News reports of research into Alzheimer's disease Jan - June 2006
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.
May
Good physical function linked to Alzheimer's delay
A study following 2,288 older adults for six years found that those whose
physical function was higher at the start of the study were three times less
likely to develop dementia than were those whose physical function was
lower.
The report appeared in the May 22 issue of Archives of
Internal Medicine.
Full reference
http://www.eurekalert.org/pub_releases/2006-05/ghcc-gpf051806.htm
Collaborative care has better outcomes for both patients and caregivers
An 18-month study involving 153 older adults with Alzheimer's disease and
their caregivers has found that restructuring the primary care practice
environment to emphasize a team approach to care significantly improved the
quality of care and behavioral and psychological symptoms of
dementia. Caregivers were also less stressed and less depressed.
The study was published in the May 10 issue of the
Journal of the American Medical Association.
Full reference
http://www.eurekalert.org/pub_releases/2006-05/iu-lai050406.htm
Link between size of hippocampus and progression to Alzheimer's
A study of 20 older adults with mild cognitive impairment has found that
the
hippocampus was
smaller in those who developed into Alzheimer's during the 3 year period.
The research appeared in the May issue of the Archives
of Neurology.
Full reference
http://www.eurekalert.org/pub_releases/2006-05/uoc--rml050406.htm
Potential new treatment strategy for Alzheimer's
A study has identified several new compounds that could play a role in
preventing or treating Alzheimer's disease and other degenerative conditions
of the nervous system. In culture, these compounds bind with a receptor
called p75NTR; a receptor that in the body binds
neurotrophins.
There is some evidence that in Alzheimer's, some of the neurons that die
express the p75NTR binding site, indicating they may be dying because
neurotrophins are binding to them. Because the new compounds bind with
p75NTR in place of neurotrophins, they may provide a means of preventing
damage that neurotrophins would otherwise be causing. The compounds were
also found to inhibit the death of
oligodendrocytes.
The study appeared in the May 17 issue of the Journal
of Neuroscience.
Full reference
http://www.eurekalert.org/pub_releases/2006-05/uoc--pnt051706.htm
Post-mortem brain studies reveal features of mild cognitive impairment
Autopsies have revealed that the brains of patients with mild cognitive
impairment display pathologic features that appear to place them at an
intermediate stage between normal aging and Alzheimer's disease. For
instance, the patients had begun developing
neurofibrillary tangles, but the number of
plaques was similar to that in
healthy patients. All patients with mild cognitive impairment had
abnormalities in their
temporal lobes, which likely caused their cognitive difficulties, and
many also had abnormalities in other areas that did not relate to the
features of Alzheimer's disease. In a second study, of 34 patients with mild
cognitive impairment who had progressed to clinical dementia before their
deaths, 24 were diagnosed (post-mortem) with Alzheimer’s, and 10 with other
types of dementia. As in the other study, all patients had abnormalities in
their temporal lobes.
The two studies appeared in the May issue of Archives
of Neurology.
Full reference
2nd
http://www.eurekalert.org/pub_releases/2006-05/jaaj-pbs050406.htm
Neurons can produce apolipoprotein E
Apolipoprotein E has been known
to be synthesized in the brain in support cells such as
astrocytes,
microglia, and
ependymal layer cells. Controversial for the last decade has been the
question of whether or not neurons can produce apoE. Using a unique mouse
model, researchers have now demonstrated that neurons can produce apoE, but
only in response to injury to the brain.
The study was published in the May 10 issue of the
Journal of Neuroscience.
Full reference
http://www.eurekalert.org/pub_releases/2006-05/gi-gsp051006.htm
April
Social networks protect against Alzheimer's
Previous studies have found that older people with more extensive social
networks are less likely to suffer cognitive impairment. Now a new study
provides evidence that social networks, like education, offers a 'protective
reserve' capacity that spares them the clinical manifestations of
Alzheimer's disease. 89 elderly people without known dementia participating
in the Rush Memory and Aging Project underwent annual clinical evaluation
and cognitive tests. To determine social network, participants were asked
about the number of children they have and see monthly; about the number of
relatives, excluding spouse and children, and friends to whom they feel
close and with whom they felt at ease and could talk to about private
matters and could call upon for help, and how many of these people they see
monthly. Their social network was the number of these individuals seen at
least once per month. Brain autopsy was done at the time of death. It was
found that, as the size of the social network increased, the same amount of
Alzheimer’s pathology in the brain (i.e., extent of
plaques and
tangles) had less effect on
cognitive test scores. In other words, for persons without much pathology,
social network size had little effect on cognition. However, as the amount
of pathology increased, the apparent protective effect on cognition also
increased.
The study will be published in the May issue of The
Lancet Neurology.
Full reference
http://www.eurekalert.org/pub_releases/2006-04/rumc-snp042106.htm
Dietary supplements offer new hope for Alzheimer's patients
A "cocktail" of dietary supplements (omega-3 fatty acids, uridine and
choline) has been found to dramatically increase the amount of membranes
that form brain cell synapses in gerbils. The treatment is now in human
clinical trials. It is hoped that such treatment may significantly delay
Alzheimer's disease. The treatment offers a different approach from the
traditional tactic of targeting amyloid plaques and tangles. Choline can be
found in meats, nuts and eggs, and omega-3 fatty acids are found in a
variety of sources, including fish, eggs, flaxseed and meat from grass-fed
animals. Uridine, which is found in RNA and produced by the liver and
kidney, is not obtained from the diet, although it is found in human breast
milk.
The study appears in the May 9 issue of Brain Research.
Full reference
http://www.eurekalert.org/pub_releases/2006-04/miot-mro042706.htm
New genetic cause of Alzheimer's disease
Amyloid
protein originates when it is
cut by enzymes from a larger precursor
protein. In very rare cases, mutations appear in the amyloid precursor
protein, causing it to change shape and be cut differently. The amyloid
protein that is formed now has different characteristics, causing it to
begin to stick together and precipitate as amyloid
plaques. A genetic study of Alzheimer's patients younger than 70 has
found genetic variations in the promoter that increases the gene expression
and thus the formation of the amyloid precursor protein. The higher the
expression (up to 150% as in Down syndrome), the younger the patient
(starting between 50 and 60 years of age). Thus, the amount of amyloid
precursor protein is a genetic risk factor for Alzheimer's disease.
The findings will appear in the June issue of
The American Journal of Human Genetics.
Full reference
http://www.eurekalert.org/pub_releases/2006-04/vfii-rda041906.htm
March
Protein identified as cause of memory loss
Researchers have identified a substance in the brain that is proven to
cause memory loss, giving drug developers a target for creating drugs to
treat memory loss in people with dementia. The substance is a form of the
amyloid-beta protein that is distinct from
plaques and has been given the
name Ab*56. Ab*56 impairs memory independently of plaques or neuronal loss,
and may contribute to cognitive deficits associated with Alzheimer's
disease.
The research was published in the March 16 issue of
Nature.
Full reference
http://www.eurekalert.org/pub_releases/2006-03/uom-uom_1031306.htm
http://www.jhu.edu/news_info/news/home06/mar06/memory.html
Reduced insulin in the brain triggers Alzheimer's degeneration
By depleting insulin and its related
proteins in the brain,
researchers have replicated the progression of Alzheimer's disease –
including plaque deposits,
neurofibrillary tangles,
impaired cognitive functioning, cell loss and overall brain deterioration –
in an experimental animal model. Brain deterioration was not related to the
pancreas, raising the possibility that Alzheimer's is a neuroendocrine
disorder, or a Type 3 diabetes.
The study was published in the
Journal of Alzheimer's Disease.
Full reference
http://www.eurekalert.org/pub_releases/2006-03/l-rii031606.htm
Pin1 enzyme key in preventing onset of Alzheimer's disease
An enzyme called Pin1,
previously shown to prevent the formation of the
tangles characteristic of
Alzheimer's brains, has now been shown to also play a pivotal role in
guarding against the development of the
plaques that are also characteristic of Alzheimer's. These findings
establish a direct link between amyloid plaques and tau tangles, and provide
further evidence that Pin1 (prolyl isomerase) is essential to protect
individuals from age-related neurodegeneration.
The study appeared in the March 23 issue of Nature.
Full reference
http://www.eurekalert.org/pub_releases/2006-03/hms-nrs032006.htm
February
Alzheimer's has higher genetic risk than thought
In a study far larger than any undertaken before, results suggest the
highest estimates of the genetic risk of developing Alzheimer’s are in fact
correct. The study involved all participants in the Swedish Twin Registry
aged 65 or older in 1998 (nearly 12,000 of them) and found 392 pairs with
evidence of Alzheimer's in at least one twin. In the model that best fit the
data, genetic influence accounted for 79% of Alzheimer's risk, with 95%
probability of being within the range 67 to 88%. The other 21% of
Alzheimer's risk was due to non- shared environmental causes. Risk from
shared environments was statistically negligible. Genetic risk for
Alzheimer's was the same for men and women after controlling for age. The
study raises doubts about the widely held view that Alzheimer's has two
forms: the "familial," with
genetic roots, and the "sporadic,"
with environmental causes. This doesn’t mean, however, that environment is
unimportant.
The study appeared in the February 2006 issue of
Archives of General Psychiatry.
Full reference
http://www.eurekalert.org/pub_releases/2006-02/uosc-aft020206.htm
Alzheimer's progresses more rapidly in highly educated people
A study of 312 New Yorkers aged 65 and older, who were diagnosed with
Alzheimer's disease and monitored for over 5 years, found that overall
mental agility declined faster for each additional year of education,
particularly in the speed of thought processes and memory, and was
independent of age, mental ability at diagnosis, or other factors likely to
affect brain function, such as depression and vascular disease. It’s
suggested this may reflect the greater ability of brains with a higher
cognitive reserve to tolerate damage, meaning the damage is greater by the
time it becomes observable in behavior. The finding confirms earlier
findings from some epidemiological studies.
The research appeared in the Journal of Neurology
Neurosurgery and Psychiatry.
Full reference
http://www.eurekalert.org/pub_releases/2006-02/bsj-adp021506.htm
Depression associated with changes in the brain in Alzheimer's
A lifetime history of depression is associated with increased
plaques and
tangles in the brains of those
with Alzheimer's disease and more rapid cognitive decline, confirming
previous indications that depression may be a risk factor for Alzheimer’s.
The study is published in the February issue of
Archives of General Psychiatry.
Full reference
http://www.eurekalert.org/pub_releases/2006-02/tmsh-ldb020306.htm
New drug reduces plaque and tangles in Alzheimer's mice
Alzheimer's mice that received
a compound known as AF267B for eight weeks performed significantly better on
a spatial memory test than untreated mice did. A different memory test that
involved associating a place with a shock was not affected. The drug was
found to reduce
plaques and
tangles in the
hippocampus but
not in the
amygdala. AF267B
seems to work in part by enhancing the activity of receptors for the
neurotransmitter
acetylcholine, and
boosting the levels of an enzyme
called
alpha secretase, which blocks
the production of beta-amyloid
proteins. Suppressing the M1 receptors worsened the condition and
performance of Alzheimer’s mice, confirming the important role of M1
receptors in modulating the plaques and tangles characteristic of
Alzheimer’s.
The report appeared in the March 2 issue of Neuron.
Full reference
http://www.sciam.com/article.cfm?chanID=sa003&articleID=000332CA-2F01-1405-AE5A83414B7F4945
Link between APOE and memory neurotransmitter
A new link in the complex chain of Alzheimer’s development has been
found. It’s been found that receptors that bind
apolipoprotein E (APOE) and those that bind
glutamate are in
fact connected, separated only by a small
protein. It may be that
inefficient or high levels of APOE are clogging these binding sites,
preventing glutamate from activating the processes necessary to form
memories. It may also be that the
APOE4 variant — associated with Alzheimer's — is less efficient at
removing lipid debris in the brain than is APOE2 or APOE3.
The study was published in the February 10 issue of the
Journal of Biological Chemistry.
Full reference
http://www.eurekalert.org/pub_releases/2006-02/gumc-nrr020906.htm
January
Use your brain, halve your risk of dementia
In the first comprehensive review of the research into 'cognitive
reserve', which looks at the role of education, occupational complexity and
mentally stimulating activities in preventing cognitive decline, researchers
concluded that complex mental activity across people’s lives almost halves
the risk of dementia. All the studies also agreed that it was never too late
to build cognitive reserve. The review covered 29,000 individuals across 22
studies.
The paper was published online October 6 and will appear in a forthcoming
issue of Psychological Medicine.
Full reference
http://www.eurekalert.org/pub_releases/2006-01/uons-uyb012406.htm
Exercise protects against Alzheimer's
A study following 1,740 seniors (aged 65 and older) over a six-year
period, found that those who exercised three or more times a week had a 30 —
40% lower risk for developing dementia compared with those who exercised
fewer than three times per week. Even modest amounts, such as walking 15
minutes a day, appear beneficial, and the more frail the person was, the
more they benefited from regular exercise.
The report appeared in the January 17 issue of Annals
of Internal Medicine.
Full reference
http://www.eurekalert.org/pub_releases/2006-01/ghcc-eil011006.htm
Blackcurrants may protect against Alzheimer's
A cultured cell study has found that compounds in blackcurrants strongly
protect neuronal cells against the types of stress caused by dopamine and
amyloid-b, a
peptide associated with
Alzheimer's disease. Blackcurrants and boysenberries contain
anthocyanins. Those that
are darker (like British blackcurrants) have more anthocyanins and are
likely to be more potent. Compounds from these berries are already known to
act as antioxidants, but a role in neuroprotection has not been demonstrated
previously.
The paper was published online 23 January and will appear in a forthcoming
issue of the Journal of the Science of Food and
Agriculture.
Full reference
http://www.eurekalert.org/pub_releases/2006-01/jws-bbb011906.htm
New compound stops brain cell degeneration in Alzheimer's disease
A new orally administered compound specifically targeted to suppress
brain cell inflammation and neuron loss associated with Alzheimer's disease
has been developed. The compound, MW01-5-188WH, is rapidly absorbed by the
brain and is non-toxic. It selectively inhibits production of
pro-inflammatory
proteins called cytokines by
glia, giving it relevance for several neurodegenerative disorders. The
compound suppressed brain inflammation and neuron dysfunction in the
hippocampus and protected against cognitive decline in
genetically engineered mice. The
compound also restored normal levels of markers of synaptic dysfunction in
the hippocampus and attenuated Alzheimer's-like behavioral deficits. The
compound represents a new approach to Alzheimer’s therapy.
The report appeared in the January 11 issue of the
Journal of Neuroscience.
Full reference
http://www.eurekalert.org/pub_releases/2006-01/nu-ncs011906.htm
Two pathways lead to Alzheimer's disease
Mild cognitive impairment (MCI), a transitional stage between normal
cognition and Alzheimer's disease, has been categorized into two sub-types
on the basis of differing symptoms. Those with the amnesic subtype (MCI-A)
have memory impairments only, while those with the multiple cognitive domain
subtype (MCI-MCD) have other types of mild impairments, such as in judgment
or language, and mild or no memory loss. Both sub-types progress to
Alzheimer's disease at the same rate. A new imaging technique has now
revealed that these types do in fact have different pathologies. The
hippocampus of
patients with MCI-A was not significantly different from that of Alzheimer's
patients (who show substantial shrinkage), but the hippocampus of those with
MCI-MCD was not significantly different from that of the healthy controls.
The report appeared in the January issue of Archives
of Neurology.
Full reference
http://www.eurekalert.org/pub_releases/2006-01/uopm-tpf010606.htm
Key genetic risk for Alzheimer's linked to myelin breakdown
Myelin, the fatty insulation coating the brain's internal wiring, builds
up in childhood, and breaks down as we age. Myelin is critical for speedy
communication between neurons. A new study supports a growing body of
evidence that myelin breakdown is a key contributor to the onset of
Alzheimer disease later in life. Moreover, it has also revealed that the
severity and rate of myelin breakdown in healthy older individuals is
associated with ApoE status. Thus
both age, the most important risk factor for Alzheimer disease, and ApoE
status, the second-most important risk factor, seem to act through the
process of myelin breakdown.
The findings are detailed in the January edition of
Archives of General Psychiatry.
Full reference
http://www.eurekalert.org/pub_releases/2006-01/uoc--isl122805.htm
Study links Alzheimer's and Down’s syndrome
New research suggests the cognitive problems observed in Alzheimer’s are
related to defects in the machinery controlling neuronal connections — PAK
enzyme signaling pathways. PAK (p21-activated kinase)
enzymes form a family that
includes two members (PAK1 and PAK3) that play critical roles in learning
and memory. Humans with genetic loss of PAK3 have severe mental retardation.
The study reveals that both PAK1 and PAK3 are abnormally distributed and
reduced in Alzheimer patients, and that
beta-amyloid was directly
involved in PAK signaling deficits. The finding suggests therapies designed
to address the PAK defect could treat cognitive problems in both patient
populations.
The paper was published online January 15 in Nature
Neuroscience.
Full reference
http://www.eurekalert.org/pub_releases/2006-01/uoc--sid012506.htm
Study links Alzheimer's disease to abnormal cell division
Neurons affected by Alzheimer’s and many other neurodegenerative diseases
often start to divide before they die. A new mouse study shows that this
abnormal cell division starts long before
amyloid plaques or other
markers of the disease appear, suggesting a new approach to therapy for
Alzheimer's. The findings also shed new light on the theory that the
accumulation of amyloid beta
in the brain causes the neuron death in Alzheimer’s, indicating that
micro-molecular aggregates (tiny clumps made up of several amyloid beta
molecules) rather than amyloid plaques may trigger the disease.
The report appeared in the January 18 issue of the
Journal of Neuroscience.
Full reference
http://www.eurekalert.org/pub_releases/2006-01/nion-sla011206.htm
