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Scientists make advance in dementia research
November 9, 2010--The preservation of a
protein found in particular synapses in the
brain plays a key role in protecting against
vascular dementia after a stroke, say
researchers at King's College London.
The study, funded by the Dunhill Medical
Trust, is published in the 9 November issue
of Neurology,
the medical journal of the American Academy
of Neurology. Researchers say the study
findings increase understanding of vascular
dementia, and highlight a possible target
for future diagnoses and treatment of the
condition.
Professor Paul Francis, King's College
London, said: 'Vascular dementia accounts
for 15 to 20 per cent of the 25 million
people worldwide with dementia, yet there is
currently no effective treatment.
It is common for people to develop vascular
dementia after suffering a stroke, which can
be devastating for patients and their carers.
'Understanding the chemical processes that
affect the brain when people develop
vascular dementia is a vital step towards
identifying potential treatments for this
common condition. The findings of this study
take us that little bit closer towards
achieving this goal.'
Vascular dementia, the second most common
form of the condition, is caused by problems
in the supply of blood to the brain, such as
a stroke, and can affect memory, thinking,
behaviour and the ability to perform
everyday activities. One in three older
people who have a stroke develop dementia
within three months, with a 10-fold
increased risk of dementia over five years.
The team, led by Professor Paul Francis at
King's in collaboration with Newcastle
University, studied differences in nerves
and synapses in the brain tissue of
individuals with and without dementia, over
half of which had also suffered a stroke
previously.
A synapse is a tiny gap between two neurones
(nerve cells) in the brain, and information
is transported across this gap by a
neurotransmitter. Synapses that use
glutamate (an amino acid) as a
neurotransmitter are known to be related to
memory and cognition, and contain a protein
called VGLUT1.
The autopsy study specifically looked at the
levels of VGLUT1 by analysing brain tissue
from 73 individuals, obtained from the
Brains for Dementia Research programme.
Forty-seven individuals had a form of
cerebrovascular disease, triggered when the
blood supply to the brain is disturbed in
some way, such as a stroke. Twenty-seven of
these people had undergone an annual
cognition test in the years before their
death as part of the Cambridge Assessment of
Mental Health for the Elderly (CAMCOG)
evaluation.
The findings show a correlation between
levels of VGLUT1 and cognition scores – the
higher the concentration of VGLUT1, the
better they did in the CAMCOG cognition
assessment.
Crucially, the study also showed that in
those individuals who did not develop
dementia after a stroke, the levels of
VGLUT1 were significantly higher.
These findings suggest that if levels of
VGLUT1 can be preserved artificially after a
stroke, the chances of developing vascular
dementia could be significantly reduced.
