News reports of research into Alzheimer's disease July - December 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.
December
Brain activity, drugs could affect Alzheimer's progression
Mouse studies have revealed that the activity of connections among
brain cells significantly affects levels of the toxic protein
beta-amyloid, suggesting
that the kind of mental activity people practice or drugs they might
take for depression or anxiety could affect their risk of Alzheimer’s or
the disease progression. The researchers suggest that enriched
environments may increase overall synaptic activity in some brain
regions and decrease it in others. Increased activity in some brain
regions might result in increased susceptibility to beta-amyloid
deposition if the activated neural circuits contain high levels of human
APP expression. Drugs used to treat neuropsychiatric disorders
directly influence neurotransmitters, and their receptors, thereby
altering synaptic activity.
The article appeared in the December 22 issue of
Neuron.
Full reference
http://www.eurekalert.org/pub_releases/2005-12/cp-bad121505.htm
Testosterone improves quality of life
A 24-week study involving 16 male patients diagnosed with mild
Alzheimer disease and 22 healthy male controls found that Alzheimer’s
patients who received daily testosterone treatment showed significant
improvement on a quality-of-life instrument that encompasses memory,
interpersonal relationships, physical health, energy, living situation
and overall well-being, however improvement in memory or other cognitive
skills using cognitive tests did not reach significance. Among healthy
controls, those receiving testosterone showed a non-significant trend
toward greater improvement in self-rated quality of life.
The study was published December 12 in an early online release of
Archives of Neurology.
Full reference
Full text at
http://archneur.ama-assn.org/cgi/content/full/63.2.nct50002v1
http://www.eurekalert.org/pub_releases/2005-12/uoc--apt120805.htm
Natural compound from 'pond scum' shows potential activity against Alzheimer's
A compound isolated from a cyanobacterium, a type of blue-green algae
(‘pond scum’) shows promise of becoming a natural drug candidate for
fighting Alzheimer's. Nostocarboline (the newly isolated compound) is a
potent inhibitor of
cholinesterase, with
a potency comparable to
galanthamine.
The study was published in the December 26 issue of the
Journal of Natural Product.
Full reference
http://www.eurekalert.org/pub_releases/2005-12/acs-ncf122705.htm
New technique finds higher levels of creatine in Alzheimer’s brains
Creatine is involved in the maintaining the energy balance in the
brain, but creatine, being small and very soluble, is difficult to
detect. A new study has now succeeded in detecting creatine in situ, in
brain tissue, and has found relatively large deposits in the hippocampus
of Alzheimer’s brains. The finding suggests an overlooked aspect of
energy disturbance in Alzheimer's disease, but further research is
needed to understand it.
The finding was reported in the November issue of the
Journal of Biological Chemistry.
Full reference
http://www.eurekalert.org/pub_releases/2005-12/uow-iar122105.htm
More light on apoE4 and Alzheimer’s
A mutant form of a protein that transports cholesterol,
apolipoprotein E (apoE) has
long been recognized as a causative factor for Alzheimer's disease, but
exactly how has been unclear. 299 amino acids are associated with apoE4,
but new research has now found which of these amino acids are toxic.
These toxic fragments all reside in the mitochondria (the “energy
powerhouse” of the cell). The finding suggests a new therapeutic
approach, involving blocking interaction of apoE4 fragments with the
mitochondria.
The findings were published in the December 20 issue of the
Proceedings of the National Academy of Science.
Full reference
http://www.eurekalert.org/pub_releases/2005-12/gi-gsl121405.htm
p25 only good in small doses
Elevated levels of a key brain regulatory
enzyme called Cdk5 and an associated regulatory
protein
called p25 have been found in
the brains of Alzheimer’s patients. A new mouse study has found that
switching on p25 in the hippocampus for only two weeks actually enhanced
learning and memory compared to normal mice; however mice in which p25
had been switched on for six weeks showed impaired learning and memory.
These mice also showed significant brain atrophy and loss of hippocampal
neurons. The two-week pulse of p25 did not cause neurodegeneration and
had long-lasting effects on enhancing memory. The researchers suggest
that p25 might be produced to compensate for the loss of Cdk5 activity
during aging, however chronically high levels lead to neuronal cell
death. The findings are consistent with several recent studies
suggesting that in the development of Alzheimer’s, compensatory
mechanisms that initially enhance neuroplasticity eventually become
maladaptive when chronically activated.
The report appeared in the December 8 issue of
Neuron.
Full reference
http://www.eurekalert.org/pub_releases/2005-12/cp-aje120505.htm
November
Alzheimer's disease onset tied to lapses in attention
A new finding may lead to another tool to detect Alzheimer’s early,
and also offers support for the idea that breakdowns in attention may be
at the heart of many of the memory problems experienced by Alzheimer’s
sufferers. The study, involving 94 older adults (average age mid-70s)
who were either healthy controls or in the early stages of Alzheimer’s,
found those in the early stages of Alzheimer's disease had greater
difficulty shifting attention back and forth between competing sources
of information in a dichotic listening task. The finding may also
explain why early-stage patients start to struggle with everyday tasks
that call for processing a lot of information, such as driving. Prior
research has found that performance on dichotic listening predicts
accident rates in commercial bus drivers.
[note: this study was briefly reported on in September, but only
mentioning its use as an early test]
The study was published in the September issue of
Neuropsychology.
Full reference
Full text is available at:
www.apa.org/journals/releases/neu195687.pdf
http://www.eurekalert.org/pub_releases/2005-11/wuis-ado110905.htm
Cholesterol treatment, including statins, may slow Alzheimer's disease progression
A study following 342 Alzheimer’s patients attending a memory clinic
for almost three years has found that the disease progressed
significantly more slowly in patients given cholesterol lowering drugs.
A larger trial will be needed to confirm the findings.
The study appeared in the December issue of the
Journal of Neurology Neurosurgery and Psychiatry.
Full reference
http://www.eurekalert.org/pub_releases/2005-11/bsj-cti111605.htm
Compound in wine reduces levels of Alzheimer's disease-causing peptides
In cell studies, resveratrol has been found to lower levels of
amyloid-beta peptides.
Resveratrol is a natural compound occurring in abundance in grapes,
berries and peanuts. The highest concentration has been reported in
wines prepared from Pinot Noir grapes. The anti-amyloidogenic effect of
resveratrol observed in cell cultures does not however necessarily mean
that the beneficial effect can result simply from eating grapes or
drinking wine. Further research aims to develop more active and more
stable compounds.
The study was published in the November 11 issue of the
Journal of Biological Chemistry.
Full reference
http://www.eurekalert.org/pub_releases/2005-11/asfb-ciw110305.htm
http://www.sciam.com/article.cfm?chanID=sa003&articleID=000581B2-EE9B-136B-AE9B83414B7F0000
Progression of Alzheimer's disease revealed
A new imaging agent is giving researchers information never before
available about how and where Alzheimer’s progresses in the brain.
Results suggest that amyloid
plaques deposit sequentially, first appearing in the
cingulate cortex/precuneus
and
frontal cortex
areas, then progressing to the
parietal and
temporal
cortex and
caudate, and
finally reaching the
occipital cortex and sensory-motor cortex. These findings may
explain why memory and judgment are often the brain functions first
affected in Alzheimer's disease.
The findings were presented at the 35th Annual Meeting of the Society
for Neuroscience, being held Nov. 12-16 in Washington, D.C.
Reference
http://www.eurekalert.org/pub_releases/2005-11/uopm-ctt111105.htm
October
A new analysis of a standard brain test may help predict dementia
A new study gives promise of early diagnosis of Alzheimer’s. A
computer analysis of an EEG (electroencephalograph) test was almost 95%
accurate in predicting those people in their 60s and 70s who would
develop dementia over the next 7 to 10 years. There were several
distinctive features in the brain waves of those who would later show
cognitive impairment. The study now needs to be replicated with a larger
sample.
The study was published online on 6 October in
Neurobiology of Aging.
Full reference
http://www.eurekalert.org/pub_releases/2005-10/dumc-ana100505.htm
Gas-blockers might slow down Alzheimer's disease
Beta-amyloid is known
to cause brain cells to make an inhibitor of an enzyme that triggers the
production of nitric oxide (iNOS). This enzyme is normally turned on
during infection and is needed to help immune cells destroy invading
pathogens, but it is not normally found in the brain, where it may cause
cellular damage that destroys neurons. Although it’s long been known
that iNOS is present in the brain lesions of Alzheimer’s patients, it
hasn’t been known whether its presence makes things worse. A new study
has now shown that Alzheimer's-prone mice that lack iNOS live twice as
long and develop fewer brain lesions than iNOS-expressing mice. The
researchers suggest that iNOS inhibitors might turn out to be an
effective in slowing the progression of Alzheimer's disease.
The study appeared in the November 7 issue of the
Journal of Experimental Medicine.
Full reference
http://www.eurekalert.org/pub_releases/2005-10/joem-gms102005.htm
New light on how amyloid beta accumulation leads to long-term memory loss
A study using genetically
engineered mice has shed new light on why the damage to brain tissue
seen in Alzheimer’s leads to the loss of long-term memories. It seems
that the accumulation of
amyloid-beta peptides can deplete key proteins in the
hippocampus, and this process can be worsened by increased activity
of an enzyme called Fyn. The conversion of new information into
long-term memories requires proteins (such as Arc and Fos) that help
strengthen the synapses between specialized neurons in the hippocampus.
Fyn is located at the synapses, where it regulates the activity of
several memory-related proteins; increases in Fyn activity significantly
increase the susceptibility of the hippocampal granule cells to the
amyloid beta-induced depletion of memory proteins.
The research was reported in two companion papers in the October 19
issue of the Journal of Neuroscience.
Full reference
2
http://www.eurekalert.org/pub_releases/2005-10/gi-szi101705.htm
Concussions increase chance of age-related cognitive impairment
A study involving retired National Football League players found
that they had a 37% higher risk of Alzheimer's than other U.S. males
of the same age. Some 60.8% of the retired players reported having
sustained at least one concussion during their professional playing
career, and 24% reported sustaining three or more concussions. Those
with three or more concussions had a five-fold greater chance of
having been diagnosed with mild cognitive impairment and a
three-fold prevalence of reported significant memory problems
compared to those players without a history of concussion. As the
study was based on self-reported answers to the health questions,
further studies are needed to confirm the findings, but it does seem
likely that head injuries earlier in life increase the chance of
developing dementia or mild cognitive impairment.
The study appeared in the October issue of
Neurosurgery.
Full reference
http://www.eurekalert.org/pub_releases/2005-10/uonc-nsa101005.htm
September
More sensitive tests for predicting Alzheimer's
The first study used data from 119 participants in the Longitudinal
Aging Study Amsterdam. The memory test scores of those who two years
later developed Alzheimer's were compared with the scores of those who
stayed healthy. Three tests were very good at predicting who would later
develop Alzheimer's: a Paired-Associate Learning Test, which cued
participants to recall five semantically related and five semantically
unrelated pairs of words; a Perceptual Identification Task, which
measured how fast participants read aloud words briefly presented on a
computer screen; a Visual Association Test, which cued participants to
recall six line drawings of common objects that had been presented
earlier in an illogical interaction with another object or cue. On the
word-pair memory test, people destined to develop Alzheimer's disease
didn't do any better when words were related than when they weren't,
suggesting they’d already lost deep semantic knowledge. On the
word-reading test, word repetition didn't help high-risk participants to
perform better, a sign that implicit learning was impaired. The popular
Mini Mental Status Exam (MMSE), a test mainly sensitive to episodic
memory, was not as good a predictor.
In the second study, a dichotic listening task, which measures how well
people process information when they hear one thing in the left ear and
another in the right ear, was found to also be predictive of
Alzheimer’s, confirming that people have problems with selective
attention very early in the disease.
The studies appear in the September issue of
Neuropsychology.
Full reference
2
Full text of the both articles is available at
www.apa.org/journals/releases/neu195629.pdf
and
www.apa.org/journals/releases/neu195687.pdf
http://www.eurekalert.org/pub_releases/2005-09/apa-pfm092105.htm
Loss of body mass linked to development of Alzheimer's disease
People with Alzheimer's disease are known to lose weight and body
mass after they have the disease, but now the
Religious Orders Study has revealed that loss in body mass index is
associated with a greater risk of developing the disease. People who
lost approximately one unit of BMI per year had a 35% greater risk than
people with no change in BMI; those with no change in BMI had a 20%
greater risk of developing the disease than that of people who gained
six-tenths of a unit of BMI per year. A similar relationship was also
found between changes in BMI and rate of cognitive decline. The findings
are supported by recently published findings of the Honolulu-Asia Aging
Study, showing that dementia-associated weight loss in Japanese-American
men begins before the onset of dementia and accelerates by the time of
diagnosis.
The research was reported in the September 27 issue of
Neurology.
Full reference
http://www.eurekalert.org/pub_releases/2005-09/nioa-lob092105.htm
Green tea ingredient prevents Alzheimer's-like brain damage in mice
A major antioxidant in green tea (epigallocatechin-3-gallate (EGCG))
has prevented Alzheimer's-like damage in the brains of genetically
engineered mice. EGCG decreased production of
beta-amyloid. It may be that EGCG dietary supplementation could help
prevent and treat the disease. However, other flavinoids in green tea
actually oppose naturally-occurring EGCG's ability to prevent the
harmful build-up of beta-amyloid; thus, drinking green tea alone is
unlikely to have a beneficial effect through the same mechanism.
The report was published in the September 21 issue of the
Journal of Neuroscience.
Full reference
http://www.eurekalert.org/pub_releases/2005-09/uosf-gti091505.htm
Gene therapy reversed memory loss in mice
A study using genetically
engineered mice has reversed the rodents' memory loss by silencing
beta-secretase (an enzyme that helps produce
amyloid plaques). The size and number of plaques were reduced by
two-thirds within a month.
The report appeared in the October 1 issue of
Nature Neuroscience.
Full reference
http://www.eurekalert.org/pub_releases/2005-09/si-tak092005.htm
August
Negative review of recommended Alzheimer's drugs
A review of the 22 published, double-blind, randomised trials of the
three
cholinesterase
inhibitors currently recommended for Alzheimer’s disease (donepezil,
rivastigmine, and
galantamine) has found
considerable flaws in the methodology of all trials, and concluded that
“Because of flawed methods and small clinical benefits, the scientific
basis for recommendations of cholinesterase inhibitors for the treatment
of Alzheimer's disease is questionable.”
The study was reported in the August 6 issue of the
British Medical Journal.
Full reference
New research suggests heart bypass surgery increases risk of Alzheimer's disease
Patients who have either coronary artery bypass graft surgery or
coronary angioplasty are at an increased risk of developing Alzheimer's
disease, according to a study involving 5,216 people who underwent
coronary artery bypass graft surgery (CABG) and 3,954 people who had a
percutaneous transluminal coronary angioplasty (PTCA) in 1996 and 1997.
The researchers suggest the trauma to the brain during surgery is the
principle cause.
The report appeared in the August issue of the
Journal of Alzheimer's Disease.
Full reference
http://www.eurekalert.org/pub_releases/2005-08/cwru-nrs082405.htm
Folates more effective in limiting Alzheimer's disease risk than antioxidants, other nutrients
Analysis of data from the Baltimore Longitudinal Study of Aging has
revealed that those with higher intake of
folates, vitamin E and vitamin B6 had a lower risk of developing
Alzheimer’s. When the three vitamins were analyzed together, only
folates were associated with a significantly decreased risk. Those who
had at least 400mcg of folates a day (the recommended daily allowance)
had a 55% reduction in risk of developing Alzheimer’s. Unfortunately,
most people who reached that level did so by taking supplements,
suggesting the difficulty of doing so through diet alone. Folates are
abundant in foods such as liver, kidneys, yeast, fruits (like bananas
and oranges), leafy vegetables, whole-wheat bread, lima beans, eggs and
milk; however, they are often destroyed by cooking or processing. No
association was found between vitamin C, carotenoids (such as
beta-carotene) or vitamin B-12 intake and decreased Alzheimer's risk.
Results appear in the inaugural issue of
Alzheimer's & Dementia: The Journal of the Alzheimer's Association.
Full reference
http://www.eurekalert.org/pub_releases/2005-08/uoc--fme081105.htm
“Default” brain activity implicated in Alzheimer's disease
Here’s an unexpected finding: imaging of the brains of 764 adults of
various ages has revealed that the regions that are active when people
are in “default mode” — not concentrating on anything in particular,
just musing to yourself — are the same regions that develop plaques in
Alzheimer’s. They also found that, when asked to concentrate on a
specific task, individuals with Alzheimer’s showed increased activity in
these posterior cortical regions, rather than the decreased activity
seen in young, healthy adults. The researchers speculate that dementia
may in fact be a consequence of normal cognitive function — a
possibility that hasn’t heretofore been considered. The findings raise
the hope of developing methods to detect precursors of the disease long
before it develops.
The study appears in the August 24 issue of the
Journal of Neuroscience.
Full reference
http://www.eurekalert.org/pub_releases/2005-08/hhmi-bai082405.htm
Biosensor reveals new information about ADDLs
A new method using nanoscale optical biosensors allows researchers to
detect and estimate the size and structure of
ADDLs in cerebrospinal fluid.
It’s believed that only ADDLs of a certain size cause problems for
neurons in the early stages of Alzheimer’s disease. It is hoped that
eventually this technology will help us diagnose Alzheimer’s accurately
in living people, and aid our understanding of how ADDLs are involved in
Alzheimer’s.
The findings were presented on August 31 at the 230th national meeting
of the American Chemical Society.
Reference
http://www.eurekalert.org/pub_releases/2005-08/acs-brn081905.htm
July
Memory loss in genetically engineered mice reversed
Mice were genetically engineered to develop dementia; the
transgene was designed
to be able to be turned off. The researchers expected that when the
transgene expressing the dementia was turned off, memory loss would
stop. Instead, they were surprised to find the loss was reversed; the
mice regained their memory. A further surprise occurred when it was
found that the neurofibrillary
tangles, thought to be one of the causes of dementia, remained, and
even increased, suggesting that the tangles are not a cause of dementia.
The results were published in the July 15 issue of
Science.
Full reference
http://www.eurekalert.org/pub_releases/2005-07/uom-uom071105.htm
Early warning signs of Alzheimer's show up years before official diagnosis
A meta-analysis of 47 studies of Alzheimer's disease has revealed that
people can show early warning signs across several cognitive domains
years before they are officially diagnosed, confirming that Alzheimer's
causes general deterioration and tends to follow a stable preclinical
stage with a sharp drop in function. People at the preclinical stage
showed marked preclinical deficits in global cognitive ability, episodic
memory, perceptual speed, and executive functioning; along with somewhat
smaller deficits in verbal ability, visuospatial skill, and attention.
There was no preclinical impairment in primary memory. There is no clear
qualitative difference between the normal 75-year old and a preclinical
Alzheimer’s sufferer; instead it seems that the normal elderly person,
the preclinical Alzheimer’s person, and the early clinical Alzheimer’s
patient represent three instances on a continuum of cognitive
capabilities.
The findings appeared in the July issue of
Neuropsychology.
Full reference
http://www.eurekalert.org/pub_releases/2005-07/apa-ews072505.htm
Missing eyeglasses impair activities for a third of nursing home patients with Alzheimer's disease
A study of nearly 100 Alzheimer’s patients in nursing homes has
determined that one third of them were not using or did not have glasses
that were strong enough to correct their eyesight. Apart from causing
disorientation, limiting mobility and increasing the chance of falls,
the loss of vision is likely to impact on mental stimulation, by making
it difficult or impossible to engage in mentally stimulating activities
such as reading or watching television.
The report appeared in the July/August issue of the
Journal of the American Medical Directors Association.
Full reference
http://www.eurekalert.org/pub_releases/2005-07/slu-mem071905.htm
Anti-inflammatory function of Alzheimer's disease drugs revealed
Current Alzheimer’s drugs focus on preventing the breakdown of
acetylcholine.
Acetylcholine-producing cells are among the first to die in Alzheimer's
patients. Research has also shown that the brains of Alzheimer's
patients are characterized by excessive immune activation and
inflammation, which are induced by overproduction of an
inflammation-producing protein called
interleukin-1 and related
compounds. Now a new study has found that current Alzheimer's drugs
cause a marked reduction in the production of interleukin-1. The
findings suggest a new interpretation of why acetylcholine is important;
when the acetylcholine increases (as a result of the drug), there is a
reduction of the production of interleukin-1. The study also describes
the use of a new drug (EN101) which produces these effects in a more
efficient way than known heretofore by destroying the molecular
antecedent (messenger RNA) of the enzyme, rather than simply blocking
the enzyme's activity.
The study was published in the May issue of Annals
of Neurology.
Full reference
http://www.eurekalert.org/pub_releases/2005-07/thuo-afo072805.htm
New light on why plaques form
Alzheimer's disease is characterized by an increasing deposit of the
amyloid-β
protein in the brain, which collect to form aggregations called 'plaques'.
New research has unraveled how certain plaques are formed. It seems the
plaques attach primarily to blood vessels, which show clear structural
damage, leading to leakage between the blood vessels and the brain.
Under normal circumstances, the blood vessels transport excess amyloid-β
protein away from the brain. The findings suggest new treatment
approaches.
The report was published in the August issue of
American Journal of Pathology.
Full reference
http://www.eurekalert.org/pub_releases/2005-07/vfii-adn072705.htm
