Use the labels in the right column to find what you want. Or you can go thru them one by one, there are only 33,991 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.
Your conclusion is totally wrong. If you want to vastly reduce stroke impairment and at least give it a fighting chance for recovery with existing therapy, you have to
Here
we report and comment on the magnitudes of post-stroke impairment
reduction currently observed using new neurotechnologies. We argue that
neurotechnology’s best use case is impairment reduction as this is
neither the primary strength nor main goal of conventional
rehabilitation, which is better at targeting the activity and
participation levels of the ICF. The neurotechnologies discussed here
can be divided into those that seek to be adjuncts for enhancing
conventional rehabilitation, and those that seek to introduce a novel
behavioral intervention altogether. Examples of the former include
invasive and non-invasive brain stimulation. Examples of the latter
include robotics and some forms of serious gaming. We argue that motor
learning and training-related recovery are conceptually and
mechanistically distinct. Based on our survey of recent results, we
conclude that large reductions in impairment will need to begin with
novel forms of high dose and high intensity behavioral intervention that
are qualitatively different to conventional rehabilitation. Adjunct
forms of neurotechnology, if they are going to be effective, will need
to piggyback on these new behavioral interventions.
Something for your doctor to keep track of, or not.
Your chances of getting dementia. MAYBE YOU WANT YOUR DOCTOR TO DO SOMETHING ABOUT THIS? UP TO YOU. Because if you don't hound your doctor, nothing will be done.
Stroke creates faulty brain circuits so ask your doctor and stroke hospital what they are doing to ensure clinical testing occurs in stroke test subjects. Nothing, then make sure they all get fired. I take no prisoners when such incompetence is openly displayed.
Red 8.3 astrocytes in the spine of a mouse. Credit: Rothstein lab
Working with mouse and human tissue, Johns Hopkins Medicine
researchers report new evidence that a protein pumped out of some—but
not all—populations of "helper" cells in the brain, called astrocytes,
plays a specific role in directing the formation of connections among
neurons needed for learning and forming new memories.
Using
mice genetically engineered and bred with fewer such connections, the
researchers conducted proof-of-concept experiments that show they could
deliver corrective proteins via nanoparticles to replace the missing
protein needed for "road repairs" on the defective neural highway.
Since such connective networks are lost or damaged by neurodegenerative diseases
such as Alzheimer's or certain types of intellectual disability, such
as Norrie disease, the researchers say their findings advance efforts to
regrow and repair the networks and potentially restore normal brain
function.
The findings are described in the May issue of Nature Neuroscience.
"We are looking at the fundamental biology of how astrocytes
function, but perhaps have discovered a new target for someday
intervening in neurodegenerative diseases with novel therapeutics," says
Jeffrey Rothstein, M.D., Ph.D., the John W. Griffin Director of the
Brain Science Institute and professor of neurology at the Johns Hopkins
University School of Medicine.
"Although astrocytes appear to all look alike in the brain, we had an
inkling that they might have specialized roles in the brain due to
regional differences in the brain's function and because of observed
changes in certain diseases," says Rothstein. "The hope is that learning
to harness the individual differences in these distinct populations of
astrocytes may allow us to direct brain development or even reverse the
effects of certain brain conditions, and our current studies have
advanced that hope."
In the brain, astrocytes are the support cells that act as guides to
direct new cells, promote chemical signaling, and clean up byproducts of
brain cell metabolism.
Rothstein's team focused on a particular astrocyte
protein, glutamate transporter-1, which previous studies suggested was
lost from astrocytes in certain parts of brains with neurodegenerative
diseases. Like a biological vacuum cleaner, the protein normally sucks
up the chemical "messenger" glutamate from the spaces between neurons
after a message is sent to another cell, a step required to end the
transmission and prevent toxic levels of glutamate from building up.
When these glutamate transporters disappear from certain parts of the
brain—such as the motor cortex and spinal cord in people with
amyotrophic lateral sclerosis (ALS)—glutamate hangs around much too
long, sending messages that overexcite and kill the cells.
To figure out how the brain decides which cells need the glutamate transporters,
Rothstein and colleagues focused on the region of DNA in front of the
gene that typically controls the on-off switch needed to manufacture the
protein. They genetically engineered mice to glow red in every cell
where the gene is activated.
Normally, the glutamate transporter is turned on in all astrocytes.
But, by using between 1,000- and 7,000-bit segments of DNA code from the
on-off switch for glutamate, all the cells in the brain glowed red,
including the neurons. It wasn't until the researchers tried the largest
sequence of an 8,300-bit DNA code from this location that the
researchers began to see some selection in red cells. These red cells
were all astrocytes but only in certain layers of the brain's cortex in
mice.
Because they could identify these "8.3 red astrocytes," the
researchers thought they might have a specific function different than
other astrocytes in the brain. To find out more precisely what these 8.3
red astrocytes do in the brain, the researchers used a cell-sorting
machine to separate the red astrocytes from the uncolored ones in mouse
brain cortical tissue, and then identified which genes were turned on to
much higher than usual levels in the red compared to the uncolored cell
populations. The researchers found that the 8.3 red astrocytes turn on
high levels of a gene that codes for a different protein known as
Norrin.
Rothstein's team took neurons from normal mouse brains, treated them
with Norrin, and found that those neurons grew more of the "branches"—or
extensions—used to transmit chemical messages among braincells.
Then, Rothstein says, the researchers looked at the brains of mice
engineered to lack Norrin, and saw that these neurons had fewer branches
than in healthy mice that made Norrin.
In another set of experiments, the research team took the DNA code
for Norrin plus the 8,300 "location" DNA and assembled them into
deliverable nanoparticles. When they injected the Norrin nanoparticles
into the brains of mice engineered without Norrin, the neurons in these
mice began to quickly grow many more branches, a process suggesting
repair to neural networks. They repeated these experiments with human
neurons too.
Rothstein notes that mutations in the Norrin protein that reduce
levels of the protein in people cause Norrie disease—a rare, genetic
disorder that can lead to blindness in infancy and intellectual
disability. Because the researchers were able to grow new branches for
communication, they believe it may one day be possible to use Norrin to
treat some types of intellectual disabilities such as Norrie disease.
For their next steps, the researchers are investigating if Norrin can
repair connections in the brains of animal models with
neurodegenerative diseases, and in preparation for potential success,
Miller and Rothstein have submitted a patent for Norrin.
More information:
Sean J. Miller et al. Molecularly defined cortical astroglia
subpopulation modulates neurons via secretion of Norrin, Nature Neuroscience (2019). DOI: 10.1038/s41593-019-0366-7Journal information:Nature Neuroscience
Medical treatments for a variety of diseases have advanced
dramatically in recent decades, but sometimes they come with a cost;
namely damage to surrounding tissues and organs. That’s where stem cell
research and regenerative medicine come in. Those fields seek to develop
new ways of repairing the damage. But how do you see if those repairs
are working? Researchers at Purdue say they have found a way to do just
that.
The researchers have developed a 3D technology that allows
them to track, map and monitor what happens with cells and tissues that are
being used to repair damage caused by disease or the treatment for the disease.
By observing the cells and tissues they can see if they are staying where they
are needed and if they are working.
The technology, published in the journalACS Nano,
uses tiny sensors placed on a flexible scaffold to monitor the new
materials in the body. Ingeniously the scaffold is buoyant, so it can
float and survive in the wet conditions found in many parts of the body.
In a news
release, Chi Hwan Lee, the leader of the research team, says the device could
help millions of people:
“Tissue
engineering already provides new hope for hard-to-treat disorders, and our
technology brings even more possibilities. This device offers an expanded set
of potential options to monitor cell and tissue function after surgical transplants
in diseased or damaged bodies. Our technology offers diverse options for
sensing and works in moist internal body environments that are typically
unfavorable for electronic instruments.”
Purdue created this video showing the device and explaining how it works.
Now if we could just accomplish this in humans. We could see which neurons are talking but no one is listening and map exactly the dead and damaged areas. Using that knowledge to target axonal sprouting and dendrite branching to overcome those missing connections. Targeting interventions using nanotechnology to correct specific neurons could then be possible. I think grandiose ideas, but at least I think about solving stroke rather than sitting on my ass like the non-existent stroke leaders we have. https://www.news-medical.net/news/20180112/Caltech-researchers-develop-new-method-to-see-neural-connections-in-living-flies.aspx
The human brain is composed of billions of neurons wired together in intricate webs and communicating through electrical pulses and chemical signals. Although neuroscientists have made progress in understanding the brain's many functions--such as regulating sleep, storing memories, and making decisions--visualizing the entire "wiring diagram" of neural connections throughout a brain is not possible using currently available methods. But now, using Drosophila fruit flies, Caltech researchers have developed a method to easily see neural connections and the flow of communications in real time within living flies. The work is a step forward toward creating a map of the entire fly brain's many connections, which could help scientists understand the neural circuits within human brains as well.
A paper describing the work appears online in the December 12 issue of eLife. The research was done in the laboratory of Caltech research professor Carlos Lois.
"If an electrical engineer wants to understand how a computer works, the first thing that he or she would want to figure out is how the different components are wired to each other," says Lois. "Similarly, we must know how neurons are wired together in order to understand how brains work."
When two neurons connect, they link together with a structure called a synapse, a space through which one neuron can send and receive electrical and chemical signals to or from another neuron. Even if multiple neurons are very close together, they need synapses to truly communicate.
The Lois laboratory has developed a method for tracing the flow of information across synapses, called TRACT (Transneuronal Control of Transcription). Using genetically engineered Drosophila fruit flies, TRACT allows researchers to observe which neurons are "talking" and which neurons are "listening" by prompting the connected neurons to produce glowing proteins.
With TRACT, when a neuron "talks"--or transmits a chemical or electrical signal across a synapse--it will also produce and send along a fluorescent protein that lights up both the talking neuron and its synapses with a particular color. Any neurons "listening" to the signal receive this protein, which binds to a so-called receptor molecule--genetically built-in by the researchers--on the receiving neuron's surface. The binding of the signal protein activates the receptor and triggers the neuron it's attached to in order to produce its own, differently colored fluorescent protein. In this way, communication between neurons becomes visible. Using a type of microscope that can peer through a thin window installed on the fly's head, the researchers can observe the colorful glow of neural connections in real time as the fly grows, moves, and experiences changes in its environment.
Many neurological and psychiatric conditions, such as autism and schizophrenia, are thought to be caused by altered connections between neurons. Using TRACT, scientists can monitor the neuronal connections in the brains of hundreds of flies each day, allowing them to make comparisons at different stages of development, between the sexes, and in flies that have genetic mutations. Thus, TRACT could be used to determine how different diseases perturb the connections within brain circuits. Additionally, because neural synapses change over time, TRACT allows the monitoring of synapse formation and destruction from day to day. Being able to see how and when neurons form or break synapses will be critical to understanding how the circuits in the brain assemble as the animal grows, and how they fall apart with age or disease.
TRACT can be localized to focus in on the wiring of any particular neural circuit of interest, such as those that control movement, hunger, or vision. Lois and his group tested their method by examining neurons within the well-understood olfactory circuit, the neurons responsible for the sense of smell. Their results confirmed existing data regarding this particular circuit's wiring diagram. In addition, they examined the circadian circuit, which is responsible for the waking and sleeping cycle, where they detected new possible synaptic connections.
TRACT, however, can do more than produce wiring diagrams. The transgenic flies can be genetically engineered so that the technique prompts receiving neurons to produce proteins that have a function, rather than colorful proteins that simply trace connections.
"We could use functional proteins to ask, 'What happens in the fly if I silence all the neurons that receive input from this one neuron?'" says Lois. "Or, conversely, 'What happens if I make the neurons that are connected to this neuron hyperactive?' Our technique not only allows us to create a wiring diagram of the brain, but also to genetically modify the function of neurons in a brain circuit."
Previous methods for examining neural connections were time consuming and labor intensive, involving thousands of thin slices of a brain reconstructed into a three-dimensional structure. A laboratory using these techniques could only yield a diagram for a single, small piece of fruit-fly brain per year. Additionally, these approaches could not be performed on living animals, making it impossible to see how neurons communicated in real time.
Because the TRACT method is completely genetically encoded, it is ideal for use in laboratory animals such as Drosophila and zebrafish; ultimately, Lois hopes to implement the technique in mice to enable the neural tracing of a mammalian brain. "TRACT is a new tool that will allow us to create wiring diagrams of brains and determine the function of connected neurons," he says. "This information will provide important clues towards understanding the complex workings of the human brain and its diseases."
Department of Chemistry and
Chemical Biology, Rutgers, The State University
of New Jersey, 610 Taylor
Road, Piscataway, New Jersey 08854, United States
Shreyas Shah
received his Ph.D. in Chemistry and Chemical Biology from Rutgers
University (New Brunswick, NJ). His doctoral research focused on
developing nanomaterial-based 2D/3D scaffolds for neural regeneration,
neural drug delivery, and neuromodulation. He is currently building a
new lab/program in Physiological Communications at Bell Labs located in
Murray Hill, NJ.
Biography
Aniruddh Solanki
received his Ph.D. in Chemistry and Chemical Biology from Rutgers
University (New Brunswick, NJ). He is currently pursuing his
postdoctoral research at Brigham and Women’s Hospital and the Harvard
Medical School.
Biography
Ki-Bum Lee
is an Associate Professor of Chemistry and Chemical Biology at Rutgers
University (New Brunswick, NJ). His research interest is to develop and
integrate nanotechnologies and chemical functional genomics to modulate
signaling pathways in cells toward specific cell lineages or behaviors.
Abstract
Conspectus
The
mammalian brain is a phenomenal piece of “organic machinery” that has
fascinated scientists and clinicians for centuries. The intricate
network of tens of billions of neurons dispersed in a mixture of
chemical and biochemical constituents gives rise to thoughts, feelings,
memories, and life as we know it. In turn, subtle imbalances or damage
to this system can cause severe complications in physical, motor,
psychological, and cognitive function. Moreover, the inevitable loss of
nerve tissue caused by degenerative diseases and traumatic injuries is
particularly devastating because of the limited regenerative
capabilities of the central nervous system (i.e., the brain and spinal
cord).
Among current approaches,
stem-cell-based regenerative medicine has shown the greatest promise
toward repairing and regenerating destroyed neural tissue. However,
establishing controlled and reliable methodologies to guide stem cell
differentiation into specialized neural cells of interest (e.g., neurons
and oligodendrocytes) has been a prevailing challenge in the field. In
this Account, we summarize the nanotechnology-based approaches our group
has recently developed to guide stem-cell-based neural regeneration. We
focus on three overarching strategies that were adopted to selectively
control this process.
First,
soluble microenvironmental factors play a critical role in directing the
fate of stem cells. Multiple factors have been developed in the form of
small-molecule drugs, biochemical analogues, and DNA/RNA-based vectors
to direct neural differentiation. However, the delivery of these factors
with high transfection efficiency and minimal cytotoxicity has been
challenging, especially to sensitive cell lines such as stem cells. In
our first approach, we designed nanoparticle-based systems for the
efficient delivery of such soluble factors to control neural
differentiation. Our nanoparticles, comprising either organic or
inorganic elements, were biocompatible and offered multifunctional
capabilities such as imaging and delivery.
Moving
from the soluble microenvironment in which cells are immersed to the
underlying surface, cells can sense and consequently respond to the
physical microenvironment in which they reside. For instance, changes in
cell adhesion, shape, and spreading are key cellular responses to
surface properties of the underlying substrate. In our second approach,
we modulated the surface chemistry of two-dimensional substrates to
control neural stem cell morphology and the resulting differentiation
process. Patterned surfaces consisting of immobilized extracellular
matrix (ECM) proteins and/or nanomaterials were generated and utilized
to guide neuronal differentiation and polarization.
In
our third approach, building on the above-mentioned approaches, we
further tuned the cell–ECM interactions by introducing nanotopographical
features in the form of nanoparticle films or nanofiber scaffolds.
Besides providing a three-dimensional surface topography, our unique
nanoscaffolds were observed to enhance gene delivery, facilitate axonal
alignment, and selectively control differentiation into neural cell
lines of interest. Overall, nanotechnology-based approaches offer the
precise physicochemical control required to generate tools suitable for
applications in neuroscience.
Scientists at the Wyss Institute for Biologically Inspired
Engineering at Harvard University developing novel nanotherapeutics for
clearing obstructed blood vessels have teamed up with researchers at
University of Massachusetts' New England Center for Stroke Research
(NECSTR) to develop a new, highly effective drug-device combination for
treating life-threatening blood clots in patients with stroke.
In a new study that will appear in the December 2015 issue of Stroke
journal, the team co-led by Wyss Institute Founding Director Donald
Ingber, M.D., Ph.D., and U. Mass Medical Professor of Radiology Ajay
Wakhloo, M.D., Ph.D., FAHA, describe their novel method to quickly
dissolve away clots that completely obstruct blood vessels in the brain.
Their approach combines an injectable clot-busting nanotherapeutic that
targets blockages with an intra-arterial device that restores blood
flow to obstructed vessels.
The Wyss Institute nanotherapeutic is composed of an aggregate of
biodegradable nanoparticles coated with a clot-busting drug called
tissue plasminogen activator (tPA), which mimics the way blood platelets
behave inside our own bodies. When blood vessels narrow, the shear
force of blood flow increases at that location to produce a physical cue
that causes platelets to stick to the vessel wall. Similarly, the
nanotherapeutic reacts to fluid shear force, releasing tPA-coated
nanoparticles in these narrowed regions where vessels are partially
occluded, binding to the blood clot and dissolving it away.
But until now, the mechanically activated nanotherapeutic would not
be effective in complete vascular blockages where there is no blood
flow, as is the case for most stroke patients. The most effective
treatment today for stroke is known as a "stent-retriever thrombectomy"
procedure, originally described by Wakhloo and his colleague Matthew
Gounis, Ph.D., Associate Professor of Radiology at UMass. The procedure
involves placing a small tube through the blockage, passing a closed
stent through it, and then opening the stent to physically pull the
large blood clot out of the vessel.
"Even with the retriever thrombectomy procedure, not all clots can be
removed with a successful outcome," said Gounis. "Clot fragments can be
dislodged, which can lead to microclots and tissue damage downstream in
the brain circulatory system, and physical dragging of the stent
through the vessel can potentially be damaging as well."
Instead,
the new advance describes using the stent not to drag out the clot, but
to create a narrow channel restoring blood flow through an opening in
the center of the vascular blockage. Doing so creates a high level of
shear force generated by restored flow, activating the nanotherapeutic
to release and target the clot-busting drug along the opened channel in
the clot. After the blood clot is fully dissolved, the stent is
re-sheathed and harmlessly removed from the vessel. If during the
process any clot fragments break off and travel away through the
circulatory system, the drug-coated nanoparticles will remain bound to
them and continue to dissolve them locally wherever they go.
"What's progressive about this approach is that the temporary opening
of a tiny hole in the clot - using a stent device that is already
commonly used clinically - results in a local rise in mechanical forces
that activate the nanotherapeutic to deploy the clot-busting drug
precisely where it can best do its job," said Ingber, who is also the
Judah Folkman Professor of Vascular Biology at Boston Children's
Hospital and Harvard Medical School and Professor of Bioengineering at
the Harvard John A. Paulson School of Engineering and Applied Sciences.
In clinically relevant large animal studies, the team has
demonstrated that the drug-device combination works very efficiently,
showing that it dissolves clots that fully occlude brain blood vessels
that are the same size as they would be in humans.
"This has been a great collaboration between experts in the field of
treating stroke and experts in mechanobiology and bioengineering," said
co-first author of the study Netanel Korin, Ph.D., former Wyss
Technology Development Fellow and current Assistant Professor in
Biomedical Engineering at the Technion, Israel, who first described the
nanotherapeutic in a 2012 Science publication with Ingber. "We hope that
one day it will have a positive impact on patients suffering from a
range of medical crises resulting from blood clot occlusions."
Source:
Wyss Institute for Biologically Inspired Engineering at Harvard
I would expect our doctors to absolutely jump for joy to have this. They could finally be able to tell us exactly what areas of our brain are dead or damaged. And with that knowledge they could start to create stroke protocols to fix the damage. And they can stop using the excuse of: 'All strokes are different, all stroke recoveries are different'.
An article discussing it here: Injectable electronic brain nets could give us a window into the mind
The research it is based upon here:
Will your doctor be using a test like this to identify your 33% chance of getting dementia post-stroke early while something can still be done about it? Does your doctor have anything better than my ideas with research to back them up? My complete list here: Dementia prevention 19 ways
http://www.spring.org.uk/2014/12/this-brain-disease-will-affect-nearly-every-family-now-nanotechnology-can-detect-it-early.php?
A new type of brain scan which can detect the toxins which cause
Alzheimer’s disease has been developed by scientists at Northwestern
University.
The test, which uses nanotechnology, identifies the early signs of
dementia and could be used to both monitor and combat the disease.
The areas of the brain which contain the amyloid beta toxins are seen on the brain scan as large dark patches.
The new test is a breakthrough because previously it was only
possible to detect the amyloid plaques — once these have developed it is
probably too late for any effective therapy.
