News reports of research into Alzheimer's disease April - December 2000
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There's a glossary of terms used in Alzheimer's research.
Disclaimer:
This section began as an offshoot of my
gathering of news items about memory. I am not a medical expert. My
background is in psychology. The information I have gathered here should
not be taken as providing any advice.
December 2000
Alzheimer sufferers recalled significantly more details of
long-ago events (68% vs 61%) when music was
played during recall. Recent memory was not affected. It is
suggested that music could be played at particular times when
better recall is desirable, such as when relatives visit.
Guardian report
Three independent studies have linked late-onset Alzheimer's
disease to a locus on chromosome 10
that affects processing of the amyloid-beta protein, a peptide
important in the formation of the characteristic amyloid plaques
found in the brains of people with Alzheimer's disease.
Researchers are optimistic the precise gene will be found in the
next few years.
Before this, a particular form of the apolipoprotein E (APOE) gene
on chromosome 19 has been the only widely recognized genetic
risk factor in late onset Alzheimer’s disease. There is also
some evidence of a risk factor gene on a region of chromosome
12.
So far, three genes have been found that are linked to the rare
early-onset Alzheimer's (when symptoms appear before age 60).
The findings are reported in the Dec. 22 issue of
Science.
http://www.eurekalert.org/pub_releases/2000-12/MCJ-Loc1-2112100.htm
A vaccine may help prevent and treat
the disabling memory loss and cognitive impairment of
Alzheimer's disease. Alzheimer's occurs when amyloid-beta
peptides accumulate in the brain, forming plaque. While previous
studies have shown that vaccinating mutated mice with this
amyloid-beta peptide could remove the plaque deposits, there was
never any evidence of improvement in brain function, until now.
The researchers also believe this study provides the final
element of proof that Alzheimer's is initiated by amyloid-beta
peptides. The researchers believe clinical trials could begin on
human subjects within the year.
The study was published in the Dec. 21-28 issue of
Nature.
http://www.eurekalert.org/pub_releases/2000-12/UoT-UoTr-1912100.htm
A chemical called
methionine (an amino acid found in beta-amyloid) may be the
source of the toxic free radicals produced by the amyloid-beta
peptide. Recent studies have demonstrated that higher than
normal doses of vitamin E may slow the advance of
Alzheimer's in some people with late stages of the disease.
The current study provides a possible explanation for this
link. Vitamin E, an antioxidant, appears to work by
destroying free radicals (oxidants) produced by amyloid.
The study was presented at the 2000 International Chemical
Congress of Pacific Basin Societies.
http://www.eurekalert.org/pub_releases/2000-12/ACS-Ript-1712100.htm
The protein alpha1-antichymotrypsin can double the
accumulation of amyloid plaque in the brains of mice,
suggesting a possible new target for therapy in humans.
Alpha1-antichymotrypsin (ACT) is a serin protease inhibitor,
or
serpin, that normally prevents enzymes
known as proteases from digesting proteins. Scientists have
known for some time that production of ACT is increased in
the brains of patients with Alzheimer's disease, but its
role has not been understood. The current study, conducted
in genetically engineered mice, reveals that increased
production of ACT in the brain strongly increases the
build-up of amyloid proteins. It is not yet clear exactly
how it does this.
The report appeared in the December issue of the
American Journal of Pathology.
http://www.eurekalert.org/pub_releases/2000-12/UoCS-Rrir-0412100.htm
November 2000
A one-year study found rivastigmine tartrate (Exelon®)
reduces the cognitive decline of people with mild to
moderate Alzheimer's disease. 545 patients completed the
initial six-month phase of the trial and 532 then agreed
to extend the trial another six months. Patients who
received the higher dose of rivastigmine from the
beginning had higher cognitive scores at the end than
those patients who received a placebo or the lower dose
during the first six months. This suggests early
treatment with a high dose may provide benefits that are
lost if treatment is delayed.
The study was published in the November issue of
European Neurology.
http://www.eurekalert.org/pub_releases/2000-11/IU-Rtrc-0811100.htm
Scientists at Johns Hopkins have demonstrated that a
specific enzyme,
beta-secretase, is
essential for nerve cells to form amyloid plaques, whose
over-abundance is characteristic of Alzheimer's. It is
one of two enzymes implicated in plaque formation. The
other is gamma-secretase. "We're really encouraged by
possible therapeutic implications because scientists are
already designing small molecules capable of crossing
the brain's blood-brain barrier." The molecules could,
in theory, be fine-tuned to inhibit such enzymes as
beta-secretase.
The research was presented at the annual meeting of the
Society for Neuroscience in New Orleans.
http://www.eurekalert.org/pub_releases/2000-11/JHMI-Hsse-0511100.htm
While the excess of amyloid plaque deposits have
long been recognised as a hallmark of Alzheimer's
disease, it has not been known whether the problem
occurs because of an over-production, or because of
a failure to remove them. A study involving mice
found that blood vessels are responsible for
removing the beta amyloid protein in healthy brain
tissue. In particular, a protein known as
LRP-1 (low density lipoprotein receptor-related
protein), rapidly shuttles beta amyloid out of the
brain and across the blood-brain barrier to the
body, which breaks it down into harmless waste
products. Not only did the researchers find that
removal of amyloid from the brain slowed
dramatically when LRP-1 was blocked, but they also
showed that healthy middle-aged mice had fewer LRP-1
molecules and shuttled amyloid out of their brains
at only half the rate as young mice. It is
speculated that healthy young people normally can
handle the load of removing amyloid, but that
plaques can occur when the LRP-1 system becomes less
efficient and the body faces other challenges
related to aging, such as decreased circulation.
It's also possible that the protein begins
accumulating more quickly, overwhelming the removal
system.
http://www.eurekalert.org/pub_releases/2000-11/UoR-Simt-0511100.htm
October 2000
A new study has demonstrated that the drug
Aricept® can "switch on" brain cells thought to
be irreparably damaged in Alzheimers sufferers.
Previous research suggested Aricept had no such
dramatic effects. The new findings may enable more
effective use to be made of the drug.
www.guardian.co.uk/Archive/Article/0,4273,4080005,00.html
April 2000
A five-month study conducted by
Janssen Research Foundation show that patients who were
treated with Reminyl® (galantamine) showed a significant
improvement in their cognitive, functional and behavioural
symptoms. "For the first time, we are able to show that Reminyl®
has benefits not only on cognition, but on patients' ability to
function, while also postponing the emergence of behavioural
symptoms."
An additional study demonstrated Reminyl's
long-term effectiveness for at least 12 months. The six month
extension study involved 353 patients with mild-to-moderate
Alzheimer's disease. Previously, 636 patients had taken part in
a six-month double-blind study, which was subsequently extended.
Importantly, patients in this group were also able to maintain
activities of daily functioning for one year.
The studies
were presented at the International Stockholm/Springfield
Symposium, a meeting of leading experts to discuss advances in
Alzheimer's therapy.
http://www.eurekalert.org/pub_releases/2000-04/K-Nroi-0604100.htm
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