Caring for someone who is ill is emotionally and often physically draining as well.
Caring for someone who has Alzheimer’s or other form of dementia can often lead to the carers themselves becoming sick, exhausted, stressed, depressed, fearful and lonely.

In Australia we have over 250,000 people living with dementia, that’s over 1% of our total population. For every person with the disease there are on average 2.5 caregivers involved in their care. Often the primary caregiver is a spouse, partner or family member. They themselves may be relatively elderly with other associated health problems and susceptibility to stress induced cardiovascular illness and increased mortality.

With the number of people living with dementia expected to triple by 2050, we need to be looking at ways not only to assist the person with the illness, but also the carers themselves: providing sufficient support and access to appropriate services.

The problem in being a carer is not only does it increase your own risk of illness and exhaustion; the ongoing stress significantly increases your risk of depression and for developing dementia.

So what can be done to help alleviate some of the strain?

Dr Helen Lavretsky from UCLA Semel Institute for Neuroscience and Human Behaviour has published the findings of a new study, which examined the value of providing yoga meditation practice for carers.

What the study showed was firstly

1. An improved level of cognitive function and lower levels of depression and

2. A reduction in stress induced cellular aging

What does this means for carers?

Carers will often report high levels of emotional distress and 50% are at risk of developing clinical depression.
In the study, 49 carers (age range 45- 91) were either taught a brief 12 minute yogic practice that included chanting meditation Kirtan Kriya, or, if they were in the control group they sat in a quiet place with their eyes closed, listening to instrumental music on a relaxation CD for 12 minutes.

After 8 weeks of those in the mediation group, 65% showed a 50% improvement on a depression rating scale, and 52% showed an improvement on a mental health score.

This compared to a 31% depression improvement and 19% mental health improvement for the relaxation group.

So learning brief yogic mediation made a significant difference in a very short time frame. One would imagine that this would provide ongoing benefit if the carer was to continue with the practice on a daily basis. Professor Lavretsky commented that the benefits appear to be specific to Kirtan Kriya, which incorporates several different elements of chanting, finger poses and visualisation.She describes this as providing “brain fitness” in addition to the stress reduction.

The other interesting finding was in relation to cellular ageing.

At the end of our chromosomes we have what are called telomeres. An enzyme called telomerase helps to maintain our telomeres. If the enzyme telomerase activity is absent, then every time our cells divide, our telomeres get shorter until eventually the cells die. Promoting or maintaining a higher level of telomerase therefore helps our telomeres to be maintained and immune cell longevity.

In the study there was a whopping difference between the two groups in terms of increase in telomerase activity.

The mediating group showed a 43% improvement in telomerase activity compared to just 3.7% in the relaxation group.

Professor Lavretsky now plans a follow up study to confirm these findings using a neuroimaging study of Kirtan Kriya meditation. She has also incorporated yoga into the caregiver program as part of the UCLA Alzheimer’s and Dementia Care program. This program aims to provide comprehensive coordinated care, resources and support to both patients and caregivers.

The great thing about this study is the huge amount of benefit provided to the carers through a simple and inexpensive yoga program.
It would be fantastic if this could be made available on a wide scale to all carers as it could make all the difference between “just surviving” and “managing well.”

Ref:
H. Lavretsky, E.S. Epel, P. Siddarth, N. Nazarian, N. St. Cyr, D.S. Khalsa, J. Lin, E. Blackburn, M.R. Irwin. A pilot study of yogic meditation for family dementia caregivers with depressive symptoms: effects on mental health, cognition, and telomerase activity. International Journal of Geriatric Psychiatry, 2012; DOI: 10.1002/gps.3790

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

Neurons may not be the superstars we think they are after all. It may be our other brain cells, the glia, the ugly ducklings of the brain, which actually have the really important role.

When you think about brain cells you would normally be thinking about neurons. These are the brain cells involved in transmitting electrical impulses between themselves, releasing a selection of over 300 neurochemicals so that we can all enjoy our thoughts, feelings and actions. We have around 85 billion of them.

But there are an equal number of other brain cells in our heads which up until recently were thought of as merely having a supporting role, providing the glue to bind our brain cells together. Indeed glia comes from the Greek word meaning “glue”. Yet our glial cells are now being revealed to be equal superstars in their own right and studies are now starting to unravel the mystery of what the true role of our glial cells may be.

Welcome to the world of glial cells.

Researchers from the Tel Aviv University have been studying glial cells and have discovered that they are central to our brain’s plasticity: the ability of our brain to form new synaptic connections between other brain cells.
One type of glial cells are called astrocytes and it is these, which appear to be involved in controlling synaptic communication.

Our brain’s plasticity enables us to learn new information, store it and adapt to changing circumstances.

Maurizio de Pitta along with other researchers from the Salk Institute, the University of California and University of Lyon have developed a computer model which incorporates the influence of the glial cells on the transfer of information at the level of the synapse.

The parts of the brain most highly involved in memory and learning are the hippocampus and the cerebral cortex. Perhaps not surprisingly these areas are abundant in glial cells as well as neurons. So much so that for every neuron in these areas there are between two to five glial cells.

So what are these glial cells doing?

The researchers believe that the glial cells work as moderators of the neurochemical information being transported at the synapses
They can either ramp things up to prompt the transfer of information or slow synaptic activity down if the synapses are overactive. The end result? The glial cells basically are orchestrating the transmission of information for optimal brain function.

They do this by “listening in” to the neurons and communicating between themselves using the same neurotransmitter receptors as neurons but without using electrical impulses.

This major difference is that whereas neurons communicate with each other serially through their multitude of synaptic connections, glia communicate more widely like radio waves and at a slower pace than the zippy neurons.

Is this relevant to better understanding certain brain diseases?

Prof Ben-Jacob notes that these findings could have important implications for a number of brain disorders such as epilepsy and neurodegenerative diseases such as Alzheimer’s.

Glial cells and epilepsy

When a person has an epileptic seizure, the activity of neurons in one location spread and take over the normal activity of other locations This is explained as the glial cells here failing to adequately regulate synaptic transmission.

In other conditions if neuronal activity is noted to be low, the glial cells act to boost transmission of information by maintaining the synaptic plasticity between brain cells.

Glial cells and Alzheimer’s

Douglas Fields asks whether in Alzheimer’s the pathology occurs as a result of a failure of the associated glia to clear waste. These specialised microglia have a particular role in destroying bacteria and by clearing away diseased tissue promoting tissue recovery and repair.

Wolfgang Streit from the University of Florida has noted that the microglia degenerate and become weaker with age. In Alzheimer’s disease much of the early neuronal loss occurs in the area of the hippocampus. Streit has demonstrated that the degeneration of microglia follows a similar pattern leading to the question of whether Alzheimer’s disease is a problem associated with ageing microglia no longer able to perform their usual function of clearing waste such as amyloid.

Glial cells and chronic pain

A number of researchers from the US, Japan and the UK have discovered that both microglia and astrocytes respond to the activity of pain circuits following injury by releasing neurochemicals to support neurons and stimulate healing. What appears to happen in some cases is that the microglia don’t turn off when the healing is complete, a bit like the never ending porridge pot, so the pain circuits continue to fire.

Glial cells and mental illness

Research into depression and schizophrenia has shown that these conditions are associated with reduced numbers of glial cells – oligodendrocytes and astrocytes. Because astrocytes are associated with regulating the amount of neurotransmitters at synapses, having lower levels of these glial cells may be a contributor to these conditions. It has been proposed that targeting these glia may provide a new method of treatment.

As this fascinating research continues to unravel the mysteries of the true function of glial cells, we may have to change our previous perspective that our brain’s super plasticity is based on neuronal activity alone. It appears that we need our glial cells to keep our neurons on task and efficient – a bit like a master coach.

Refs:
Maurizio De Pittà, Vladislav Volman, Hugues Berry, Eshel Ben-Jacob. A Tale of Two Stories: Astrocyte Regulation of Synaptic Depression and Facilitation. PLoS Computational Biology, 2011; 7 (12): e1002293 DOI: 10.1371/journal.pcbi.1002293

Scientific American Mind: R. Douglas Fields The Hidden Brain May/June 2011 Pages 53 – 57