Use the labels in the right column to find what you want. Or you can go thru them one by one, there are only 34,245 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.
Changing stroke rehab and research worldwide now.Time is Brain!trillions and trillions of neuronsthatDIEeach day because there areNOeffective hyperacute therapies besides tPA(only 12% effective). I have 523 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:
My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. 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 lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.
A team of Chinese collaborators has reported experiments
in the Oxford academic journal Cerebral Cortex titled "Functional
gradients in prefrontal regions and somatomotor networks reflect the
effect of music training experience on cognitive aging" which are stated
to show that music training enhances the functional separation between
regions across prefrontal and somatomotor networks, delaying
deterioration in working memory performance and prefrontal suppression
of prominant but irrelevant information. I'm passing on the abstract and
a clip from the paper's conclusion, and can send interested readers the
whole article. I think it is an important article but I find it is
rendered almost unintelligble by Chinese to English translation issues.
I'm surprised the journal let this article appear without further
editing.
Studies showed that the top-down control of the prefrontal
cortex (PFC) on sensory/motor cortices changes during cognitive aging.
Although music training has demonstrated efficacy on cognitive aging,
its brain mechanism is still far from clear. Current music intervention
studies have paid insufficient attention to the relationship between PFC
and sensory regions. Functional gradient provides a new perspective
that allows researchers to understand network spatial relationships,
which helps study the mechanism of music training that affects cognitive
aging. In this work, we estimated the functional gradients in four
groups, young musicians, young control, older musicians, and older
control. We found that cognitive aging leads to gradient compression.
Compared with young subjects, older subjects presented lower and higher
principal gradient scores in the right dorsal and medial prefrontal and
the bilateral somatomotor regions, respectively. Meanwhile, by comparing
older control and musicians, we found a mitigating effect of music
training on gradient compression. Furthermore, we revealed that the
connectivity transitions between prefrontal and somatomotor regions at
short functional distances are a potential mechanism for music to
intervene in cognitive aging. This work contributes to understanding the
neuroplasticity of music training on cognitive aging.
From the conclusion paragraph:
In a nutshell, we demonstrate the top-down control of
prefrontal regions to the somatomotor network, which is associated with
inhibitory function and represents a potential marker of cognitive
aging, and reveal that music training may work by affecting the
connectivity between the two regions. Although this work has
investigated the neuroplasticity of music on cognitive aging by
recruiting subjects of different age spans, the present study did not
include the study of longitudinal changes of the same group. Further
studies should include longitudinal follow-up of the same groups over
time to more accurately evaluate the effect of music intervention on the
process of cognitive aging.
Martin et al. offer
an open source article that describes a smartphone intervention that
enhances real-world memory and promotes differentiation of hippocampal
activity in older adults. I have downloaded the HippoCamera smartphone
App described in the text from the Apple App Store, and found a research
passcode is required, for which the following clip of text from the
article is relevant: "As of the time of writing, this is a
research-dedicated application that
requires an access code that can be obtained from a corresponding
author."
Significance
The ability to vividly recollect our past declines with
age, a trend that negatively impacts overall well-being. We show that
using smartphone technologies to record and replay brief but rich memory
cues from daily life can improve older adults’ ability to reexperience
the past. This enhancement was associated with corresponding changes in
the way memories were stored in the brain. Functional neuroimaging
showed that repeatedly replaying memory cues drove memories apart from
one another in the hippocampus, a brain region with well-established
links to memory function. This increase in differentiation likely
facilitated behavior by strengthening memory and minimizing competition
among different memories at retrieval. This work reveals an easy-to-use
intervention that helps older adults better remember their personal
past.
Abstract
The act of remembering an everyday experience influences how
we interpret the world, how we think about the future, and how we
perceive ourselves. It also enhances long-term retention of the recalled
content, increasing the likelihood that it will be recalled again.
Unfortunately, the ability to recollect event-specific details and
reexperience the past tends to decline with age. This decline in
recollection may reflect a corresponding decrease in the distinctiveness
of hippocampal memory representations. Despite these well-established
changes, there are few effective cognitive behavioral interventions that
target real-world episodic memory. We addressed this gap by developing a
smartphone-based application called HippoCamera that allows
participants to record labeled videos of everyday events and
subsequently replay, high-fidelity autobiographical memory cues. In two
experiments, we found that older adults were able to easily integrate
this noninvasive intervention into their daily lives. Using HippoCamera
to repeatedly reactivate memories for real-world events improved
episodic recollection and it evoked more positive autobiographical
sentiment at the time of retrieval. In both experiments, these benefits
were observed shortly after the intervention and again after a 3-mo
delay. Moreover, more detailed recollection was associated with more
differentiated memory signals in the hippocampus. Thus, using this
smartphone application to systematically reactivate memories for recent
real-world experiences can help to maintain a bridge between the present
and past in older adults.
I want to pass on references to two new approaches to relieving the symptoms of post-traumatic stress disorder (PTSD). Nuwer describes
a new study showing that MDMA (known as the party drug Ecstasy, or
Molly) can bring relief to PTSD when used in conjunction with talk
therapy. Ressler et al.
address the problem that human patients cannot be directly re-exposed
to trauma-cues of the sort that have been used in animal studies to
induce and then disrupt reconsolidation of traumatic memories. They
devise a procedure for covertly capturing and attenuating a
hippocampu-dependent fear memory in male rats, a procedure that might
prove to be useful in human therapy. Here is their abstract:
Reconsolidation may be a viable therapeutic target to
inhibit pathological fear memories. In the clinic, incidental or
imaginal reminders are used for safe retrieval of traumatic memories of
experiences that occurred elsewhere. However, it is unknown whether
indirectly retrieved traumatic memories are sensitive to disruption.
Here we used a backward (BW) conditioning procedure to indirectly
retrieve and manipulate a hippocampus (HPC)-dependent contextual fear
engram in male rats. We show that conditioned freezing to a BW
conditioned stimulus (CS) is mediated by fear to the conditioning
context, activates HPC ensembles that can be covertly captured and
chemogenetically activated to drive fear, and is impaired by
post-retrieval protein synthesis inhibition. These results reveal that
indirectly retrieved contextual fear memories reactivate HPC ensembles
and undergo protein synthesis-dependent reconsolidation. Clinical
interventions that rely on indirect retrieval of traumatic memories,
such as imaginal exposure, may open a window for editing or erasure of
neural representations that drive pathological fear.
Scientists have come closer to understanding why people seem to age at different rates.
(Image credit: Shutterstock)
Some people's hearts stay strong well into their 60s, but their
kidneys begin to fail. Others may have the kidneys of a 30-year-old but
fall victim to constant infection.
Now, scientists may be one step closer to understanding why the aging process varies so drastically between people.
Even
within a single person, aging unfolds at different rates in different
tissues, sometimes striking the liver before the heart or kidney, for
example. People fall into distinct categories depending on which of
their biological systems ages fastest, and someday, doctors could use
this information to recommend specific lifestyle changes and design
personalized medical treatments, according to a new study, published
Jan. 13 in the journal Nature Medicine.
What's your "ageotype"?
The
research team behind the study sorted 43 people into aging categories,
or "ageotypes," based on biological samples collected over the course of
two years. The samples included blood, inflammatory substances,
microbes, genetic material, proteins and by-products of metabolic
processes. By tracking how the samples changed over time, the team
identified about 600 so-called markers of aging — values that predict
the functional capacity of a tissue and essentially estimate its
"biological age."
So far, the team has identified four distinct
ageotypes: Immune, kidney, liver and metabolic. Some people fit squarely
in one category, but others may meet the criteria for all four,
depending on how their biological systems hold up with age.
"Now,
it's going to be a lot more than just four categories," said senior
author Michael Snyder, a professor and the chair of genetics at the
Stanford University School of Medicine in California. For instance, one
participant in the study appeared to be a cardiovascular ager, meaning
their cardiac muscle accumulates wear-and-tear at a greater rate than
other parts of their body. "If we [surveyed] 1,000 people, I'm sure
we'll find other cardio agers and that category will become better
defined." And with more research, even more patterns of aging may
emerge, Snyder added.
In the past, scientists have hunted formarkers of aging
in enormous datasets for large populations, Snyder, told Live Science.
Researchers pinpointed markers of aging by comparing data from young
people to that of older people, but for individuals, that kind of data
captures only a specific moment in time. It cannot reveal how a given
person might change as they age, Snyder said.
In
a clinical setting, that means population-based markers might not be
the best measure to determine how a patient is aging, or what
combination of medical treatments might suit them best, he added.
"Population-based decisions are crude at best," Synder said. They won't necessarily hold up for you, per se."
By
tracking specific people through time, Snyder and his co-authors hoped
to learn how aging markers differ between individuals. Their study
participants ranged in age from 29 to 75 and provided at least five
biological samples over the course of two years. Even within that
relatively short time frame, several patterns of aging emerged.
For example, immunological agers accumulated more markers of inflammation through time, while metabolic agers accrued more sugar in their blood,
indicating that their bodies were metabolizing glucose less
efficiently. Similar to scores on a personality test, each individual's
aging "profile" included a combination of traits, mixed and matched from
different ageotypes.
Personalized medicine
Snyder
and his co-authors plan to follow the study participants to see how
their aging profiles morph over time. They also aim to develop a simple
ageotype test that could be used in the doctor's office to quickly
assess a patient's health status, and potentially point them toward the
best possible treatment options.
"There
are drugs and various kinds of dietary interventions and lifestyle
interventions through which it may be possible to modulate some of these
aging processes," Dr. James Kirkland, a gerontologist and head of the
Kogod Center on Aging at the Mayo Clinic in Rochester, Minnesota, told NBC News.
"But
in order to apply those correctly, we have to know which people to
apply which drugs or which dietary interventions in order to get the
most bang for the buck," said Kirkland, who was not involved in the new
study.
While existing drugs, diets and exercise regimes can target some signs of aging, other markers aren't fully understood yet.
For
example, over the course of Snyder's study, a marker of poor kidney
function decreased in 12 individuals, eight of whom took statins. The
marker, a waste product called creatinine,
accumulates in the blood as muscle tissue naturally breaks down, but
the kidneys typically filter the substance and expel it through the
urine. Creatinine levels fell in the eight individuals on statins,
suggesting that the medication improved their kidney function, though
it's unclear why levels also dipped in four additional people, the
authors noted.
The
team also found that concentrations of several microbes seem to change
with age, but we don't yet know how that may affect health. Certain
microbes may proliferate in response to age-related changes in the
body, while others help drive them, Snyder said. The authors also
spotted differences in how diabetic and pre-diabetic people aged as
compared to insulin-sensitive people, but it's unclear whether these
markers indicate meaningful differences in health status. Many studies
suggest that insulin plays a central role in aging throughout the
animal kingdom, but more research is needed to clarify its exact
influence over human aging.
For
now, ageotypes present as many questions as they do answers about human
aging. Until scientists understand what various aging markers really
mean, clinicians will continue to rely on standard vital sign
assessments to track patients' health over time. In the near future,
perhaps ageotypes could serve to motivate people to take better care of
areas of their body that appear to be aging faster than others, Snyder
said. For instance, if someone fits the profile of a cardiovascular
ager, they might focus on improving their cardiovascular health and
undergoing relevant medical tests to check on their progress.
"As
we collect a lot more information, we are going to be better able to
follow how people are aging, [as well as] what interventions they did
that actually reduced their aging," Snyder said.
I perk up whenever I see a reference relevant to 'inflamaging,' the slow
rise of cellular inflammation that accompanies - as I am too well aware
in my own case - aging. Neuroflammation is an underlying component of
dementias and alzheimer's disease. Sanmarco et al.
at Brigham and Women's Hospital in Boston have now discovered a new
subset of brain cells that fight inflammation with instructions from the
gut microbiome. Here are excerpts from their research brief that are a bit easier to follow than the technical abstreact of the article:
Astrocytes are the most abundant type of cells within the
central nervous system (CNS).. Researchers have long assumed that
astrocytes’ primary function is to provide nutrients and support for the
brain’s more closely scrutinized nerve cells; over the years, however,
increasing evidence has shown that astrocytes can also actively promote
neurodegeneration, inflammation, and neurological diseases. Now, a team
led by researchers from Brigham and Women’s Hospital, has shown that a
specific astrocyte sub-population can do the opposite, instead serving a
protective, anti-inflammatory function within the brain based on
signals regulated by the bacteria that reside in the gut.
The researchers used refined gene- and protein-analysis
tools to identify the novel astrocyte subset. The astrocyte population
resides close to the meninges (the membrane enclosing the brain) and
expresses a protein called LAMP1, along with a protein called TRAIL,
which can induce the death of other cells. These features help the
LAMP1+TRAIL+ astrocytes limit CNS inflammation by inducing cell death in
T-cells that promote inflammation... They found that a particular
signaling molecule, called interferon-gamma, regulates TRAIL expression.
Moreover, they found that the gut microbiome induces the expression of
interferon-gamma in cells that circulate through the body and ultimately
reach the meninges, where they can promote astrocyte anti-inflammatory
activities.
Understanding the mechanisms driving the anti-inflammatory
functions of LAMP1+TRAIL+ astrocytes could enable researchers to develop
therapeutic approaches to combat neurological diseases, like multiple
sclerosis. For example, they are exploring probiotic candidates that can
be used to regulate the astrocytes’ anti-inflammatory activity.
I did the same and got a bottle of 10mg astaxanthin. Don't listen to me, I'm not medically trained. Of course I have no idea how much to take and nobody in the world that would know the answer anyway.
On reading this article by Yook et al. I promptly ordered a bottle of 10 mg astaxanthin capsules to add to my normal array of supplements (and exercise). Significance
Leptin (LEP, a small protein hormone), produced and acting in the
hippocampus, mediates enhancement by mild exercise (ME) of
hippocampus-related memory and neurogenesis, which are further increased
by an antioxidant carotenoid, astaxanthin (AX). Both are facilitated by
the administration of ME or AX alone. The up-regulation of the LEP gene
and LEP protein expression in the hippocampus by ME is further elevated
when combined with AX. Consistently, the combined interventions
increased hippocampal LEP protein. In LEP-deficient ob/ob mice, LEP
replacement in the brain restored the ability of ME+AX to enhance
hippocampal function. Thus, a combined lifestyle intervention based on
ME, including yoga and tai chi, and specific dietary supplements that
include antioxidants may together improve cognition and possibly retard
cognitive decline in humans.
Abstract
Regular exercise and dietary supplements with antioxidants each have the
potential to improve cognitive function and attenuate cognitive
decline, and, in some cases, they enhance each other. Our current
results reveal that low-intensity exercise (mild exercise, ME) and the
natural antioxidant carotenoid astaxanthin (AX) each have equivalent
beneficial effects on hippocampal neurogenesis and memory function. We
found that the enhancement by ME combined with AX in potentiating
hippocampus-based plasticity and cognition is mediated by leptin (LEP)
made and acting in the hippocampus. In assessing the combined effects
upon wild-type (WT) mice undergoing ME with or without an AX diet for
four weeks, we found that, when administrated alone, ME and AX
separately enhanced neurogenesis and spatial memory, and when combined
they were at least additive in their effects. DNA microarray and
bioinformatics analyses revealed not only the up-regulation of an
antioxidant gene, ABHD3, but also that the up-regulation of LEP gene
expression in the hippocampus of WT mice with ME alone is further
enhanced by AX. Together, they also increased hippocampal LEP (h-LEP)
protein levels and enhanced spatial memory mediated through AKT/STAT3
signaling. AX treatment also has direct action on human neuroblastoma
cell lines to increase cell viability associated with increased LEP
expression. In LEP-deficient mice (ob/ob), chronic infusion of LEP into
the lateral ventricles restored the synergy. Collectively, our findings
suggest that not only h-LEP but also exogenous LEP mediates effects of
ME on neural functions underlying memory, which is further enhanced by
the antioxidant AX.
With this, young blood and young gut bacteria would your recovery from stroke become much easier? We'll never know because we have NO central place to go to to update a strategy.
Deric Bownds has a good summary of senescence in this blog post:
What protocol is your doctor following for getting your motor skills consolidated during sleep. Therapy in the evening? Naps after therapy? Does your doctor know ANYTHING AT ALL?
This is completely applicable to us as stroke survivors. You have to challenge yourself all the time, however don't be as stupid as me, I can and will do anything, so far I haven't seriously injured myself.
Read DERIC BOWNDS MIND BLOG and then ask your doctor what the hell is the downside of doing this post-stroke? Other than the lazy f*cking excuse that it is not standard of care.
