Professor Emeritus
A. David Smith of the University of Oxford has worked at the frontiers of
neuroscience for more than 50 years.In
particular he has been at the forefront of research into novel treatments and techniques
for Alzheimer’s disease and dementia.
A packed audience sat enthralled as
Emeritus Professor A. David Smith (University of Oxford, UK) spoke of his
research into novel treatments and techniques for Alzheimer’s disease and
Dementia during the BRNZ Inaugural Public Lecture on 3 February 2016 sponsored
by the Neurological Foundation and Brain Research New Zealand.
Then came this question from the
audience:
“Can we prevent Alzheimer’s?”
“Yes, we can!” was Prof. Smith’s
resounding reply.
Here’s How:
Prof. A. David Smith’s recommendations:
·
Stop
smoking.
·
30
minutes of brisk exercise each day (enough to get you puffing and sweating).
·
If
you have diabetes and/or high blood pressure, take drugs that effectively treat
these.
·
Increase
the Mediterranean elements of your diet, especially your 5+ a day of fruit and
vegetables.
·
Eat
fish once or more a week.
·
Watch
your blood glucose.
·
Make
sure your vitamin D and B12 status is good.
·
If you do have memory
problems, get your homocysteine checked.
(Homocysteine
is a common amino acid in your blood. You get it mostly from eating meat. High
levels of it are linked to early development of heart disease. In fact, a high
level of homocysteine is a risk factor for heart disease. It's associated with
low levels of vitamins B6, B12, and folate, as well as renal disease.)
·
If
it’s high, take B vitamins in consultation with your GP.
·
Keep
mentally and socially active
Here’s Why
Prof. Smith
cited, (among others), the Caerphilly Cohort Study. Read the full study
Twenty-five
years ago, 2,235 men between the ages of 45 and 59 agreed to take part in a
longitudinal study. They were tested
again in 2013.
The group who
had adopted these healthy behaviours:
·
Non-smoking
·
Consuming
more than 3 portions of fruit / vegetables a day
·
Consuming
less than 30% of calories as fat
·
Taking
daily exercise
·
Drinking
less than 3 units of alcohol per day
had a 64%
lower risk of dementia. It’s as simple
as that! (Visit the Neurological
Foundation for a full coverage of Professor Smith’s presentation.)
Is Alzheimer’s inherited?
When asked if
Alzheimer’s Disease is caused by our genes, Prof. Smith dispelled that myth.
‘Less than 1%
of dementia cases are entirely genetic’.
About 20% of
the population has common gene mutations (called susceptibility genes) which
may slightly increase the risk of developing dementia, but in 99% of all cases,
dementia does not have genetic causes.
Most common risk factors for dementia
are NOT genetic. Here they are:
·
Age
·
Smoking
·
Mid-life
high blood pressure, high cholesterol and obesity
·
Depression
·
Low
social activity
·
Physical
inactivity
·
Low
education
·
Diabetes
and high blood sugar
·
Low
intake of omega-3 fatty acids
·
High
blood homocysteine (due to low levels of B vitamins)
Here’s the best news! Dementia CAN be
prevented.
Please find below links
to an overview of Professor Smith's lecture on Dementia and his presentation.
1. Click here
for Professor Smith's presentation
2. Click here
for an overview of Professor Smith lecture
Science Note:
What’s the difference between Dementia
and Alzheimer’s Disease?
Dementia is
an umbrella term used to describe a group of conditions that affect how well
our brains work.
The most
common form of dementia is Alzheimer’s disease – which around two-thirds of
people with dementia have.
The symptoms
each person experiences depends on the parts of the brain that are affected.
However, the most common dementia symptoms include changes in memory, thinking,
behaviour, personality and emotions. These changes affect a person’s ability to
perform everyday tasks and interfere with their everyday lives.
Why does Alzheimer’s affect people
differently?
QUESTION: Both my mother and my father-in-law
suffer from Alzheimer’s disease. We’re told that they both seem to be at about
the same point in the physical progression of the disease. But my father-in-law
has remained fairly lucid, while my mother is more confused and forgetful. What
could account for this?
Harvard Medical School’s Adviser gives
the answer:
ANSWER: The tremendous number of nerve cells
and connections between cells in a healthy brain provide a seemingly infinite
capacity for processing information. It also provides a margin of safety in
case some cells are damaged. In Alzheimer’s disease, however, the wholesale
destruction of nerve cells eliminates this safety net, especially in the brain
areas involved in memory and cognition.
But as you’ve
noted, the disease doesn’t always affect people in the same way or with similar
severity. Consider two older people with the same amount of Alzheimer’s
disease–related plaques and tangles in their brains. One person has some memory
miscues now and then, but continues to lead a relatively normal life. The other
has the severe loss of memory and other cognitive deficits that typify
Alzheimer’s disease.
Why the difference? One explanation is that
they had differing amounts of cognitive reserve. Cognitive reserve can protect
you from the effects of Alzheimer’s and other diseases that affect the brain.
Cognitive reserve can be thought of as
having two parts, hardware and software. The hardware consists of brain cells,
or neurons, and connections between those brain cells, which are called
synapses. The theory is that people with more brain cells and synapses at their
disposal are better able to maintain cognitive functions even after important
brain cells are damaged.
The software
is the brain’s capacity for finding alternative circuits and neural networks if
disease or injury is blocking the usual ones. People’s cognitive abilities can
stay roughly the same if their brains are adept at these workarounds.
Brain reserve
capacity — the term sometimes used for the hardware — is, in large part,
genetically determined. But the human brain is capable of generating new
synapses and neurons throughout life, and the input of stimulating experiences
has been shown to alter brain structure.
There is
plenty of research to back up this idea. Brain scans of people learning to
juggle show increases in the size of brain structures linked with the visual
processing of movement. MRIs of the brains of London taxi drivers have shown
that they have larger-than-normal posterior hippocampi, an area of the brain
involved in spatial memory.
Formal
educational achievement is an important factor, but virtually any mentally
challenging or engaging activity seems to have a positive effect on cognitive
reserve.
Some research
has found that crossword puzzles, Sudoku and other “brain exercise” activities
have a narrow effect: That is, if you do Sudoku puzzles, you become better at
doing Sudoku puzzles and little else.
But a study
showed that Sudoku and other puzzles also made older people more open to trying
new things, so there’s still much more to be learned in this area.
Physical
activity may be just as important as mental activity for brain health and
building up cognitive reserve. Dozens of studies have shown it to have a
pronounced effect, and aerobic exercise that gets your heart rate up may be
especially important.
Exercise
seems to affect the brain directly, increasing the number of synapses and
enhancing the action of neurotransmitters, the chemicals that make brain
cell-to-brain cell communication possible. It also increases the production of
brain-derived neurotrophic factor (BDNF), a “brain juice” protein that promotes
the production of new brain cells and the survival of existing ones.
Physical
activity also has indirect effects. If your heart and lungs are strong and
healthy, more oxygen-rich blood will circulate to the brain. And exercise
controls and reduces the risk of conditions like diabetes and high blood
pressure that can put brain cells in harm’s way.
For the brain
and the rest of the body, the wisdom of Hippocrates may be as true today as it
was 2,400 years ago: That which is used develops that which is not used, wastes
away.
Start your
brain training today!
(Sources: Memory Foundation, 8 April 2012, Neurological
Foundation of New Zealand, 3 February 2016))
