News reports of research into Alzheimer's disease Jan - June 2005
To search by subject, go to Alzheimer's subject index.
Return to Alzheimers main page for monthly index
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.
June
New memory aid helps dementia sufferers remember
An innovative memory aid based on an interactive multimedia computer
system aims to stimulate more enjoyable, rewarding conversation between
sufferers and those who care for them. CIRCA (Computer Interactive
Reminiscence and Conversation Aid) involves a simple touch-screen with
easy-to-follow instructions; it displays a choice of three random categories
(entertainment, local life etc) and three media (music, photo, video). The
images, video or sound clips then act as a memory trigger and conversation
prompt. During development, CIRCA was tested on 40 dementia sufferers with
very encouraging results. CIRCA could become available on the market in 2-3
years.
http://www.eurekalert.org/pub_releases/2005-06/eaps-nma061505.htm
New memory drug works best in combination with older drug
An experimental drug – a compound known as SGS742 – has been successful
in animal studies in improving memory, and is now in human clinical trials.
The drug works by blocking certain chemicals that interfere with memory
formation, thus enabling better acquisition and retention of new
information. It alters the activity of gene control machinery that is
important for memory consolidation. It was most effective when used in
conjunction with Aricept, an established Alzheimer’s drug.
The findings were described in the June issue of
Neuropharmacology.
Full reference
http://www.eurekalert.org/pub_releases/2005-06/jhu-nmd060905.htm
Non-invasive MRI technique distinguishes between Alzheimer's and frontotemporal dementia
A new study has found that a non-invasive imaging technique called
arterial spin labeling is just as accurate and much faster and cheaper
compared to invasive scanning techniques in distinguishing Alzheimer's
disease from frontotemporal dementia (FTD). Frontotemporal dementia is the
second-most common dementia after Alzheimer's disease. The present study
aimed simply at differentiating the two types of dementia; further research
needs to be done to confirm that the technique can be used to diagnose an
individual patient.
The results were presented at the first International Conference on
Prevention of Dementia, held June 18-21 in Washington, D.C.
http://www.eurekalert.org/pub_releases/2005-06/uoc--nmt061605.htm
Abnormal cell division possible precursor of Alzheimer's
A study of genetically engineered mice sheds more light on the causes of
Alzheimer’s. The study looked at what the reasons for neuron death apart
from neurofibrillary tangles; they found an abnormal type of cell division
occurring in tau proteins that may activate a cascade of abnormal events.
The study was reported in the June issue of The
Journal of Neuroscience.
Full reference
http://www.eurekalert.org/pub_releases/2005-06/ani-asa062005.htm
Alzheimer's disease linked to early inflammation
A new study of dementia in identical twins suggests that exposure to
inflammation early in life quadruples one's risk of developing Alzheimer's
disease. The study involved sifting the 20,000 participants in the Swedish
Twin Registry for the 109 "discordant" pairs where only one twin had been
diagnosed with dementia. Answers to health questions in the survey enabled
the researchers to build a crude indicator of periodontal disease, measured
indirectly by teeth lost or loose. Because this is not a direct measure of
inflammation, the results need to be confirmed, but they do suggest that an
inflammatory burden early in life, as represented by chronic gum disease,
may have severe consequences later. The study also found that mental
activities at age 40 did not seem to lower the risk of developing
Alzheimer's, and the level of education was not a large factor once genes
were taken into account (nevertheless, those with less high school and
college education had 1.6 times the risk of dementia). Previous studies have
shown that Alzheimer's is strongly genetic: If one twin has the disease, his
or her identical twin has a 60% chance of developing it.
The study was presented at the first Alzheimer's Association International
Conference on Prevention of Dementia, to be held June 18-21 in Washington,
D.C.
http://www.eurekalert.org/pub_releases/2005-06/uosc-adl061605.htm
http://www.msnbc.msn.com/id/8281581/
New computer program may enable early prediction of Alzheimer's risk
Researchers have developed a brain scan-based computer program that
quickly and accurately measures metabolic activity in the hippocampus, a key
brain region that shrinks with the development of Alzheimer’s. The study
followed 53 normal subjects aged 54 to 80 for at least 9 years and in some
cases for as long as 24 years, and found that hippocampal glucose metabolism
was significantly reduced on the first scan of those 25 individuals who
would later experience cognitive decline related to either mild cognitive
impairment or to Alzheimer's. The findings bring hope of being able to
predict who will develop Alzheimer’s at least 9 years ahead of symptoms.
The technical details of the program were published in the June issue of
Neurology.
Full reference
http://www.eurekalert.org/pub_releases/2005-06/nyum-ncp061505.htm
Expert system gives non-experts diagnostic accuracy of Alzheimer's disease from PET scans
A computer program has been developed that enhances the diagnostic
accuracy of PET scans with Alzheimer's patients. A PET scan is a very
reliable noninvasive test, but only in the hands of an experienced
investigator. The new program enables even inexperienced doctors to diagnose
reliably, hopefully enabling diagnosis to occur earlier.
The findings were presented at the Society of Nuclear Medicine's 52nd Annual
Meeting in Toronto.
Reference
http://www.eurekalert.org/pub_releases/2005-06/sonm-esd061605.htm
May
Hopeful results from interrupted Alzheimer's vaccine study
Phase 2 of a human clinical trial vaccinating patients with beta-amyloid
was halted in 2002 when some participants developed brain inflammation.
Participants continued to be monitored, however, and results show that
participants whose immune systems mounted a response against beta amyloid
performed significantly better on a series of memory tests than those who
received a placebo injection (but not on 5 tests often used to diagnose
dementia). There were also signs of reduced levels of tau protein (a protein
considered a sign of cell death) in those who had an immune response. As a
result, new trials are underway, this time using humanized antibodies rather
than beta amyloid itself. The antibodies should help trigger the immune
system to attack beta amyloid, but will be cleared by the body soon after
injection.
Two papers were published in the May 10 issue of
Neurology.
Full reference 1
Full reference 2
http://www.eurekalert.org/pub_releases/2005-05/uomh-hrf050505.htm
Finding an Alzheimer's switch
One prominent theory of the cause of Alzheimer's involves the so-called
"amyloid beta protein cascade," in which a protein called APP is clipped
into shorter pieces by enzymes known as secretases. If the portion of APP
clipped by the beta form of secretase is further clipped by a third form,
gamma secretase, the resulting fragments are amyloid beta peptides, A-beta
40 and A-beta 42. A-beta 42 in particular is toxic and causes the formation
of amyloid plaques. A new study has uncovered an unsuspected subunit of
gamma-secretase, the protein CD147, which apparently regulates the
production of the toxic peptides that cause amyloid plaques. CD147 is
expressed in many tissues and has many functions besides its role in tumor
invasion, including reproduction, inflammation, and protein transport and
sorting within cells. It also has a role in neural function: when the CD147
gene is deleted in mice, the result is defective nervous system development,
loss of working memory, spatial learning deficits, and disorientation —
behaviors remarkably suggestive of Alzheimer's disease. Future research will
attempt to uncover exactly how CD147 prevents excessive production of A-beta
42 peptides, and what causes it to fail.
The study was reported online before print May 12 in
Proceedings of the National Academy of Sciences.
Full reference
http://www.eurekalert.org/pub_releases/2005-05/dbnl-faa051305.htm
April
Clinical diagnosis of Alzheimer's may be delayed with donepezil
In a study of people with mild cognitive impairment, those who took the
drug donepezil were at reduced risk of progressing to a diagnosis of
Alzheimer's during the first years of the trial, but by the end of the
3-year study there was no benefit from the drug. Of the 769 participants,
212 developed possible or probable Alzheimer’s within the 3-year study
period; the donepezil group's risk of progression to a diagnosis of
Alzheimer’s was reduced by 58% one year into the study, and 36% at 2 years,
but no risk reduction at the end of three years. Vitamin E was also tested
in the study and was found to have no effect at any point in the study.
However, it should be noted that an earlier study found an effect of Vitamin
E only when taken in combination with Vitamin C.
The findings were reported in the April 14 online issue of
The New England Journal of Medicine, and will appear in the June 9
print issue.
Full reference
http://www.eurekalert.org/pub_releases/2005-04/nioa-cdo041205.htm
http://www.eurekalert.org/pub_releases/2005-04/mc-dia041105.htm
Protein studies may lead to new Alzheimer's test
A new technique has identified more than 400 proteins in human spinal
fluid — 40 times more than previously known. On average, one of every five
proteins identified was substantially changed in patients with Alzheimer's
disease compared to older people without neurological disease. The finding
may lead to a new test for diagnosing Alzheimer’s.
The study appeared in the April issue of the Journal
of Alzheimer's Disease.
Full reference
http://www.eurekalert.org/pub_releases/2005-04/uow-psm041905.htm
Exercise slows development of Alzheimer's-like brain changes in mice
Population-based studies have provided evidence that various lifestyle
interventions might help slow the onset and progression of Alzheimer’s. A
mouse study now provides a clue how that might work. Physical activity
enhanced the learning ability of mice genetically engineered to develop
amyloid plaques and decreased the level of plaque-forming beta-amyloid
protein fragments in their brains. The mice were divided into mice with
access to running wheels or no access. The findings are supported by another
recent study that found that beta-amyloid levels decreased in the brains of
another kind of transgenic mice when they were housed in groups and in
environments that were enriched with running wheels, colored tunnels, and
toys.
The study appeared in the April 27 issue of The
Journal of Neuroscience.
Full reference
http://www.eurekalert.org/pub_releases/2005-04/nioa-esd042605.htm
How Alzheimer's impacts important brain cell function
Researchers have found that synaptic proteins, proteins involved in brain
cell communications, decrease in the brains of Alzheimer's patients compared
to healthy brains from people in the same age range. The decrease in the
frontal cortex was more severe than in other portions of the brain. They
also found synaptic protein levels were even lower in the brains of patients
in the early stages of Alzheimer's disease, suggesting that the loss of
these proteins happens very early in the disease process. The reduction of
synaptic proteins may be caused by mitochondrial dysfunction, a
well-documented occurrence in Alzheimer's.
The research was reported in the April issue of the
Journal of Alzheimer's Disease.
Full reference
http://www.eurekalert.org/pub_releases/2005-04/ohs-ord040605.htm
Gene therapy slows cognitive decline in trial
The first human clinical trial of gene therapy for Alzheimer’s, involving
8 volunteers, has found an increase in the brain’s use of glucose — a sign
of brain activity — and a significant slowing of the patients’ rate of
cognitive decline in the 6 patients who completed the procedure safely.
The study was published online on April 24 in Nature
Medicine.
Full reference
http://www.eurekalert.org/pub_releases/2005-04/uoc--acd041805.htm
Some benefit from memantine for moderate-to-severe Alzheimer’s
A review of nine published studies comprising 2,339 participants has
concluded that memantine has a small but significant cognitive benefit for
moderate-to-severe Alzheimer’s patients. It also seems to prevent the onset
of agitation. Although there was some indication of benefit for those with
mild to moderate Alzheimer’s, the effects were not significant. Researchers
caution that the drug treats the symptoms only, slowing the progress of the
disease only.
The review appears in the April issue of The Cochrane
Library.
http://www.eurekalert.org/pub_releases/2005-04/cfta-sap041505.htm
March
Link between insulin and Alzheimer's
A new study has found that insulin and its related proteins are produced
in the brain as well as the pancreas, and that reduced levels of these
contribute to the degeration of brain cells, an early symptom of Alzheimer's
disease. The finding raises the possibility of a Type 3 diabetes.
The findings are reported in the March issue of the
Journal of Alzheimer's Disease.
Full reference
http://www.eurekalert.org/pub_releases/2005-03/l-rdl030205.htm
Enriched environment delays onset of Alzheimer's in mice
A study of genetically engineered mice has found that an enriched
environment, with more opportunities to exercise, explore and interact with
others, can dramatically reduce levels of beta-amyloid peptides, hallmarks
of Alzheimer's disease. The mice also showed greater activity for several
genes involved in memory and learning, the growth of new nerve cells, cell
survival, and the growth of new blood vessels within the brain. As with
humans, mice in the enriched environment showed varying levels of activity.
The most active were found to have the least beta-amyloid. Researchers
suggested the reason may simply be a matter of blood flow; physical and
mental activity can stimulate growth of new blood vessels and keep existing
vessels open and functional.
The report appeared In the 11 March 2005 issue of
Cell.
Full reference
http://www.eurekalert.org/pub_releases/2005-03/uocm-eed030705.htm
Chemical decoy shows promise for slowing Alzheimer's
A chemical polymer shows promise in cell culture studies of slowing
Alzheimer’s by blocking the toxic brain proteins thought to cause the
disease. The likely candidate for any drugs developed from this approach
would be people at increased risk of Alzheimer’s, who haven’t yet developed
signs of the disease.
The finding was presented on March 17 at the 229th national meeting of the
American Chemical Society.
Reference
http://www.eurekalert.org/pub_releases/2005-03/acs-ds030705.htm
Fish oil may help prevent Alzheimer's
A study involving genetically engineered mice has found that a diet high
in docosahexenoic acid, or DHA — an omega-3 fatty acid found in relatively
high concentrations in cold-water fish — dramatically slowed the progression
of Alzheimer's, by cutting the harmful brain plaques that mark the disease.
An earlier study showed that DHA protected against damage to the "synaptic"
areas where brain cells communicate and enabled mice to perform better on
memory tests. Food sources of omega-3 fatty acids include fish such as
salmon, halibut, mackerel and sardines, as well as almonds, walnuts, soy,
and DHA-enriched eggs.
The results appear in the March 23 online edition of the
Journal of Neuroscience.
Full reference
http://www.eurekalert.org/pub_releases/2005-03/vrcs-foh032405.htm
Beta amyloid accumulation shown to be trigger for onset of Alzheimer's
A study using genetically engineered mice has determined that early beta
amyloid accumulation within neurons is the trigger for the onset of memory
decline in Alzheimer's. The study found that decline in long-term memory
retention began with the buildup of beta amyloid in neurons of the
hippocampus, amygdala and cerebral cortex regions of the mice's brains,
although the plaques and tangles characteristic of Alzheimer’s had not yet
developed. When the beta amyloid was cleared away, the memory impairments
disappeared; the reemergence of beta amyloid inside the neurons marked again
the onset of memory problems.
The report appeared in the March 3 issue of Neuron.
Full reference
http://www.eurekalert.org/pub_releases/2005-03/uoc--uri030105.htm
http://www.sciencentral.com/articles/view.htm3?type=article&article_id=218392512
February
Smoking now found detrimental for Alzheimer’s
Previous animal studies had suggested that nicotine reduces the number of
amyloid plaques; a new study, however, has found that chronic nicotine
exposure increases neurofibrillary tangles.
The paper appeared in the February 22 issue of
Proceedings of the National Academy of Sciences.
Full reference
http://www.eurekalert.org/pub_releases/2005-02/uoc--ctp020805.htm
Progress toward a more targeted treatment of Alzheimer's disease
A major role in the process by which plaques develop is played by
γ-secretase, an enzyme that cuts proteins in a particular place. Sometimes
the γ-secretase cleavage goes wrong, causing the creation of a by-product
that sticks together and precipitates (plaques). Although γ-secretase is
divided into several entities, it’s been assumed that the complex acts as a
homogeneous unit. However, new research has found that γ-secretase's various
sub-units exhibit very diverse, tissue-specific activity. The findings
should make it possible to develop medicines that are targeted on a single
sub-unit and thereby have a much more specific action, with fewer unwanted
side-effects.
The paper appeared in the February 1 issue of
Proceedings of the National Academy of Sciences.
Full reference
http://www.eurekalert.org/pub_releases/2005-02/vfii-pta013105.htm
Drugs used to treat Alzheimer's in nursing homes are worsening sufferers' illness
A study of 93 patients with dementia has found that quetiapine, an
anti-psychotic drug commonly used in nursing homes to treat agitation and
related symptoms in people with Alzheimers' disease, actually worsens
patients' illness, significantly speeding up their rate of cognitive
decline. Unfortunately, quetiapine had been regarded as one of the safer of
the antipsychotic drugs available. There have been safety concerns with the
two most commonly used antipsychotic drugs in people with dementia,
risperidone and olanzapine, because of increased risk of stroke.
Participants in the trial who were taking rivastigmine showed little or no
worsening of their illness. Neither drug had any effect on agitation.
The paper appeared in the April 16 issue of the
British Medical Journal.
Full reference
http://www.eurekalert.org/pub_releases/2005-02/bmj-dut021605.htm
January
Weight loss may be an early sign of dementia in the elderly
An analysis of data from 1,890 men who were participants in The
Honolulu-Asia Aging Study has found that the weight loss common in people
with dementia begins 2-4 years before the onset of clinical dementia
symptoms. It’s possible that treatment interventions directed toward
maintaining optimal nutrition and preventing excess weight loss could slow
the disease.
The study appeared in the January issue of Archives of
Neurology.
Full reference
http://www.eurekalert.org/pub_releases/2005-01/jaaj-wlm010505.htm
New test is first step in early detection of Alzheimer's disease
A new technique called bio-bar-code amplification (BCA) technology has
been found to be able to detect miniscule amounts of ADDL in human
cerebrospinal fluid, bringing promise of an early diagnostic test for
Alzheimer’s. The researchers hope to develop the technology so that the test
could be done using a blood or urine sample instead of cerebrospinal fluid,
which is more difficult to obtain.
The findings were published online the week of January 31 in the
Proceedings of the National Academy of Sciences.
Full reference
http://www.eurekalert.org/pub_releases/2005-01/nu-nti012805.htm
http://www.eurekalert.org/pub_releases/2005-01/nsf-nds012805.htm
Antibody treatment partially reverses nerve damage in Alzheimer disease
A mouse study has had success in significantly decreasing structural
nerve damage in the brains of mice with Alzheimer’s, by administering an
beta amyloid antibody treatment to the brain surface.
The study appeared online on January 20 in advance of print publication in
the February 1 issue of the Journal of Clinical
Investigation.
Full reference
http://www.eurekalert.org/pub_releases/2005-01/joci-atp011305.htm
http://news.bbc.co.uk/go/pr/fr/-/1/hi/health/4188677.stm
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