brain glycogen was used by the neurons as a fuel reserve during times when blood glucose levels were low i.e as in when exercising. In prolonged exercise, our muscular glycogen stores will typically get depleted, so the scientists looked at measuring muscle and brain glycogen in the rats after running them on treadmills at varying intervals of 30, 60 and 120 minutes and comparing levels to a non exercising group.

What they found was that after 30 and 60 minutes of running, the muscle and liver glycogen stores were depleted whilst the rat brain glycogen levels remained the same. But after 120 minutes running, the brain glycogen levels dropped in 5 different areas of brain, consistent with respective blood and brain glucose levels. In other words the glycogen stores from the astrocytes had been broken down and the energy released, and subsequently used by the energy hungry neurons.

In 2012 the same group of scientists did further studies,(again using rats)this time looking at the effect of exhaustive running on brain glycogen levels after a single running session and after 4 weeks of regular moderate intensity running.

After the single session of running on the treadmill, the rats were allowed to rest and feed prior to having their brain glycogen levels measured. What the scientists found was that the rats brains had over compensated with up to 60% more glycogen being stored in the astrocytes. This then dropped back to normal levels within 24 hours.
In the second case, after four weeks of exercise training this extra compensation level became the new “normal”, especially in those areas of the brain associated with learning and memory. The longer lasting super compensation of the cortex and hippocampus is thought to probably be a training adaptation to meet the increased energy demand of a brain in someone who exercises regularly.

So what does this imply for us as exercising humans?

Having a greater amount of fuel reserve in the astrocytes may explain why our thinking skills improve if we exercise regularly. Our brain then has a better and larger fuel supply to enable us to think and remember better.

So next time you have been for a bit of a burn, don’t forget to top up afterwards with a carbohydrate rich snack such as a banana to boost your brain glycogen levels.

Refs:
Matsui T, Soya S, Okamoto M, Ichitani Y, Kawanaka K, Soya H. Brain glycogen decreases during prolonged exercise. J Physiol. 2011 Jul 1;589 (Pt 13):3383-93. Epub 2011 Apr 26.

Matsui T, et al. Brain glycogen supercompensation following exhaustive exercise. J Physiol. 2012 Feb 1;590 (Pt 3):607-16. Epub 2011 Nov 7.

It used to be cancer that was hidden, something that people didn’t want to talk about because of the associated connotations of illness, pain and dying.
The big taboo of today remains on the table, with as yet too little serious or major concerted input particularly on the part of Governments, to put this subject on everybody’s lips and get some action happening, and quickly.

What is this taboo?

It’s called dementia, the disease we are scared of, too scared to move out of the blaring headlights that are warning us of the impending tsunami of people likely to be living with or caring for someone with this disease.

The release of the film “The Iron Lady” may help with this, by encouraging discussion between families, between friends and perhaps politicians to really look at what dementia actually is, and what we can all do to help ourselves to resist the onset of this disease as well as to know what to do if we ourselves, or our partner or family member is affected.

In a newspaper article in the London Evening Standard Jan 11th the British Government Minister for Mental Healthcare Paul Burstow commented on the fact that there are over 40,000 people living in London who have dementia and are unaware of it. Now that is a worry.

There are already 65,000 people in London who have been diagnosed with dementia, with 26,00 receiving some form of treatment.
He worries that this lingering taboo means many of these people face a delay in diagnosis or appropriate help because of the stigma attached. It’s easier to ignore or deny a parent’ s increasing forgetfulness and memory lapses until the crunch time occurs. This condemns them, to what he believes is a more miserable life and who will in the long run end up in hospital, receiving poorer care that may not be dementia specific. It of course removes the precious time remaining to them, when they and their families could be receiving advice and counselling about the management options and help care that is available.

This undiagnosed group is similar to those people who do not know they have diabetes. It has been known for a long time that there are probably an equivalent number of people who have diabetes, but do not know it, as there are people diagnosed with the condition.

If you have dementia and do not know it, what impact does that have on your own personal safety and those of others if for example you are out and about or driving a car?

Paul Burstow believes it is vital to bring dementia “out of the shadows” and wants London to become the first capital city in the world to be recognised as being “dementia-friendly” where staff in shops, Tube stations, superstores and cinemas are specially trained in helping confused people.

Whether you live in London, Sydney or Timbuktu, the primary message is that it is vital we are not afraid to speak up and talk about dementia.

We need to give ourselves permission to find out if we have memory problems, whether we do have a condition such as dementia and what we can do to ensure we keep safe while living in the community and to be able to access appropriate help.

As we reach our forties and fifties, we start to notice a few changes with our brain. We forget things more easily, we experience more “tip of the tongue moments” and find it harder to stay focused or on task. We put it down to the fact that our speed of mental processing is slowing down. We may even have a couple of fleeting worrying thoughts that our brain might be showing the first signs of actual cognitive decline.

One of the biggest fears people express about ageing, is the loss of our mental faculties. That loss of that of course, has a significant impact on our ability to remain self-caring and independent.

Until now, the onset of actual cognitive decline has been thought to occur in our sixties. The clinical onset of Alzheimer’s disease typically occurs around age 65 or older, although it is well recognized that the actual condition slowly and silently develops over the preceding couple of decades. Brain scans can now show the pathological changes in younger brains, before the clinical signs of disease.
Those showing the greatest amount of pathological change in their brains are also known to be at greatest risk of developing clinical signs of dementia in later life.

Findings from a couple of studies (including a longitudinal study from Seattle, which has been following a group of 500 individuals since 1956) have suggested that cognitive decline did not start before the age of 60.
Those findings have now been challenged by a new study recently published in the British Medical Journal which has found that the age of onset of cognitive decline may be significantly earlier than previously thought: actually starting in our mid forties.

This study of 10308 men and women civil servants aged 45 to 70 years from London UK was set up to examine whether different age groups showed differing levels of cognitive decline over a ten-year period. The group underwent tests of memory, reasoning, vocabulary, phonemic and semantic fluency in three different assessments over the ten-year period.

The results of the study showed the following:

Between the age of 65 and 70, men on average showed a -9.6% decline in cognition,
women -7.4%. This was not unexpected.

However results of the younger age group age 45 to 49 also showed evidence of cognitive decline, albeit at a lower percentage; -3.5% cognitive decline for men and -3.6% for women.

The implications of this study suggest that we need to be taking a much closer note of how we are performing in midlife. Along with midlife obesity, high blood pressure and high cholesterol, our midlife cognitive function appears to be very important in determining how we will fare as we age.

If cognitive decline is picked up in our midlife, then at least that provides some valuable time to be putting into place specific strategies to to minimize any further decline and attempt to build cognitive reserve. What we don’t know (and requires further study) is whether midlife cognitive decline will lead to actual dementia – however it would seem prudent to do whatever we can, to keep our brains intact.

So what is the best thing we need to be doing in our midlife?

It’s all about maintain and improving brain function by adopting brain healthy lifestyles:

Eat healthily with a wide variety of green vegetables, fruit, lean proteins, seeds and nuts and keeping away from pies, pasties, cakes and biscuits, hot chips and fried foods.

Maintain a positive attitude to life. Being social engaged and active helps to keep stress levels down and stave off anxiety and depression.

Use your brain to learn new skills. Aim to include mental activities every day that are outside our usual habits. Card games, Sudoku, brain games, and apps are all useful.

Move your body. One of the biggest things we can do for our brain is to ensure we spend a minimum of thirty minutes every day doing some form of physical exercise – enough to get the heart rate up.

So next time you have a memory lapse, forget an appointment or lose your keys while it might simply a slower speed of processing, it could be an indication of a more serious reduction in your cognitive ability. So rather than ignoring it, be proactive and take the time every day to help restore your mental sharpness. Your brain may depend on it.

Ref:

Singh-Manoux,A.et al Timing of onset of cognitive decline: results from Whitehall 11 prospective cohort study. British Medical Journal 2012; 344 doi: 10.1136/bmj.d7622

During the last twelve months I have done a lot of writing – a book, my blog posts, some articles, presentations and workshops. They have all been completed with me being in a certain position i.e. sitting at a desk in front of my computer.

I’ve never had to spend so much time on my derriere before and I have to say I noticed a few things.

Firstly something which I can only describe as “writers bottom”, an intense desire to get up, jump up and down or move to do anything physically that would relieve me from the torment of having to sit a moment longer.

I have always endeavoured to ensure I exercise daily, with a 30 to 40 minute walk, some yoga plus a swim a couple of times a week, but this no longer felt adequate to help keep my brain cells firing.

Thirdly I started experiencing backache and various other aches and pains I had never had before. Was it my age I pondered? It was only when I took action to help my sore back by having some physio, doing some cycling and doing yoga that the penny finally dropped – I had advanced “sitting disease” which was impacting my physical and mental well being. Time to change!

But how many of us are not in the position to allow for that change? Luckily I won’t be as dormant next year, as my work will be involving a lot more movement with walking and standing. But if you are a sedentary worker having to sit every day in front of your desk how can you do things differently and overcome the sitting disease?

And it’s not just our bottom, which feels the impact; our tummy muscles lose tone and we tend to put on weight too. The spread of the derriere is accompanied by a spread around the middle. So if your clothes are getting a bit tight and your tummy is protruding more than it used to, perhaps it’s time to consider how much time you are sitting and find a way to sit less.

This week a colleague shared this video clip from Dr Mike, which is one of the best health promotion videos I have seen for a while. He explains exactly WHY exercise is the best prescription your doctor could ever prescribe because it is the remedy to assist so many of our modern day ailments: obesity, depression, hypertension, diabetes, heart disease, arthritis and dementia.

So do yourself a favour, no make that two…..

Firstly watch this video and then commit to filling in your daily prescription of “finding thirty” every day.
And why am I going on about sitting too much? Because of the negative effect it has on our brain function. We evolved to move because it stimulates the production of neurochemicals that support and nurture our existing brain cells as well as promoting the production of new neurons every day.
We need to “find thirty” every day as a minimum to keep our brain working at it’s very best.

So let’s make “sitting disease” and “writer’s bottom” a thing of the past and look to creating a more “brain fit” you.

It’s always good to hear encouraging news, especially when it is about a potential treatment for Alzheimer’s disease. A recent report on the evening news spoke about a vaccine being developed through the University of Sydney.

Associate Professor Lars Ittner from Sydney’s Brain and Mind Research Institute is leading a study into developing a vaccine that targets a specific brain protein called tau that is associated with Alzheimer’s disease and fronto- temporal dementia.

In people with dementia, the tau protein forms what are called neurofibrillary tangles, which leads to neuronal death and loss of brain function.

In this study on mice, the vaccine was shown to slow down the development of further neurofibrillary tangles. There was no effect on those tangles that had already formed. So the prospect is that it might be possible if future development of this vaccine occurs for this to be be used in humans once the diagnosis of dementia has been made, and slow down progression of the disease. It is not a cure, but it could buy the person more time for cognitive functioning and possibly work as a preventative if someone is perceived to be at higher risk of developing dementia.

Other researchers around the world have also been looking to develop a vaccine, one to either target tau or amyloid.

Professor Ittner commented that in many studies, vaccines were being trialled in mice with dementia, prior to the onset of clinical symptoms. This study is the first to show that a vaccine targeting tau can be effective once the disease has set in. It is known that the pathological changes associated with Alzheimer’s disease start many years before the clinical onset of symptoms. Having a treatment to slow down further progression would be huge step in the right direction.

Earlier this year I wrote a blog about a nasal spray being developed to minimise the potential risk of vascular dementia.

Researchers at Georgetown University, Washington D.C have found that if an antibody is given later in the progression of Alzheimer’s the greater the chance that it will trigger brain inflammation.

In their studies, mice with Alzheimer’s symptoms were given an antibody called PFA1, which was designed to clear amyloid from their brains. Those mice with the greatest amount of amyloid present at the beginning of treatment showed a greater inflammatory response. The take home from this was that the greatest benefit to lower the amount of amyloid would be obtained by using it early on i.e. in the early stages of the disease.

In Germany, researchers at the University of Rostock are investigating a protein ABCC1, which has been shown to help remove amyloid from mice brains. They have also been using a drug commonly used for treating nausea and vomiting (thiethylperazine) to activate this protein, suggesting that using this drug could be of potential benefit to prevent the development of amyloid plaques.

In the US, Scott Webster at the Georgia Health Sciences University in Augusta is also working on an Alzheimer’s vaccine. His vaccine is targeted versus two brain proteins: amyloid and RAGE (receptor for advanced glycation end-products). The RAGE protein helps the amyloid get into the brain and contributes to the inflammatory process that the amyloid causes to the brain’s neurons.

Webster’s vaccine is different in that it targets these two proteins. The vaccine uses the body’s own immune system to protect against the overproduction of RAGE and amyloid. His vaccine is different also in that it can be taken orally thus using the gut’s bacteria which are vital to our immune system. Previous vaccines developed elsewhere that have targeted just amyloid, have failed to show benefit in clinical trails and some have also had significant side effects. By targeting the two proteins, Webster is more hopeful that this combination effect will lead to reducing or eliminating the toxic effects of the brain inflammation. Early results in animal studies have been encouraging so far, so the next step will be to use the vaccine trialled in larger animal studies.

With all this amazing work going on around the world we are surely moving closer to having more effective treatments that will be able to stop Alzheimer’s in it’s tracks.

Refs:

Bi M, Ittner A, Ke YD, Götz J, Ittner LM (2011) Tau-Targeted Immunization Impedes Progression of Neurofibrillary Histopathology in Aged P301L Tau Transgenic Mice. PLoS ONE 6(12): e26860. doi:10.1371/journal.pone.0026860

American Friends of Tel Aviv University (2011, February 28). An Alzheimer’s vaccine in a nasal spray?. ScienceDaily. Retrieved December 10, 2011, from http://www.sciencedaily.com¬ /releases/2011/02/110228104310.htm

Markus Krohn, Cathleen Lange, Jacqueline Hofrichter, Katja Scheffler, Jan Stenzel, Johannes Steffen, Toni Schumacher, Thomas Brüning, Anne-Sophie Plath, Franziska Alfen, Anke Schmidt, Felix Winter, Katja Rateitschak, Andreas Wree, Jörg Gsponer, Lary C. Walker, Jens Pahnke. Cerebral amyloid-β proteostasis is regulated by the membrane transport protein ABCC1 in mice. Journal of Clinical Investigation, 2011; DOI: 10.1172/JCI57867

Georgia Health Sciences University (2011, September 26). Research points new way to possible Alzheimer’s vaccine. ScienceDaily. Retrieved December 10, 2011, from http://www.sciencedaily.com¬ /releases/2011/09/110926104609.htm