Protect your brain
It is by no means a certainty that we lose some of our cognitive abilities as we grow older. There are steps that can be taken to preserve brain health.
A while back, Malaysia left the ranks of developing countries to join the world community as a Newly Industrialised Country (NIC). We are now in the post-industrial age. Citizens young and old now face a brave new world in which new gadgets seem to be launched every few months (at least it feels like it).
While the young can rapidly learn to use each new gizmo, the not-so-young labour to master these mysterious technologies, be they automated teller machines, cell phones, digital cameras or remote controls.
It is not possible to survive as a Luddite (defined in MSN Encarta as an opponent of new technology), even in Malaysia.
What this means is that, each of us, young and old, are required to keep our wits about us and to try and maintain our brain function for as long as possible.
The good news is that significant loss of mental ability is no longer considered to be part of normal ageing. Mental decline is therefore not inevitable.
Our cognitive function – that is, the ability to remember, learn, think, and reason – can in theory, be preserved right up to advanced old age.
Severe mental decline, termed dementia, is caused by disease processes: it is not a predestined part of ageing.
Keeping mentally agile
A healthy lifestyle with satisfying work and social engagement goes a long way towards preserving our brain health. But can we, on our part, do more to enhance this benefit?
For this to be achieved, we look to medical science for answers: a lot of research is in progress with this objective in mind.
Like all successful projects, to tap the brain’s full potential, conditions have to right from the moment of conception (choose your parents!), and subsequently nurturing development in the womb and through early childhood.
This foundation must be built upon with an up-bringing which promotes intellectual and social development. It is then maintained through continued life-long learning and engaging in activities to stimulate the brain to compensate for cell loss and injury.
Your diet should contain brain-enhancing nutrients. It should be low in saturated fat, without excess of carbohydrates, and contain adequate amounts of fruits, nuts and vegetables to provide vitamins, minerals and essential fatty acids.
To maintain mental agility, avoid causing damage to your brain. Other than accidents, the major cause of head injury in young people is high risk sports and recreational activities.
You don’t have to be a boxer to be at risk of serious brain damage. A recent study done in Canada showed that brain concussion in youth may result in subtle mental and physical malfunction even 30 years later.
And of course, it is well known that alcohol and drug abuse cause damage to the brain.
Understanding normal brain ageing
Scientists are making significant progress in understanding what constitutes normal brain ageing.
While brain scans appear to indicate that brain size is reduced with advancing years, it has been shown, to our pleasant surprise, that the actual number of nerve cells does not seem to decline with age.
A study done at the Harvard Medical School on 27 normal people, aged between 56 and 103 years, found that reduced brain size was due to loss of nerve cell architecture, rather than fewer numbers of neurons.
Another long-held dogma is that the mature brain is incapable of growing new cells. In fact, recent experiments showed that the adult brain is capable of generating new nerve cells in the hippocampus (a region of the temporal lobe), indicating that the brain has the ability, albeit limited, to repair itself.
Brain regeneration
While brain repair is theoretically possible, it is obviously insufficient to heal the massive damage seen in diseases of neuro-ageing such as stroke, Alzheimer’s disease and Parkinson’s disease. What’s needed are large numbers of brain cells to replace those lost in such conditions.
You may remember that President Barack Obama’s campaign platform included the call to promote embryonic stem cell research. Perhaps not coincidentally, now that he has been inaugurated, the US Federal Drug Administration has approved the first human trials of embryonic stem cells, which are cultured from human embryos.
In this preliminary study, nerve cells derived from such stem cells will be tested for their ability to repair nerve damage in a small group of spinal-cord injury patients.
However, the use of such embryo-derived stem cells is the subject of ethical debate.
Earlier, researchers at the University of Florida had demonstrated in animal studies that mature human brain cells were also able to generate new brain tissue. These cells could be induced to multiply into large numbers and could in theory serve as brain tissue transplants.
The authors claimed that these “findings document for the first time the ability of common human brain cells to morph into different cell types …”
Therefore, to circumvent the objection to the use of embryonic stem cells, much work is now focussed on adult stem cells, which are obtained at present mostly from the bone marrow (the soft tissue within our large bones). These primitive cells can be coaxed to change backward to a more immature form and later stimulated to differentiate into more specialised cells such as nerve, kidney, heart or other kinds of tissue – a case of one step backward, two (or more) steps forward.
Stem cell transplants are still a long way off from being a viable treatment. Of much greater immediate potential is the development of cell populations (micro test kits, so to speak) to investigate the safety and effectiveness of new drugs.
For example, there is an urgent need in patients with acute stroke for salvage treatments to prevent other at-risk cells from dying. This is termed neuroprotection, that is, mechanisms which protect neurons from cell death and/or apoptosis (cell suicide), following any form of damage.
It is also possible to induce these cells to produce nerve growth factors (neurotrophins) which could help brain tissue repair and revive, by altering their DNA programming.
What’s available for treatment: today, and in the future
Handling of cellular junk
A number of the diseases of brain ageing have been found to be associated with the accumulation of cellular junk. A well known example is Alzheimer’s disease, which causes dementia (loss of brain function). In this condition, the cell debris consists of amyloid plaques which are composed of abnormal mis-folded proteins.
Strategies being developed to overcome this include blocking the formation of amyloid and vaccines which stimulate the immune system to attack the amyloid.
Sirtuins are proteins which play an important role in ageing, cancer, diabetes and obesity. They mediate the effect of resveraterol, the active principle in red wine.
A study found that one such inhibitor of sirtuin 2 mitigated the toxic effects of cellular junk (in the form of inclusion bodies) in an experimental model of Parkinson’s disease.
Enhancing impaired nerve function
Identifying which nerve circuits fail in Alzheimer’s disease allows us to target our treatments.
·Cholinergic drugs
Nerve cell loss in Alzheimer’s disease is most profound in the cholinergic pathways where acetylcholine acts as neurotransmitter (a chemical that transmits the nerve signal from one neuron to the next). Acetylcholine is broken down by the cholinesterase enzyme. Cholinesterase inhibitors are formulated to augment cholinergic nerve transmission. Members of this class of drugs are donezepil, rivastigmine and galantamine.
·Anti-glutamatergic drugs
On another front, it is believed that a malfunction of glutamatergic circuits results in overstimulation of the N-methyl-D-aspartate (NMDA) receptor, thereby causing excitotoxicity. This can be reduced by an antagonist of NMDA receptors such as the drug memantine.
Neuroprotection
Neuroprotection has long been a goal in the approach to neuro-ageing diseases. There are hints that this benefit may come from a number of drugs: some old, and others still under study.
·Monoamine oxidase inhibitors
Monoamine oxidase B (MAO-B) is an enzyme which breaks down dopamine and other chemical transmitters during normal brain functioning. This process leads to formation of hydrogen peroxide, a noxious substance which contributes to oxidative stress and cell death.
Propargylamines are the first of these medications to show promising results in human studies. Selegiline and rasagiline are two members of this class of MAO-B inhibitors which are already in use for Parkinson’s disease.
·Multi-function drugs
Ladostigil is the first of new class of multi-function drugs now under study in Alzheimer’s disease. It is a dual acetylcholine-butyrylcholine-esterase and MAO inhibitor which has effects on cognition and depression, as well as conferring neuroprotection.
Iron chelators with radical scavenging and MAO inhibitory actions are also under development.
Beverages and the brain
Polyphenols are natural compounds present in tea and red wine. One class of these, the flavonoids, have multifunctional activities as iron chelators, radical scavengers, anti-inflammatory agents and neuroprotectants. In particular, a major constituent of green tea extract, (EGCG) is now under study.
As for coffee, there is an interesting inverse relationship between its intake and Parkinson’s disease. How it confers this benefit is not yet understood.
It is known that caffeine is a natural antagonist of adenosine receptors, which play a role in slowing down brain metabolism. Novel compounds are being developed which have combined effects of MAO inhibition and adenosine antagonism.
All things considered, that after-dinner beverage might do more good than simply washing down your meal!
- THE STAR
A while back, Malaysia left the ranks of developing countries to join the world community as a Newly Industrialised Country (NIC). We are now in the post-industrial age. Citizens young and old now face a brave new world in which new gadgets seem to be launched every few months (at least it feels like it).
While the young can rapidly learn to use each new gizmo, the not-so-young labour to master these mysterious technologies, be they automated teller machines, cell phones, digital cameras or remote controls.
It is not possible to survive as a Luddite (defined in MSN Encarta as an opponent of new technology), even in Malaysia.
What this means is that, each of us, young and old, are required to keep our wits about us and to try and maintain our brain function for as long as possible.
The good news is that significant loss of mental ability is no longer considered to be part of normal ageing. Mental decline is therefore not inevitable.
Our cognitive function – that is, the ability to remember, learn, think, and reason – can in theory, be preserved right up to advanced old age.
Severe mental decline, termed dementia, is caused by disease processes: it is not a predestined part of ageing.
Keeping mentally agile
A healthy lifestyle with satisfying work and social engagement goes a long way towards preserving our brain health. But can we, on our part, do more to enhance this benefit?
For this to be achieved, we look to medical science for answers: a lot of research is in progress with this objective in mind.
Like all successful projects, to tap the brain’s full potential, conditions have to right from the moment of conception (choose your parents!), and subsequently nurturing development in the womb and through early childhood.
This foundation must be built upon with an up-bringing which promotes intellectual and social development. It is then maintained through continued life-long learning and engaging in activities to stimulate the brain to compensate for cell loss and injury.
Your diet should contain brain-enhancing nutrients. It should be low in saturated fat, without excess of carbohydrates, and contain adequate amounts of fruits, nuts and vegetables to provide vitamins, minerals and essential fatty acids.
To maintain mental agility, avoid causing damage to your brain. Other than accidents, the major cause of head injury in young people is high risk sports and recreational activities.
You don’t have to be a boxer to be at risk of serious brain damage. A recent study done in Canada showed that brain concussion in youth may result in subtle mental and physical malfunction even 30 years later.
And of course, it is well known that alcohol and drug abuse cause damage to the brain.
Understanding normal brain ageing
Scientists are making significant progress in understanding what constitutes normal brain ageing.
While brain scans appear to indicate that brain size is reduced with advancing years, it has been shown, to our pleasant surprise, that the actual number of nerve cells does not seem to decline with age.
A study done at the Harvard Medical School on 27 normal people, aged between 56 and 103 years, found that reduced brain size was due to loss of nerve cell architecture, rather than fewer numbers of neurons.
Another long-held dogma is that the mature brain is incapable of growing new cells. In fact, recent experiments showed that the adult brain is capable of generating new nerve cells in the hippocampus (a region of the temporal lobe), indicating that the brain has the ability, albeit limited, to repair itself.
Brain regeneration
While brain repair is theoretically possible, it is obviously insufficient to heal the massive damage seen in diseases of neuro-ageing such as stroke, Alzheimer’s disease and Parkinson’s disease. What’s needed are large numbers of brain cells to replace those lost in such conditions.
You may remember that President Barack Obama’s campaign platform included the call to promote embryonic stem cell research. Perhaps not coincidentally, now that he has been inaugurated, the US Federal Drug Administration has approved the first human trials of embryonic stem cells, which are cultured from human embryos.
In this preliminary study, nerve cells derived from such stem cells will be tested for their ability to repair nerve damage in a small group of spinal-cord injury patients.
However, the use of such embryo-derived stem cells is the subject of ethical debate.
Earlier, researchers at the University of Florida had demonstrated in animal studies that mature human brain cells were also able to generate new brain tissue. These cells could be induced to multiply into large numbers and could in theory serve as brain tissue transplants.
The authors claimed that these “findings document for the first time the ability of common human brain cells to morph into different cell types …”
Therefore, to circumvent the objection to the use of embryonic stem cells, much work is now focussed on adult stem cells, which are obtained at present mostly from the bone marrow (the soft tissue within our large bones). These primitive cells can be coaxed to change backward to a more immature form and later stimulated to differentiate into more specialised cells such as nerve, kidney, heart or other kinds of tissue – a case of one step backward, two (or more) steps forward.
Stem cell transplants are still a long way off from being a viable treatment. Of much greater immediate potential is the development of cell populations (micro test kits, so to speak) to investigate the safety and effectiveness of new drugs.
For example, there is an urgent need in patients with acute stroke for salvage treatments to prevent other at-risk cells from dying. This is termed neuroprotection, that is, mechanisms which protect neurons from cell death and/or apoptosis (cell suicide), following any form of damage.
It is also possible to induce these cells to produce nerve growth factors (neurotrophins) which could help brain tissue repair and revive, by altering their DNA programming.
What’s available for treatment: today, and in the future
Handling of cellular junk
A number of the diseases of brain ageing have been found to be associated with the accumulation of cellular junk. A well known example is Alzheimer’s disease, which causes dementia (loss of brain function). In this condition, the cell debris consists of amyloid plaques which are composed of abnormal mis-folded proteins.
Strategies being developed to overcome this include blocking the formation of amyloid and vaccines which stimulate the immune system to attack the amyloid.
Sirtuins are proteins which play an important role in ageing, cancer, diabetes and obesity. They mediate the effect of resveraterol, the active principle in red wine.
A study found that one such inhibitor of sirtuin 2 mitigated the toxic effects of cellular junk (in the form of inclusion bodies) in an experimental model of Parkinson’s disease.
Enhancing impaired nerve function
Identifying which nerve circuits fail in Alzheimer’s disease allows us to target our treatments.
·Cholinergic drugs
Nerve cell loss in Alzheimer’s disease is most profound in the cholinergic pathways where acetylcholine acts as neurotransmitter (a chemical that transmits the nerve signal from one neuron to the next). Acetylcholine is broken down by the cholinesterase enzyme. Cholinesterase inhibitors are formulated to augment cholinergic nerve transmission. Members of this class of drugs are donezepil, rivastigmine and galantamine.
·Anti-glutamatergic drugs
On another front, it is believed that a malfunction of glutamatergic circuits results in overstimulation of the N-methyl-D-aspartate (NMDA) receptor, thereby causing excitotoxicity. This can be reduced by an antagonist of NMDA receptors such as the drug memantine.
Neuroprotection
Neuroprotection has long been a goal in the approach to neuro-ageing diseases. There are hints that this benefit may come from a number of drugs: some old, and others still under study.
·Monoamine oxidase inhibitors
Monoamine oxidase B (MAO-B) is an enzyme which breaks down dopamine and other chemical transmitters during normal brain functioning. This process leads to formation of hydrogen peroxide, a noxious substance which contributes to oxidative stress and cell death.
Propargylamines are the first of these medications to show promising results in human studies. Selegiline and rasagiline are two members of this class of MAO-B inhibitors which are already in use for Parkinson’s disease.
·Multi-function drugs
Ladostigil is the first of new class of multi-function drugs now under study in Alzheimer’s disease. It is a dual acetylcholine-butyrylcholine-esterase and MAO inhibitor which has effects on cognition and depression, as well as conferring neuroprotection.
Iron chelators with radical scavenging and MAO inhibitory actions are also under development.
Beverages and the brain
Polyphenols are natural compounds present in tea and red wine. One class of these, the flavonoids, have multifunctional activities as iron chelators, radical scavengers, anti-inflammatory agents and neuroprotectants. In particular, a major constituent of green tea extract, (EGCG) is now under study.
As for coffee, there is an interesting inverse relationship between its intake and Parkinson’s disease. How it confers this benefit is not yet understood.
It is known that caffeine is a natural antagonist of adenosine receptors, which play a role in slowing down brain metabolism. Novel compounds are being developed which have combined effects of MAO inhibition and adenosine antagonism.
All things considered, that after-dinner beverage might do more good than simply washing down your meal!
- THE STAR
MOHD ADHA MOHD ZAIN (ADHA ZAIN)
Blogger Informasi
