Use the labels in the right column to find what you want. Or you can go thru them one by one, there are only 12151 posts. Searching is done in the search box in upper left corner. I blog on anything to do with stroke.DO NOT DO ANYTHING SUGGESTED HERE AS I AM NOT MEDICALLY TRAINED, YOUR DOCTOR IS, LISTEN TO THEM. BUT I BET THEY DON'T KNOW HOW TO GET YOU 100% RECOVERED. I DON'T EITHER, BUT HAVE PLENTY OF QUESTIONS FOR YOUR DOCTOR TO ANSWER.
Deans' stroke musings
Changing stroke rehab and research worldwide now.Time is Brain!Just think of all thetrillions and trillions of neuronsthateach daybecause there areeffective hyperacute therapies besides tPA(only 12% effective). I have 493 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.
What this blog is for:
Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It's quite disgusting that this information is not available from every stroke association and doctors group. My back ground story is here:http://oc1dean.blogspot.com/2010/11/my-background-story_8.html
These always seem to need more followup to be useful rather than doing it
right in the first place and doing some real research. Regardless, I
bet your doctor does nothing with this information. A. Because s/he never read it. B. Because s/he could not be bothered to understand how to implement it in a protocol. C. It is not my job. I am waiting for SOMEONE ELSE TO SOLVE THE PROBLEM. Namely 100% recovery for all my stroke patients.
Ischemic injury induces neurogenesis in the subventricular zone (SVZ)
of the lateral ventricles and subgranular zone (SGZ) of dentate gyrus
(DG), and it promotes the migration of neuroblasts, guided by blood
vessels, into the ischemic damaged area. Recently, we have shown that
docosahexaenoic acid (DHA; 22:6n-3) therapy improves functional and
histological outcomes following experimental stroke. The objective,
hence, is to determine whether DHA administration enhances endogenous
neurogenesis after cerebral ischemia.
Twenty-one male SD rats were anesthetized with isoflurane and subjected
to 2 h of middle cerebral artery occlusion (MCAo) by intraluminal
filament. DHA (5 mg/kg, n=10) or saline (n=11) was administered
intravenously at 3 h after onset of MCAo (n = 7-10 per group). BrdU was
injected on days 4, 5 and 6. DCX (doublecortin), NeuN (a marker for
mature neurons), ki-67 (marker for cell proliferation) have been used to
test the proliferation, migration and differentiation of neural
precursor cells. Behavioral tests were conducted on days 1, 2 and 3 and
weeks 1 and 2. Immunohistochemistry with BrdU and ki-67, DCX or NeuN,
and histopathology were performed on day 14.
DHA-treated animals showed improved neurologic scores compared to the
saline group during the two-week survival period. Total, cortical and
subcortical infarct areas in the DHA-treated group were significantly
attenuated at multiple bregma levels as well as total, cortical and
subcortical infarct volumes by 42.4 %, by 47.5 %, and by 31.2 % compared
to the vehicle-treated group. The number of BrdU+/ki-67+
cells in DHA-treated rats was increased in cortex by 88 %, SVZ by 40 %
and DG by 270 % compared to saline-treated rats. DHA treatment increased
the number of BrdU+/DCX+ cells in the cortex by
65 %, the SVZ by 29 % and the DG (by 58 %) compared to saline-treated
group. In addition, the numbers of BrdU+/NeuN+ cells were increased in the cortex by 49 %, SVZ by 28 % and DG by 48% compared to vehicle treatment.
DHA increased neurogenesis by proliferation, differentiation and
migration of neural stem cells in the DG, SVZ and peri-infarct area two
weeks after ischemic stroke. In addition, DHA promoted neurobehavioral
recovery and reduced infarct volume.
Molecular mechanisms underlying stroke-induced neurogenesis have not
been fully investigated. The microRNA 17-92 cluster (miR17-92) regulates
proliferation and differentiation of adult neural progenitor cells
(NPCs). The present study investigated whether the miR17-92 cluster in
NPCs is required for stroke-induced neurogenesis.
Methods and Results: Mice with inducible and conditional knockdown of the miR17-92 cluster in nestin lineage NPCs (nestin-CreERT2/miR17-92-/-,
17-92-cKO, n=9) and wild-type litters (WT, n=9) were treated by
tamoxifen. Administration of tamoxifen resulted in more than 60%
reduction of individual members of the miR-17-92 cluster (miR-17: 1.0 vs
0.4; miR-19a: 1.0 vs 0.3; miR-19b: 1.0 vs 0.2; miR-20a: 1.0 vs 0.4;
miR-92a: 1.0 vs 0.4 fold in WT, p<0.05) in NPCs localized to the
subventricular zone (SVZ). Two days after termination of tamoxifen
treatment, these mice were subjected to permanent right middle cerebral
artery occlusion (MCAO) and sacrificed 28 days post-MCAo. Compared to WT
mice, 17-92-cKO mice exhibited significant (p<0.05) reduction of
proliferation of NPCs measured by the number of Ki67+ cells (226±43 vs 471±100 cells/mm2) and the number of DCX+
neuroblasts (11±2% vs 24±4% ) in the ischemic SVZ. Cultured NPCs
harvested from ischemic cKO mice showed significant (p<0.05)
reduction of BrdU+ cells (37±2% vs 61±4% WT , n=3/group), Tuj1+ neuroblasts (5±0.2% vs 9±0.4% ), GFAP+ cells (33±3% vs 53±2% ), and NG2+
oligodendrocyte progenitor cells (OPCs, 3±0.1% vs 5±0.5%). These in
vivo and in vitro data indicate that reduction of the miR17-92 cluster
suppresses stroke-induced neurogenesis and gliogenesis. Western blot
analysis showed that miR17-92 cKO significantly (p<0.05) increased
and reduced a cytoskeleton-associated protein, Enigma homolog1 (ENH1,
1.6 vs 1.0 fold), and its down-stream transcription factor, inhibitor of
differentiation1 (ID1, 1.0 vs 0.6 fold), respectively. ENH1 is a
putative target of the miR17-92 cluster.
Our data indicate that the miR17-92 cluster in adult nestin lineage
NPCs is required for stroke-induced neurongenesis and gliogenesis, and
that the miR17-92 cluster possibly targets ENH1/ID1 signaling.
Variation in an animal’s spatial environment can induce
variation in the hippocampus, an area of the brain involved in spatial
cognitive processing. Specifically, increased spatial area use is
correlated with increased hippocampal attributes such as volume and
neurogenesis. In the side-blotched lizard (Uta stansburiana), males
demonstrate alternative reproductive tactics and are either territorial -
defending large, clearly defined spatial boundaries - or
non-territorial - traversing home ranges that are smaller than the
territorial males’ territories. Our previous work demonstrated cortical
volume (reptilian hippocampal homologue) correlates with these spatial
niches. We found that territorial holders have larger medial cortices
than non-territory holders, yet these differences in the neural
architecture demonstrated some degree of plasticity as well. Although we
have demonstrated a link among territoriality, spatial use, and brain
plasticity, the mechanisms that underlie this relationship are unclear.
Previous studies found that higher testosterone levels can induce
increased use of the spatial area and can cause an upregulation in
hippocampal attributes. Thus, testosterone may be the mechanistic link
between spatial area use and the brain. What remains unclear, however,
is if testosterone can affect the cortices independent of spatial
experiences and whether testosterone differentially interacts with
territorial status to produce the resultant cortical phenotype. In this
study, we compared neurogenesis as measured by the total number of
doublecortin-positive cells and cortical volume between territorial and
non-territorial males supplemented with testosterone. We found no
significant differences in the number of doublecortin-positive cells or
cortical volume among control territorial, control non-territorial, and
testosterone-supplemented non-territorial males, while
testosterone-supplemented territorial males had smaller medial cortices
containing fewer doublecortin-positive cells. These results demonstrate
that testosterone can modulate medial cortical attributes outside of
differential spatial processing experiences but that territorial males
appear to be more sensitive to alterations in testosterone levels
compared with non-territorial males.
Your doctor will need to determine what can be changed in your recovery
protocols even though this was just tested in mice. You do want the
kitchen sink thrown at your recovery, don't you? So ask your fucking
doctor what interventions that are not yet clinically proven in humans
s/he is testing on you. http://www.nature.com/articles/srep42946
designed to increase adult hippocampal neurogenesis (AHN) may have
therapeutic potential for reversing memory impairments. H3
receptor antagonists/inverse agonists also may be useful for treating
cognitive deficits. However, it remains unclear whether these ligands
have effects on AHN. The present study aimed to investigate the effects
of a 28-day treatment with S 38093, a novel brain-penetrant
antagonist/inverse agonist of H3 receptors, on AHN
(proliferation, maturation and survival) in 3-month-old and in aged
16-month-old mice. In addition, the effects of S 38093 treatment on
7-month-old APPSWE Tg2576 transgenic mice, a model of Alzheimer’s
disease, were also assessed. In all tested models, chronic treatment
with S 38093 stimulated all steps of AHN. In aged animals, S 38093
induced a reversal of age-dependent effects on hippocampal brain-derived
neurotrophic factor (BDNF) BDNF-IX, BDNF-IV and BDNF-I transcripts and
increased vascular endothelial growth factor (VEGF) expression. Finally,
the effects of chronic administration of S 38093 were assessed on a
neurogenesis-dependent “context discrimination (CS) test” in aged mice.
While ageing altered mouse CS, chronic S 38093 treatment significantly
improved CS. Taken together, these results provide evidence that chronic
S 38093 treatment increases adult hippocampal neurogenesis and may
provide an innovative strategy to improve age-associated cognitive
Your doctor will need to determine what can be changed in your recovery protocols even though this was just tested in rats. You do want the kitchen sink thrown at your recovery, don't you? So ask your fucking doctor what interventions that are not yet clinically proven in humans s/he is testing on you. http://www.mdpi.com/1422-0067/18/2/455/htm
Jing Luo 1,†,
Haiqing Zheng 1,†,
Liying Zhang 1,†,
Qingjie Zhang 1,
Lili Li 1,
Zhong Pei 2
Xiquan Hu 1,*
Department of Rehabilitation Medicine, The Third Affiliated Hospital, Sun Yat-Sen University, Guangzhou 510630, China
Department of Neurology, The First Affiliated Hospital, Sun Yat-Sen University, Guangzhou 510080, China
Received: 16 November 2016 / Accepted: 10 February 2017 / Published: 20 February 2017
Repetitive transcranial magnetic stimulation
(rTMS) has rapidly become an attractive therapeutic approach for stroke.
However, the mechanisms underlying this remain elusive. This study
aimed to investigate whether high-frequency rTMS improves functional
recovery mediated by enhanced neurogenesis and activation of
brain-derived neurotrophic factor (BDNF)/tropomyosin-related kinase B
(TrkB) pathway and to compare the effect of conventional 20 Hz rTMS and
intermittent theta burst stimulation (iTBS) on ischemic rats. Rats after
rTMS were sacrificed seven and 14 days after middle cerebral artery
occlusion (MCAO), following evaluation of neurological function.
Neurogenesis was measured using specific markers: Ki67, Nestin,
doublecortin (DCX), NeuN and glial fibrillary acidic protein (GFAP), and
the expression levels of BDNF were visualized by Western blotting and
RT-PCR analysis. Both high-frequency rTMS methods significantly improved
neurological function and reduced infarct volume. Moreover, 20 Hz rTMS
and iTBS significantly promoted neurogenesis, shown by an increase of
Ki67/DCX, Ki67/Nestin, and Ki67/NeuN-positive cells in the peri-infarct
striatum. These beneficial effects were accompanied by elevated protein
levels of BDNF and phosphorylated-TrkB. In conclusion, high-frequency
rTMS improves functional recovery possibly by enhancing neurogenesis and
activating BDNF/TrkB signaling pathway and conventional 20 Hz rTMS is
better than iTBS at enhancing neurogenesis in ischemic rats.
is a major cause of neurological disability that leads to serious
clinical consequences. It has been estimated that 90% of stroke
survivors suffer permanent neurological deficits . At present, rehabilitation therapy is the best approach for treating neurological deficits after stroke .
However, it is not ideal because most stroke survivors remain
neurologically impaired after rehabilitation. Thus, there is an urgent
need for the development of novel approaches to stroke rehabilitation.
One promising strategy for stroke rehabilitation is to enhance
endogenous pathways that support restoration after brain damage . Neural stem cell (NSC) plays a key role in endogenous restoration following stroke .
NSC persists in the rostral subventricular zone (SVZ) and subgranular
zone (SGZ) of the hippocampal dentate gyrus (DG) throughout life in
mammals . More importantly, NSC can proliferate and migrate into damaged brain regions following ischemic stroke [3,4,6]. Therefore, the promotion of endogenous neurogenesis is an attractive strategy for stroke rehabilitation.
transcranial magnetic stimulation (rTMS) is a noninvasive
neuromodulatory technique which affects brain physiology through
magnetic pulses. Different rTMS techniques have been applied to stroke
and, interestingly, they can produce different modulatory effects. For
example, high-frequency rTMS (>5 Hz) stimulates cortical excitability
and generates long-term potentiation (LTP)-like effects. In contrast,
low-frequency rTMS (<1 Hz) reduces cortical excitability and produces
long-term depression (LTD) . Intermittent theta burst stimulation (iTBS) is a novel form of high-frequency rTMS .
Conventional high-frequency rTMS procedures last between 20 and 45 min,
as compared to TBS paradigms that require 1 to 3 min of stimulation .
Recently, some studies have suggested that iTBS applied to the
ipsilateral side of human or animals has similar or better efficacy in
treating stroke compared to conventional rTMS [11,12].
Whether iTBS is better than conventional high-frequency rTMS on
improvement of functional recovery in ischemic rats is still unknown.
Moreover, it is reported that high-frequency rTMS enhances neurogenesis
in ischemic rats . However, the underlying mechanism remains elusive.
possible mechanism might be an increase in the expression of
brain-derived neurotrophic factor (BDNF) after high-frequency rTMS .
BDNF is a member of the neurotrophin family, which has recently been
shown to play a role both in protection and in recovery of function
after stroke . BDNF promotes NSC migration and proliferation via its receptor, tropomyosin-related kinase B (TrkB) [16,17].
Therefore, this study aimed to investigate whether the beneficial
effect of rTMS on functional recovery is mediated via enhanced
neurogenesis and activation of the BDNF-TrkB signaling pathway and to
compare the effect of conventional 20 Hz rTMS and iTBS on neurogenesis
in ischemic rats
Alcohol abuse is an important concern of many societies. Hippocampal neurogenesis regulates abusing drugs in a positive manner. The aim of this study was to identify factors that regulate neurogenesis in isolation period that increase preference for alcohol and salt.
Materials and Methods:
In this study sixteen rats were randomly divided into two groups: Pair (social) and isolation. Rats in the isolation group were isolated for 14 days plus one week for acclimatization
. Rats in pair group also were kept in the same condition for 14 days. In this period BrdU (50 mg/kg/day/i.p.) was injected.
At the end of the experiment, rats examined for copper, zinc, malondialdehyde (MDA), neurogenesis, salt consumption and alcohol preference.
Zinc in serum reduced in isolated rats, but copper in serum paradoxically increased in isolated rats. Neurogenesis reduced in isolated rats. Also, MDA in serum, salt consumption, and alcohol consumption increased in the isolated group.
Social isolation with reduction of neurogenesis predisposes rats to consume more alcohol and also salt. The reduction in neurogenesis is associated with paradoxical balance of zinc and copper and increase in MDA in serum. So, regulation of copper and zinc may have beneficial effects on neurogenesis, sensitization and alcohol preference.
If you have high blood pressure, you’re well aware of the types of foods you shouldn’t be eating. Your doctor
has probably shoved a lengthy list of don’ts down your throat: Don’t
eat red meat; steer clear of too much salt. At a certain point, you’ve
probably asked yourself, “What can I eat?” The good news is, there’s still plenty you can enjoy.
For folks with high blood pressure, it’s important to be cognizant of how diet will ultimately lower, or contribute, to their high blood pressure. The American Heart Association (AHA)
says, “Eating a heart-healthy diet is important for managing your blood
pressure and reducing your risk of heart attack, stroke, and other
We’ve done some digging, and have found 10 foods that will help keep those BP numbers where they need to be. Check it out.
2. Whole grains
3. Low-fat yogurt
7. Olive oil
9. Lean chicken
10. Leafy greens
Slightly more information at the link but nothing even
remotely close to a protocol. Once again you are completely
on your own to figure out your recovery and prevention interventions.
Donepezil, a medication that is approved to treat people with
Alzheimer's disease, should not be prescribed for people with mild
cognitive impairment without a genetic test. UCLA School of Nursing
researchers discovered that for people who carry a specific genetic
variation -- the K-variant of butyrylcholinesterase, or BChE-K --
donezpezil could accelerate cognitive decline. BACKGROUND
Mild cognitive impairment is a transitional state between normal
age-related changes in cognition and dementia. Because many people with
the condition display symptoms similar to those caused by Alzheimer's
disease, some physicians prescribe donepezil, which is marketed under
the brand name
Aricept and is the most-prescribed medication for Alzheimer's.
Donepezil was tested as a possible treatment for mild cognitive
impairment in a large, federally funded study published in 2005, but it
was not approved by the FDA. Still, doctors have often prescribed the
drug "off-label" -- meaning that it is not approved for that specific
disorder -- for their patients with mild cognitive impairment. METHOD
From data collected during the 2005 trial, the researchers looked at
the association between BChE-K and changes in cognitive function. Using
two tests that measure cognitive impairment, the Mini-Mental State
Examination and the Clinical Dementia Rating Sum of Boxes, they found
that people with the genetic variation who were treated with donepezil
had greater changes in their scores than those who took placebos. They
also found that those who took donepezil had a faster cognitive decline
than those who took the placebo. IMPACT
Physicians are increasingly using personalized medicine, including
pharmacogenetics -- the study of how genetics affect a person's response
to a drug -- to tailor their patients' care. The findings reinforce the
importance of physicians discussing the possible benefits and risks of
this treatment with their patients.
Wisdom and grace come with age, but so do
mental slowing and increased risk for dementia. As the elderly
population continues to grow, preserving brain health to maintain
independence and quality of life into older age is a pressing concern.
Researchers have identified some unsurprising factors that reduce one's
risk for cognitive decline, including education, exercise or a healthy diet.
But a more controversial question that continues to perplex scientists
is whether alcohol consumption might also stave off cognitive impairment
The aging brain on alcohol
Anyone who's experienced the fatigue and brain fog that follow a night of heavy drinking doesn't need science to explain the dangers of excessive alcohol
intake. These health risks may be especially impactful to the older
brain, which is already particularly vulnerable to environmental
stressors. However, in moderation, a glass of wine or beer may not only
be harmless, but may in fact also confer resilience to the aging brain
against cognitive decline. Numerous studies have reported that moderate
drinking is associated with lower rates of dementia, better cognitive performance, and slower decline in memory and executive functions.
Yet, not all studies support the notion that a nightcap can help keep
the brain sharp into late life. These discrepant findings raise two
obvious questions. First, why are some patterns of drinking
neurobiologically healthy, while others are toxic? And second, how can
we better identify drinking behaviors that promote the healthiest
trajectories of cognitive aging? Neuroprotective in moderation, neurotoxic in excess
In excess, alcohol works as a neurotoxin on may levels. Studies in animals have shown that binging on ethanol kills neurons and impairs neurogenesis–the
birth of new neurons–in the hippocampus, a region critical to creating
new memories. Furthermore, alcohol-induced dementia results from brain
damage that occurs with prolonged alcohol abuse. The reasons for the
observed benefits of alcohol are less clear. In contrast to binge
drinking, moderate alcohol intake increases neurogenesis
and may help combat oxidative stress to neurons. It's well documented
that what's good for the heart is good for the brain, and indeed,
vascular dysfunction often co-exists with or precipitates many forms of
dementia. A prevailing theory is that the neuroprotective properties of
drinking stem largely from their positive effects on cerebrovascular
health. Alcohol can reduce risk for stroke and heart disease, lower
blood pressure and increase HDL ("good") cholesterol. However, some
evidence that wine is more strongly neuroprotective than other forms of
alcohol suggests that resveratrol, a potent antioxidant found in red
wine, may also play a role. Although resveratrol minimizes dementia
pathology in animals, the extremely high doses required make it unlikely
to be the primary source of neuroprotection from alcohol.
Unraveling healthy drinking patterns for the aging brain
For our aging population to reap the greatest benefit from alcohol,
it will be essential to determine patterns of healthy drinking that are
optimized for the individual. This will require, foremost, a
comprehensive understanding of how alcohol distinctly affects you versus
me based on our genetics, sex or lifestyle. For example, alcohol has
been found to differentially influence brain structure and risk for
dementia or cognitive impairment
for those with and without the apolipoprotein E4 gene, a strong risk
factor for Alzheimer's disease. Furthermore, studies have inconsistently
reported sex differences in how drinking influences cognitive decline, which may be explained by differences in how men and women metabolize alcohol.
Despite overwhelming evidence that moderate alcohol intake can be
healthy for the aging brain, there are striking incongruences across
findings–which may be due to differences in study design or confounding
factors–that muddle our understanding of alcohol's benefits. 'Survival
bias,' in which healthier individuals participate in studies for longer,
is an unavoidable complication in longitudinal studies of aging. This
could significantly skew results if unhealthy drinkers drop out early,
leaving only "healthy" drinkers to be studied in very old age.
Furthermore, most human studies on alcohol and brain aging rely on
observed associations, which can be replete with confounding factors.
For instance, it's known that drinkers tend to live more healthy
lifestyles (e.g., they may exercise more or follow a Mediterranean
diet), or may drink more often simply because they're more socially
active, which alone is known to be brain-healthy. What's more, effects of alcohol on cognitive aging may depend on the type of alcohol
consumed, how alcohol intake is measured, or the definition of
"non-drinkers." Many studies group life-long abstainers together with
quitters, who may avoid alcohol due to poor health or may have developed
health problems from alcohol abuse. However, my postdoctoral adviser
Linda McEvoy, who studies effects of alcohol on brain aging at UC San
Diego, explains that "Randomized controlled trials offer a better
alternative to more definitely answer the question of how moderate alcohol intake
affects cognitive function. Such trials have demonstrated beneficial
cardiometabolic effects in those randomized to drink moderate amounts of
alcohol." A prescription for alcohol?
Despite some uncertainties in the research so far, it appears that regular moderate drinking
is unlikely to be hazardous to cognitive function and may even support
healthy brain aging. Until we have further clarification, McEvoy offers
some advice to those hoping to preserve brain health into late life: "If
a person consumes alcohol, I would advise drinking moderate amounts of
alcohol (one or two drinks) with dinner. If the person does not drink, I
would not advise starting. Some individuals have a hard time
controlling the amount they drink, and heavy drinking has detrimental
effects on brain health and cognitive function."
Our blood stem cells generate around a thousand billion new blood
cells every day. But the blood stem cells’ capacity to produce blood
changes as we age. This leads to older people being more susceptible to
anaemia, lowered immunity and a greater risk of developing certain kinds
of blood cancer. Now for the first time, a research team at Lund
University in Sweden has succeeded in rejuvenating blood stem cells with
established reduced function in aging mice. The study is published in
When we are young, our blood stem cells produce an even and
well-balanced number of red and white blood cells according to need. As
we age, however, the capacity of the blood stem cells to produce the
number of blood cells we need declines.
“This type of age-related change can have major consequences as it
can lead to an imbalance in stem cell production. For example, a reduced
production of immune cells or excessive production of other types of
cells can be a precursor to leukaemia”, explains David Bryder, who
headed the study at Lund University.
Tracking old stem cells
A fundamental question was whether
blood stem cells age differently within a single individual or whether
all blood stem cells are equally affected by advancing age. In an
initial stage, it was therefore important to genetically mark old blood
stem cells, to enable the identification and tracking of those most
affected by age. In the next step, these traceable cells were
reprogrammed to another type of stem cell – known as iPS cells, which
can generate all cells in an individual and not only blood cells. When
the cells are reprogrammed, their identity is ‟re-set”; when these
reprogrammed iPS cells formed new blood stem cells, the researchers
observed that the re-set had entailed a rejuvenation of the cells.
“We found that there was no difference in blood-generating capacity
when we compared the reprogrammed blood stem cells with healthy blood
stem cells from a young mouse. This is, as far as we know, the first
time someone has directly succeeded in proving that it is possible to
recreate the function of young stem cells from a functionally old cellˮ,
says Martin Wahlestedt, the first author of the study.
Not caused by mutations
The research team’s studies have also
thereby shown that many age-related changes in the blood system cannot
be explained by mutations in the cells’ DNA. If the changes depended on
permanent damage at the DNA level, the damage would still be present
after the re-set. Instead, epigenetic changes appear to underlie the
decline in function associated with advancing age.
“Our findings justify further research to improve the function of
human blood stem cells and thereby address diseases such as anaemia,
leukaemia and other blood disorders”, concludes David Bryder. The research was funded by: the Swedish Cancer Society, the
Swedish Research Council, the Swedish Pediatric Leukemia Foundation,
Knut and Alice Wallenberg foundation, ERC consolidator grant http://www.nature.com/articles/ncomms14533 Full bibliographic informationClonal reversal of ageing-associated stem cell lineage bias via a pluripotent intermediate
Wahlestedt, Eva Erlandsson, Trine Kristiansen, Rong Lu, Cord
Brakebusch, Irving L. Weissman, Joan Yuan, Javier Martin-Gonzalez &
Really? This has been known for decades. And I bet this still will not result in looking for a tPA replacement.
You mean this poster from World Stroke Day was lying?
American Stroke Association Meeting Report – Session A17 – Abstract
116 Many ischemic stroke patients do not get tPA, which can decrease
their chances for recovery. Blacks, Hispanics, women and “Stroke
Belters” are less likely to get tPA. Patients treated in large, urban
hospitals, stroke-certified hospitals and hospitals participating in
the American Heart Association’s Get With The Guidelines®─Stroke program
are more likely to get tPA. Patients with private insurance were more
likely to receive tPA than those with Medicare.
Although tPA treatment for stroke is increasing over time,
minorities, women and residents of 11 southeastern states that make up
the “Stroke Belt” are left behind when it comes to receiving tPA,
according to research presented at the American Stroke Association’s
International Stroke Conference 2017.
Tissue plasminogen activator, or tPA, is the only treatment approved
by the Food and Drug Administration for ischemic stroke, the most common
kind of stroke. If administered within 4.5 hours of the first signs of
stroke, tPA can dissolve the blood clot and restore blood flow to the
affected part of the brain.
“Hospitals, governments and other organizations are undertaking
efforts to increase the number of patients who receive tPA,” said Tracy
Madsen, M.D., Sc.M., lead researcher and Assistant Professor of
Emergency Medicine at Brown University in Rhode Island. “We wanted to
see if these quality improvement efforts were making a difference.”
The study reviewed records from the National Inpatient Sample of
563,087 patients (median age 74) who had an ischemic stroke between 2005
and 2011. Overall, 3.8 percent of patients received tPA, with the
number growing each year.
Blacks were 38 percent less likely than whites to receive tPA. Hispanics were 25 percent less likely than whites to receive tPA. Women were 6 percent less likely than men to receive tPA. Those with private insurance were 29 percent more likely to receive tPA compared to those with Medicare. Residents of the “Stroke Belt” were 31 percent less likely than those living elsewhere to receive tPA. Researchers
also found that patients discharged from a designated stroke center or a
hospital participating in the American Heart Association’s Get With The
Guidelines®─Stroke program were more likely to receive tPA. Likewise,
patients were more likely to receive tPA at large, urban, or teaching
hospitals compared to hospitals discharged from small, rural, or
Madsen said that the growing number of hospitals participating in the
Get With The Guidelines®─Stroke program and legislation requiring
emergency services to take stroke patients to regional stroke centers
are likely to increase the number of patients receiving tPA.
“Some previous studies have found that up to three-fourths of
patients arrived after the time window for tPA had closed,” Madsen said.
“Many patients across all groups do not arrive at the hospital in time,
but this is particularly true for underrepresented minorities.”
An important limitation of the study data is that researchers could
not determine why patients did not receive tPA. The study is also
limited because we were not able to adjust for patient level factors
such as time to arrival and other tPA exclusion criteria, stroke
severity, patient education, and socioeconomic status. “More research
needs to be done to help figure out why many patients do not receive
tPA,” Madsen said.
“There is also a lot of work to do in the realm of stroke education
so that patients recognize stroke symptoms and call EMS immediately,”
According to the American Heart Association’s Heart Disease and
Stroke Statistical Update, 795,000 Americans have a stroke every year,
causing almost 129,000 deaths. Residents of the Stroke Belt—Alabama,
Arkansas, Georgia, Indiana, Kentucky, Louisiana, Mississippi, North
Carolina, South Carolina, Tennessee and Virginia—suffer even higher
rates of stroke and stroke death.
The National Inpatient Sample is the largest publicly available database of inpatient health care in the U.S.
Coauthors are Shannon Melluzo, B.A.; Charles R. Wira III, M.D.;
Zainab Magdon-Ismail, Ed.M., M.P.H.; David Day, B.S.; and Toby I.
Author disclosures are on the abstract.
The study was funded by the American Heart Association/American
Stroke Association Founders Affiliate, and the Northeast Cerebrovascular
Consortium. http://newsroom.heart.org/news/many-stroke-patients-do-not-receive-life-saving-therapy?preview=13bffffcc15f8d35a03f7314a3b1eded Full bibliographic informationAHA/ASA
International Stroke Conference 2017 Session A17 - Abstract 116
Minorities, Women, and Stroke Belters Left Behind in t-PA Use Despite
Quality Improvement Efforts
You probably want your doctor to get this so the nutritionist can create a diet protocol with this included. What berries? How much? How often? Are grapes considered red? What form do the berries need to be in? Raw? Cooked? Fermented? Do pies count? http://science.sciencemag.org/content/355/6327/808.8?
John F. Foley
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Science 24 Feb 2017: Vol. 355, Issue 6327, pp. 808-809 DOI: 10.1126/science.355.6327.808-h
Greece, February 23, 2017 - Greek researchers demonstrated the potential
of a self-administered virtual supermarket cognitive training game for
remotely detecting mild cognitive impairment (MCI), without the need for
an examiner, among a sample of older adults. MCI patients suffer from
cognitive problems and often encounter difficulties in performing
complex activities such as financial planning. They are at a high risk
for progressing to dementia however early detection of MCI and suitable
interventions can stabilize the patients' condition and prevent further
It has been shown that virtual reality
game-based applications and especially virtual supermarkets can detect
MCI. Past studies have utilized user performance in such applications
along with data from standardized neuropsychological tests in order to
detect MCI. The team that conducted this study was the first scientific
team to achieve reliable MCI detection using a virtual reality
game-based application on its own. In that previous study ,
administration of the virtual super market (VSM) exercise was conducted
by an examiner. The present study eliminated the need for an examiner by
calculating the average performance of older adults using a special
version of the VSM application, the VSM Remote Assessment Routine
(VSM-RAR), at home on their own, for a period of one month. It is the
first instance where a self-administered virtual reality application was
used to detect MCI with a high degree of reliability.
The research team included scientists from
the Aristotle University of Thessaloniki (AUTH), the Centre for Research
and Technology Hellas/Information Technologies Institute (CERTH/ITI),
the Greek Association of Alzheimer's Disease and Related Disorders
(GAADRD) and the Network Aging Research (NAR) of the University of
In an article published in the Journal of Alzheimer's Disease,
the researchers have indicated that the virtual supermarket remote
assessment routine (VSM-RAR) application displayed a correct
classification rate (CCR) of 91.8% improving VSM's CCR as assessed in
the previous VSM study while achieving a level of diagnostic accuracy
similar to the most accurate standardized neuropsychological tests,
which are considered the gold standard for MCI detection.
Self-administered computerized cognitive training exercises/games are
gaining popularity among older adults as an easy and enjoyable means of
maintaining cognitive health. Such applications are especially popular
among older adults who consider themselves healthy and are not inclined
to visit specialized memory clinics for cognitive assessment. If
self-administered games and exercises could also detect cognitive disorders,
initial cognitive screening could be conducted remotely. The wide
implementation of this method of remote screening would facilitate the
detection of cognitive impairment at the MCI stage thus allowing for
more efficient therapeutic interventions.
This preliminary study indicates that automated, remote MCI screening
is feasible. This method could be utilized to screen the majority of
the older adult population, as it dramatically lowers
examination-related costs. The social and economic benefits, especially
caregiver and healthcare service burden, of the early detection of
cognitive disorders could be enormous. At the same time, as older adults
are becoming increasingly computer savvy, it is important to create
software that meets their needs and allows them to remain healthy and
active. Out team continues its research on the VSM with the aim of
improving its usability, shortening its administration time and
supplementing the science behind VSM with additional data.
Stelios Zygouris et al, A
Preliminary Study on the Feasibility of Using a Virtual Reality
Cognitive Training Application for Remote Detection of Mild Cognitive
Impairment, Journal of Alzheimer's Disease (2017). DOI: 10.3233/JAD-160518
HOUSTON -- Triple antiplatelet
therapy doesn't help prevent recurrent ischemic stroke or transient
ischemic attack (TIA) but does increase bleeding, the TARDIS randomized
Intensive therapy with aspirin, clopidogrel (Plavix), and dipyridamole (Persantine) had no better 90-day functional outcome in terms of stroke or TIA recurrence and severity as
indicated by score shifting on an ordinal modified Rankin Scale
analysis (adjusted common odds ratio 0.93, 95% CI 0.70-1.23) compared
with aspirin and dipyridamole dual therapy or clopidogrel alone as
indicated in U.K. guidelines.
same was true for fatal stroke (aOR 1.62, 95% CI 0.67-3.93) and for
most subgroups, although triple therapy tended to be better for milder
strokes (NIHSS ≤3, P=0.026 for interaction but no significant treatment effect in that group alone).
"Stick with the guideline," Philip Bath, MBBS, MD,
of the University of Nottingham, England, concluded in presenting the
findings here at the International Stroke Conference. "What our study
says is the sweet spot ... is not at three drugs. It's somewhere at one
or two, and perhaps nearer two than one."
Bleeding risk was clearly increased with triple therapy, with an
adjusted common OR of 2.49 in the ordinal analysis for bleeding
occurrence and severity at 90 days (95% CI 2.00-3.10). The net
risk-to-benefit ratio came up neutral across all endpoints and
combination endpoints considered.
The findings were "fairly definitive" and consistent with prior
antiplatelet prophylaxis evidence across multiple other conditions,
commented Mark Alberts, MD, of the Hartford Hospital, and spokesperson for the American Stroke Association on the press conference panel.
"The more antiplatelet treatments you add on and the longer the
treatment, you increase risk of hemorrhagic or bleeding complications,
not just in the brain but throughout the body, such as gastrointestinal
hemorrhage," he said.
terms of generalizability, the findings fit with U.S. guidelines too,
Alberts said, although even dual therapy is not typical in U.S. stroke
U.K. guidelines switched during the TARDIS trial as clopidogrel went
generic to recommend monotherapy with that drug over dual aspirin and
dipyridamole and then aspirin monotherapy as third line.
While triple therapy looked better on efficacy when compared with the
aspirin/dipyridamole combo than against clopidogrel alone, Bath
cautioned against concluding that clopidogrel is more effective than the
dual therapy combination.
Physicians' choice between those two types of U.K. guideline-directed
therapy was not randomized, he noted. The trial protocol allowed
physicians to chose between the two strategies for their standard
therapy group but were locked into that choice to minimize selection.
TARDIS, the first vascular prevention trial to prospectively adopt
ordinal outcomes on primary endpoints, included 3,069 patients, shy of
the planned 4,100 due to early termination. It was an international,
open-label but blinded-endpoint trial with "very inclusive" entry
criteria: age over 50, 48 or more hours after stroke onset, acute
non-cardioembolic ischemic stroke of any severity or acute TIA with an
ABCD2 score of at least 4 or more than one event in the prior week.
Bath noted that the findings were interim but "very close to the
final lock" on the data. "I don't think anything fundamental will
The trial was
funded by the British Heart Foundation, NIHR Health Technology
Assessment program, with additional indirect funding from the Stroke
Association and the NIHR Stroke Research Network/CRN Stroke.
Bath disclosed having no relevant conflicts of interest.
HOUSTON -- Nimodipine didn't
improve cognition when ischemic stroke patients with vascular mild
cognitive impairment (MCI) started taking the calcium channel blocker
within a week of their event, researchers reported here.
In a randomized controlled trial from 23 sites in China, patients had
no differences in change in Mini-Mental State Exam (MMSE) scores at 6
months whether they were on the drug or placebo, Huaguang Zheng, MD, of
Beijing Tiantan Hospital in China and colleagues reported at the International Stroke Conference meeting here.
our trial, we found that nimodipine didn't benefit vascular MCI
patients, but it may have marginal positive effects on specific
cognitive domains, such as executive function, and it won't increase the
risk of stroke or other adverse events," Zheng said during a press
More than half of stroke patients develop vascular MCI during the
first three months of follow-up, he explained, and about 30% to 50% will
develop dementia within 5 years.
While there are currently no effective therapies for vascular MCI and
dementia, some studies have suggested that nimodipine may have
cognitive benefits, he said.
To assess whether that's the case, Zheng and colleagues randomized
654 patients to either placebo or to 30 mg nimodipine three times a day.
The primary endpoint was the change in cognition function on the MMSE
and on the Alzheimer's Disease Assessment Scale Cognitive Subscale
(ADAS-Cog) over 6 months.
Overall, outcomes were similar between the two groups, with no significant advantage for nimodipine, Zheng said.
was, however, an advantage for nimodipine in terms of the proportion of
patients who had an ADAS-Cog score of 0 or greater at 6 months (34%
versus 47%), and there was some indication that the drug may benefit
specific brain areas, particularly executive function, he noted.
Zheng added that nimodipine didn't increase the risk of stroke and other adverse events.
He acknowledged that the study was limited because it didn't evaluate
Global Cognitive Index scores, neurological outcome, or subcortical
dementia, and the sample size was too small. Mark Alberts, MD,
of Hartford Healthcare, said it was "reasonable to investigate"
nimodipine given that it's been shown to potentially have
neuroprotective effects. But the problem of cognitive decline following
stroke is a "vexing issue" because the pathophysiology is so
"If you have a stroke, and you develop dementia after the stroke, is
that vascular dementia related to the stroke? Having a stroke, you take
out millions of neurons," he told MedPage Today. "Most people,
including myself, think it's a combination, that there's some underlying
degenerative process, and vascular disease on top of that is just
accelerating it perhaps."
said it's best to focus on risk factor control in patients with
cognitive impairment after a stroke -- treating diabetes,
hypertension, and hypercholesterolemia, for instance. For patients who
progress to dementia, he offers rehabilitation programs or the
cholinesterase inhibitor donepezil (Aricept). Amytis Towfighi, MD,
of the University of Southern California and director of neurological
services at the Los Angeles County department of health, agreed that
risk factor control is the main therapeutic strategy for cognitive
impairment following stroke.
"Currently there are no proven treatments. We don't know if
medications that have been tested in Alzheimer's would be effective,"
she told MedPage Today. "Generally we recommend lifestyle changes -- the same things you would recommend to prevent stroke. Prevention is the key."
The study was
supported by the National Key Technology Research and Development
Program of the Ministry of Science and Technology of China. Bayer
provided additional support.
Zheng disclosed no financial relationships with industry.