This is a review of “Beat City” – a Nintendo DS (2D) game that I believe has all the hallmarks of something that, although designed purely for pleasure, may actually improve brain function. A recent scientific review outlined several video games that, despite being developed only with gameplay and sales in mind, were nonetheless found to improve visual perception, sustained attention, task switching, rapid option selection and several other vital aspects of cognition. With this in mind I’ve been keeping an eye out for other games that might fall into this category.
Kids who play a musical instrument boast better language development than their peers who do not. The Einstein Aging Study found that elderly participants who regularly play a musical instrument exhibited greater cognitive reserve than those that did not – helping them keep the ravages of Alzheimer’s at bay for longer.
The upshot is that whether you’re very old, very young or somewhere in between, not only can playing a musical instrument create a torrent of activity in your brain’s pleasure pathways, but it can also be of long term benefit for a variety of different brain areas that support several cognitive functions.
Beat City involves travelling around a comic book stylised world on a mission to bring music back into the lives of local inhabitants – by tapping along to the beat of a variety of electronic tunes. You are the “Synchroniser,” a brave inhabitant of Beat City who is hell-bent on freeing his fellow citizens from their banal tuneless existence. En route you encounter several bizarre characters with whom you must do battle by tapping, swiping and holding the beat in time to music of varying complexity. Although upon first appearances it may seem to be aimed at younger audiences, this game gets tough – tough enough to provide even those naturally musical people out there (even my girlfriend who reached grade 8 in three different musical instruments!) with a challenge as you progress through harder and harder levels.
For the rest of us even the early levels can prove quite taxing. Hitting a rich vein of form is rewarded with a visual technicolour treat. The muted greys of Beat City are yanked out of their dreary and monotonous existence by your beat perfect music making, with the screen springing into life with a vivid burst of colour (and the characters ending up wearing increasingly bizarre fancy dress outfits.)
Reproducing a beat with accurate timing taxes a fair few different brain areas. The auditory cortex – distributed predominantly across the upper level of the temporal lobes (see diagram on the right) – crunches the soundwaves into what we actually hear through a division of labour across different patches of brain cortex which each extract different types of information. Firstly, the sound is separated out into its different frequencies at the cochlea in the inner ear and ferried to the primary auditory cortex (shown inset on the right). Some specialist areas are involved in establishing the rhythm. Others find and create the perception of melody. Functional units residing predominantly in left side of most people’s brain will extract the meaning from words in a song. Others, mainly in the right half of the brain, extract the emotional tone of the music. Then there are the brain areas involved in tapping along to the beat: pre-motor regions of the frontal cortex plan the movements and the motor strip triggers them. In order to get the timing just right, the cerebellum – hanging off the back of the brain – finesses the signal on its journey from brain to finger muscles to ensure that the stylus hits the touch screen precisely in time with the beat as opposed to a little too early or late. In Beat City, the accuracy with which you time each tap is indicated on screen by the size and colour of a musical note.
To recap: different brain areas simultaneously extract different features from the sounds that reach the ear to creates sense of hearing in our everyday lives. Patterns in the sound are automatically extracted and we naturally anticipate when the next sound is likely to occur, enabling us to synchronise our actions according to the patterns in the sounds. This instinctive impact of rhythmical sound on movement is where the urge to dance comes from.
Clapping, singing or playing a musical instrument requires different cognitive functions to operate simultaneously and interactively. Having to listen to, follow the rhythm of and anticipate changes in a musical score in order to producing carefully coordinated finger, hand (and for wind instruments: also mouth and respiratory tract) movements is a highly cognitively demanding task. Growth of extra connections (and therefore increased efficiency) in brain areas involved in perceiving sounds and producing accurately timed, precise, carefully coordinated movements are just the front and back ends of the brain workout.
In addition, prefrontal brain areas responsible for working memory, anticipation, vigilance, error correction and many other cognitive functions are also put through their paces by virtue of having to ensure that the two processes are properly integrated.
At the end of the day even if Beat City doesn’t inspire the desire to play a proper musical instrument, enabling the full brain-benefits of musical engagement to be earned, I believe it is nonetheless an effective way of challenging and thus improve your capacity for working memory, concentration and fine motor control that will come in useful in everyday life as well.
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This brainpost complements Dr Jack’s recent appearance on ITV1 on Fri 12th August 2011. It’s tricky to do such an important brain topic as AGING GRACEFULLY justice in just a 10 min slot on THIS MORNING (ITV’s flagship live daytime magazine show in the UK). Talking openly and honestly about highly emotive topics like Alzheimer’s disease, and dementia in general, is a very delicate matter. Given the prevailing time pressures of live television and the quick/punchy explanations that it requires, there is always the potential to be misunderstood. This means that really hot topics must occasionally be left out in case they have the unintended effect of causing undue anxiety as opposed to the specific intention: inspiring the public with what we can do to hang onto our marbles well into old age. This brainpost reveals a new breakthrough in our understanding of Alzheimer’s disease, deemed too risky to mention on live television in case it was misconstrued, but which may one day be instrumental in keeping dementia at bay in each and every one of us.
COLUMBO’S DEMISE FLAGS MECHANISM FOR ACCELERATED DEMENTIA
A recent article in the Daily Mail described how Peter Falk, the actor who played Lieutenant Columbo in the famous 70′s detective series by the same name, rapidly declined from mild into severe dementia in just one year. In early 2007 he was acting in a feature film, but by the end of that same year, after a series of dental operations, his daughter was in court filing for legal guardianship of her father because he could no longer recognise familiar people, places or objects. Such tragic stories inspired recently published research investigating possible links between acceleration of progression from mild to severe dementia and seemingly unrelated health problems.
Professor Clive Holmes and colleagues at the University of Southampton published a paper in last month’s Neurology journal, which may provide an explanation for the mighty Columbo’s rapid descent into severe dementia. They monitored a group of 300 people with dementia over 6 months and found that, when certain elements of the immune system were mobilised, the incidence of certain neuropsychiatric symptoms doubled. This may suggest that Peter Falk’s rapid decline into severe dementia may have been caused not by the series of dental operations per se, but rather his immune system’s response to those operations. Professor Holmes’s investigation observed elevated concentrations of tumour necrosis factor (TNF), amongst others, in individuals whose dementia-related “sickness behaviour” worsened during the 6 month monitoring period.
TUMOUR NECROSIS FACTOR – double-edged sword
TNF is involved in the inflammatory response to tissue damage and its major role is to regulate the function of immune cells. TNF is also something of a grim reaper as far as cells in our bodies are concerned, as it can induce apopotosis – programmed cell death. Apoptosis might sound like a bad idea but it is actually very important for cells to have a self-destruct button, otherwise removal of malfunctioning cells would be impossible. TNF is a natural component of our immune system that kills off, amongst other things, dangerous damaged cells that start to multiply out of control i.e cancerous tumour cells: Tumour – cancer; Necrosis – killing; Factor – agent. So, when you see TNF, think “Cancer Killing Agent.” However in a person with Alzheimer’s disease, whose brain cells are being increasingly clogged up with neurofibrillary tangles and stuck together with the accumulating amyloid plaques, it seems that high levels of TNF make matters worse by accelerating the onset of severe dementia.
HALTING DEMENTIA with ARTHRITIS DRUGS?
TNF has long been implicated in autoimmune illnesses such as rheumatoid arthritis. Many drug companies have invested vast sums of money in order to bringing anti-TNF drugs to market as an effective treatment for rheumatoid arthritis. Many severely arthritic individuals across the globe are currently enjoying significantly improved quality of life as a result of using such “biologics” to reduce the swollen joints that often leave people with terrible pain and significantly reduced mobility. But that’s not all. Recent studies have revealed that TNF plays a significant role in the development of Alzheimer’s disease and that treatment with anti-TNF drugs can improve dementia symptoms considerably. Indeed, more than 10 years ago a Danish study revealed that levels of TNF in elderly people were elevated and that TNF levels were positively correlated with dementia. An American study came to a similar conclusion. But of course back then these marvellous anti-TNF drugs hadn’t yet hit the market.
Unfortunately the anti-TNF drugs currently taken by individuals with arthritis are largely ineffective in combating dementia. This is because they simply cannot get from the blood stream into the brain (unless they are injected directly into the spine.) This is because the Blood Brain Barrier (BBB), which wraps around every blood vessel that passes through the brain, tightly regulates which molecules are allowed into the brain. Large molecules like these dementia-smashing anti-TNFs are most definitely “not on the list” so although there are many elderly arthritis sufferers with plenty of the good stuff sloshing around in their blood stream, it simply can’t get into the party. In their current form these drugs are unlikely to play a significant role in keeping dementia at bay given how impractical, not to mention dangerous (given the infection risk), repeated spinal injections are.
TROJAN HORSE TO THE RESCUE?
Brand new drug technologies can however attach therapeutic compounds to naturally-occuring molecules that are on the BBB list – a so-called “molecular Trojan horse.” Special transporter proteins embedded in the BBB “recognise” the shape of the naturally-occuring molecule as friend rather than foe, allowing it to attach to the transporter protein and be pulled, along with the attached anti-TNF compound, inside the brain. Once drug companies have managed to create anti-TNF Trojan molecules, acceleration of dementia can be prevented by suppressing TNF activity in the brain. In the not too distant future, we might all soon find ourselves keeping Alzheimer’s at bay with anti-TNF drugs that ride Trojan horses to the rescue by defending our brains from the perils of TNF “friendly fire.”
In addition to these weekly brainposts you can also catch Dr Jack’s daily #braintweet by following him on Twitter.
Contrast the lifestyles of people in their seventies who do and do not suffer from Alzheimer’s disease and clues about how to keep your brain ticking over nicely, well into old age, jump right out at you. Those who do not suffer with this dreaded disease tend to have been more committed to a regular exercise regime throughout their later years; hitting it as hard as their inevitable physical infirmities would allow (TOP TIP: Tai Chi is an excellent example of a low impact physical exercise which improves strength and flexibility at any age. It requires no equipment and can be practiced wherever you happen to be). They tend to have been more engaged in a wider array of social activities. They tend to have been careful with their diet in the long term, favouring a healthy Meditteranean-style diet (see below for more) over a typical modern Western diet (often high in saturated fats and sugars). They also tend to have been more proactively involved with their local community and more motivated to seek regular mental stimulation. People are now being advised to adopt a variety of brain-healthy habits if they wish to reduce the likelihood of developing cognitive deficits that the progression of Alzheimer’s disease can, but does not always, induce.
Alzheimer’s disease is the most common of the many different types of dementia, affecting 10% of those over 65 and almost 50% of people over the age of 85 (Evans et al, 1989). Dementia describes a syndrome that involves progressive cognitive decline occurring at an accelerated pace compared to the very gradual loss of mental faculties associated with normal aging. Dementia can involve the deterioration of reasoning, judgement, thinking, mood control, language, understanding and, most famously of all, memory. Colloquially-speaking, Alzheimer’s disease is an almighty metabolic cock-up: a brain protein (beta-amyloid) is not constructed properly due to a misprint in the genetic recipe, causing it to form tiny sticky clumps (plaques) that develop between brain cells, preventing them from communicating with each other properly and eventually killing them off entirely. To make matters worse neurofibrillary tangles accumulate within brain cells, which also ultimately leads to cell death.
Depending upon which brain structures these plaques form in, different mental functions can be disturbed. For instance, a brain structure that typically gets more than its fair share of amyloid plaques and neurofibrillary tangles in Alzheimer’s is the hippocampus. As I’ve described in a previous brainpost this brain structure is critical for the formation of memories and so when its function is compromised by the plaques and tangles of Alzheimer’s, people can become extremely forgetful.
To date, scientific research has yet to come up with a treatment to stop the formation of these amyloid plaques and neurofibrillary tangles, but there is evidence that drug treatments designed to boost the cholinergic neurotransmitter system can make symptoms less severe. Furthermore and extensive body of studies has gradually accumulated over the past 20 years to indicate that some people are able to tolerate the disruption caused by these plaques better than others (e.g. Katzman et al, 1988). The Katzman study described individuals who had shown no cognitive impairment whatsoever in life, yet post-mortem examination of their brains revealed that telltale signs of Alzheimer’s disease (the plaques and tangles) which had progressed to a considerable degree. This disparity begs the question: if two people’s brains are affected by the same degree of plaque damage, why does one continue to enjoy normal mental faculties, whilst the other suffers severe impairments to their memory, thinking and mood? The concept of “cognitive reserve” was introduced to describe brains which seemed to be able to compensate for the damage done by Alzheimer’s, presumably by using other brain networks not affected by the metabolic damage to take over certain cognitive tasks.
A separate study, this time involving 593 individuals in New York over the age of 60 and on an “at risk of dementia” register, concluded that “increased educational and occupational attainment may reduce the risk” of developing Alzheimer’s disease. A more recent study conducted in the UK concluded that cognitive reserve is almost entirely mediated by childhood cognitive ability and educational attainment, whilst whether people had successful careers or not had very little influence. So does this mean that the only way to “plaque-proof” yourself is to study hard at school and stay in education for as long as possible? Well, yes and no. Yes – in the sense that this certainly seems to protect you from the ravages of amyloid plaque buildup. No – because there ARE things you can do to build up your cognitive reserve in later life, they just have nothing to do with what you do for a living and how good you are at it.
Diet may well influence the rate at which Alzheimer’s disease progresses, probably due to the negative influence of a modern Western diet on the brain’s blood vessels. In a recent article, prominent Alzheimer’s researcher Dr Scarmeas describes a study providing evidence that a traditional Meditteranean diet – characterised by lots of fish, unsaturated fats, vegetables, fruit and cereals – seems to protect against the development of Alzheimer’s disease. In a different study which used a mouse model of the disease it was suggested that coffee may help to slow the progress of Alzheimer’s disease by preventing build up of amyloid plaques.
A recent NYT article describes research into bilingual people who seem to develop the symptoms of Alzheimer’s on average 5 or 6 years later than those who speak only one language. This suggests that the cognitive demands of regularly switching between two or more languages may delay the onset of Alzheimer’s. Although this has yet to be proven, it is thought that speaking two languages may increase cognitive reserve by improving the function of prefrontal brain areas involved in executive control. Executive control involves mental functions like holding relevant information in working memory whilst ignoring irrelevant distractions, as well as other faculties relating to problem solving, planning and decision making.
In the not-so-distant future it may be possible to replace brain cells damaged by the abberent metabolic processes of Alzheimer’s with fresh ones created from a person’s own skin cells. Other recent research has suggested that the amyloid plaques might cause memory problems by attaching to certain important neurotransmitters, and that drugs preventing this from happening may help to ease the symptoms of memory loss associated with Alzheimer’s disease. In light of the importance of early intervention to catch the disease before it causes too much damage new scanning techniques have already been developed to spot the disease before it induces any clinical deficits.
A variety of lifestyle changes can build up cognitive reserve, helping to keep dementia at bay and improving quality of life to boot!
In addition to these fortnightly brainposts you can also get DrJack’s daily #braintweet by following him on twitter.