MEMORY LOSS
BRAIN CELLS CAN REGENERATE
Dr. Fred Gage and colleagues at the Salk Institute for
Biological Studies in California, together with doctors
at the Sahlgrenska University Hospital in Sweden have shown
that new neurons do develop after birth.
This flies in the face of conventional wisdom, which suggests
that brain cells, unlike all other cell types, do not reproduce.
Dr. Gage's team took post-mortem brain tissue from 5 patients
who had received an intravenous injection of bromodeoxyuridine
as part of their treatment for squamous cell carcinoma.
This drug is a thymidine analogue and is therefore taken
up into the newly synthesised DNA of dividing cells. Because
of this property, bromodeoxyuridine is sometimes used to
check for tumour cell proliferation. Using immunofluorescence
techniques and a laser microscope, which can optically section
through individual cells, the team was able to detect the
presence of the drug in all 5 postmortem specimens.
In addition to showing that new cells were present in the
brain, the team also confirmed that these cells were neurons
by looking for two other markers which can differentiate
between neuronal cells and glial cells.
The brain tissue studied by Dr. Gage's team comes from
the dentate gyrus, the part of the brain which acts as a
relay station between the cortex and the hippocampus and
is important in memory and learning.
BMJ no.7168 (7th Nov '98) p1272
A PRELIMINARY STUDY OF DIETARY ALUMINIUM INTAKE AND RISK
OF ALZHEIMER’S DISEASE
Epidemiological studies of the relationship between aluminium
exposure and Alzheimer’s disease have focused on aluminium
in drinking water. For most people, the greatest source
of aluminium is in food, but no studies have been conducted
into the relationship between Alzheimer’s and the
consumption of foods containing large amounts of aluminium
Therefore, a pilot study was conducted to determine whether
dietary intake of aluminium additives varies in individuals
with and without the disease. 46 participants (23 matched
sets) with and without newly diagnosed Alzheimer’s
were selected. Next of kin provided lifestyle and dietary
history. The consumption of foods with high levels of aluminium
was compared between cases and controls. The crude odds
ratio for daily intake of foods containing high levels of
aluminium was 2.0 and, when adjusted for covariates, was
8.6 (p = 0.19). The intake of bread and biscuit products
differed significantly (p = 0.025), between cases and controls.
Adjusted odds ratios were also raised for a number of other
products, but not for tea consumption.
As the past consumption of foods containing high levels
of aluminium varied between those participants with Alzheimer’s
and controls, results suggest that dietary intake of aluminium
may affect the risk of developing the disease.
Rogers, M.A.M. et al
AGE AND AGEING 1999, 28 (2) 205-209
SUPPLEMENT COMBINATION OF IRON AND VITAMIN C IS SAFE AND
EFFECTIVE
There have been concerns that through increasing the bioavailability
of iron, a known oxidant, supplemental vitamin C may actually
increase free radical generation in the body. Therefore
scientists examined the effect of co-supplementing healthy
adults with iron and vitamin C on antioxidant status, platelet
function and low-density lipoprotein oxidation. Results
revealed that supplementation with a combined formulation
had a highly beneficial effect on the parameters investigated
and there was no evidence of any pro-oxidant effect.
It was concluded that iron supplements containing vitamin
C as a synergistic factor are more beneficial to health
than a supplement containing only iron, and are perfectly
safe for long-term daily use.
EUR. J. CLIN. NUTR. 1999, 53 (5) 367-74
VITAMIN E AND VITAMIN C SUPPLEMENTATION AND RISK OF ALZHEIMER
DISEASE
A study was carried out to evaluate the association between
the supplementation of vitamins C and E and the incidence
of Alzheimer’s disease in 633 healthy subjects 65
years of age and over. After an average follow-up period
of 4.3 years, 91 subjects had been diagnosed with probable
Alzheimer’s disease. None of the 27 users of vitamin
E or the 23 users of vitamin C supplements had Alzheimer
disease. These data suggest that supplementation with high-dose
vitamins E and C may reduce the risk of Alzheimer disease.
Morris M.C. et al,
ALZHEIMER DISEASE AND ASSOC. DISORDERS 1998, 12, 121-126
VITAMIN E AND VITAMIN C SUPPLEMENTATION AND RISK OF ALZHEIMER
DISEASE
A study was carried out to evaluate the association between
the supplementation of vitamins C and E and the incidence
of Alzheimer’s disease in 633 healthy subjects 65
years of age and over. After an average follow-up period
of 4.3 years, 91 subjects had been diagnosed with probable
Alzheimer’s disease. None of the 27 users of vitamin
E or the 23 users of vitamin C supplements had Alzheimer
disease. These data suggest that supplementation with high-dose
vitamins E and C may reduce the risk of Alzheimer disease.
Morris M.C. et al,
ALZHEIMER DISEASE AND ASSOC. DISORDERS 1998, 12, 121-126
VITAMIN E HELPS PREVENT INTELLECTUAL DECLINE
Researchers in Austria studied over 1,700 adults aged between
50 and 75 to test their intellectual capacity. They found
that those with higher levels of vitamin E were less likely
to have low scores in the test. A diet rich in vitamin E
may help prevent free radical damage and slow the progression
of age-related mental decline.
Schmidt, R. et al,
J. AM. GERIATR. SOC. 1998, 46, 1407-10
EFFECT OF OESTROGEN ON BRAIN ACTIVATION PATTERNS IN POSTMENOPAUSAL
WOMEN DURING WORKING MEMORY TASKS
Declining oestrogen levels characterise menopause with
effects on a range of systems including, in addition to
the reproductive system, the cardiovascular and skeletal
systems. Furthermore, there is evidence that oestrogen affects
basic neural processes. Therefore, a study was carried out
to investigate the effects of oestrogen on brain activation
patterns in post-menopausal women as they performed verbal
and non-verbal working memory tasks.
The study group consisted of 46 post-menopausal women aged
33 to 61 years. The trial consisted of a 21-day treatment
with conjugated equine oestrogens, 1.25 mg/d, randomly crossed
over with identical placebo and a 14-day washout between
treatments. Brain activation patterns were measured using
functional magnetic resonance imaging during tasks involving
verbal and non-verbal working memory. It was found that
treatment with oestrogen increased activation in the inferior
parietal lobule during storage of verbal material and decreased
activation in the inferior parietal lobule during storage
of non-verbal material. Oestrogen also increased activation
in the right frontal gyrus during retrieval tasks, accompanied
by greater left-hemisphere activation during encoding. Oestrogen
did not affect actual performance of the verbal and non-verbal
memory tasks.
Thus, oestrogen in a therapeutic dosage alters brain activation
patterns in post-menopausal women in specific brain regions
during the performance of the sorts of memory function that
are called upon frequently during any given day. These results
suggest that oestrogen affects brain organisation for memory
in post-menopausal women.
Shaywitz, S.E. et al
J.A.M.A. 1999, 281 (13) 1197-1202
FREE RADICAL DAMAGE PINPOINTED IN ALZHEIMER’S DISEASE
Oxidative damage to brain cells may be principal indicator
of Alzheimer’s disease activity, according to new
research that has identified increased concentrations of
free radicals in certain areas of patient’s brains.
Researchers at the University of Pennsylvania in Philadelphia
and colleagues at the Florida Institute of Technology in
Melbourne, Florida, have discovered that the measurement
in body tissue of compounds called isoprostanes can accurately
reflect the amount of neurological oxidative damage. The
investigators used scanning techniques to measure the amount
of isoprostanes in tissue samples obtained from 43 brains.
19 of the brains came from patients known to have had Alzheimer’s
disease, 16 from patients with either Parkinson’s
disease or schizophrenia, and 8 from normal controls. They
found that isoprostane concentrations were markedly raised
in samples from both the frontal and temporal poles in patients
known to have had Alzheimer’s disease but were normal
in these areas in the samples taken from other brains.
Oxidative damage to cells is caused by the activity of
free radicals, which are released during normal cell processes.
This results in oxidative stress, a process that is believed
to result in tissue inflammation, long suspected to be a
cause of Alzheimer’s disease. Brain tissue is particularly
susceptible to free radical damage because, unlike many
other tissues, it does not contain large amounts of protective
antioxidant compounds. Previously there has been no reliable
means for assessing the degree of oxidative stress in brain
tissue.
BMJ no.7173 p1616
THE ROLE OF HERPES SIMPLEX VIRUS TYPE 1 IN ALZHEIMER'S
DISEASE
Researchers at the Molecular Neurobiology Laboratory, UMIST,
have discovered that when the Herpes Simplex virus type
1 is present in the brain of people carrying certain genetic
information (apoE4 allele), they have a high risk of developing
Alzheimer's disease. Neither the virus nor the allele is
a risk on its own.
HUMANE RESEARCH TRUST NEWS REVIEW 1998
OESTROGEN THERAPY IN POSTMENOPAUSAL WOMEN - EFFECTS ON
COGNITIVE FUNCTION AND DEMENTIA
Researchers carried out a literature search of studies
published from January 1996 to June 1997 to determine whether
postmenopausal oestrogen therapy improves cognition, prevents
development of dementia, or improves dementia severity.
Biochemical and neurophysiologic studies suggest several
mechanisms by which oestrogen may affect cognition: promotion
of cholinergic and serotonergic activity in specific brain
regions, maintenance of neural circuitry, favourable lipoprotein
alterations, and prevention of cerebral ischaemia. In trials
assessing the effects of oestrogen on cognitive function
cognition seems to improve in perimenopausal women, possibly
because menopausal symptoms improve, but there is no clear
benefit in asymptomatic women. Meta-analysis of studies
concerning the effects of postmenopausal oestrogen use on
the risk of developing dementia suggests a 29% decreased
risk among oestrogen users, but the findings of the study
are heterogeneous. Large placebo-controlled trials are required
to address oestrogen’s role in prevention and treatment
of Alzheimer disease and other dementias.
The researchers conclude that, given the known risks of
oestrogen therapy, it is not recommended that oestrogen
be given for the prevention or treatment of Alzheimer disease
or other dementias until adequate trials have been completed.
Yaffe, K. et al
J.A.M.A. 1998, 279 (9) 688-95
PLACEBO-CONTROLLED DOUBLE-BLIND RANDOMISED TRIAL OF AN
EXTRACT OF GINKGO BILOBA FOR DEMENTIA
A multi-centre, placebo-controlled, double-blind randomised
trial in 6 US research centres was carried out with 309
out-patients, over a period of one year, to investigate
the efficacy of Ginkgo biloba in the treatment of Alzheimer’s
disease and multi-infarct dementia. The Ginkgo group scored
better than the placebo group. It was concluded that Ginkgo
biloba was safe and appears capable of stabilising and,
in a substantial number of cases, improving, the cognitive
performance and the social functioning of demented patients
for 6 months to 1 year.
Prof. E. Ernst comments favourably on this trial and points
out that research has shown that Ginkgo enhances blood fluidity,
increases microcirculatory flow, eliminates free radicals
and acts on the muscarinic cholinergic system.
Le Bars P.O., Katz M.M., Berman N, Turan M, Freedman
A.M., Schatzberg A.F.
JAMA 1997, 278(16) 1327-32
FACT 1998, Vol. 3 (1)
ALUMINIUM, ALZHEIMER’S DISEASE AND BONE FRAGILITY
The incidence of fragility fractures has increased epidemically,
especially in patients with senile dementia (including Alzheimer’s
disease). Aluminium inhibits bone mineralisation, is neurotoxic
and may, in addition to genetic factors, play a role in
the development of Alzheimer’s disease by contributing
to the formation of the characteristic beta-amyloid and
neurofibrillary tangles. A pilot study of 26 hip-fracture
patients (13 patients with Alzheimer’s disease and
13 controls) was carried out.
The aluminium content, determined mass-spectrometrically,
was higher in trabecular bone biopsies from the patients
with Alzheimer’s disease than from the controls. The
aluminium content was also higher in the younger of the
26 patients. The findings agree with the hypothesis that
aluminium plays a role in the development of Alzheimer’s
disease and bone fragility.
Mjoberg, B et al.
ACTA. ORTH. SCAND. 1997, 68 (6) 511-14
