Reserve pool neuron transmitter respecification: Novel neuroplasticity

I guess I'll have to understand transmitter receptors also.
http://onlinelibrary.wiley.com/doi/10.1002/dneu.20920/abstract
Keywords:

Neuronal plasticity;
activity-dependent plasticity;
neurotransmitter switching;
dopamine and GABA coexpression;
sensory stimulation;
development

Abstract

The identity of the neurotransmitters expressed by neurons has been thought to be fixed and immutable, but recent studies demonstrate that changes in electrical activity can rapidly and reversibly reconfigure the transmitters and corresponding transmitter receptors that neurons express. Induction of transmitter expression can be achieved by selective activation of afferents recruited by a physiological range of sensory input. Strikingly, neurons acquiring an additional transmitter project to appropriate targets prior to transmitter respecification in some cases, indicating the presence of reserve pools of neurons that can boost circuit function. We discuss the evidence for such reserve pools, their likely locations and ways to test for their existence, and the potential clinical value of such circuit-specific neurotransmitter respecification for treatments of neurological disorders. © 2011 Wiley Periodicals, Inc. Develop Neurobiol, 2011.

Stroke Arm Longitudinal study at the University of Gothenburg,

It says it is a longitudinal study but doesn't seem to be able to tell us anything.
http://7thspace.com/headlines/383955/salgot___stroke_arm_longitudinal_study_at_the_university_of_gothenburg_prospective_cohort_study_protocol.html
Recovery patterns of upper extremity motor function have been described in several longitudinal studies, but most of these studies have had selected samples, short follow up times or insufficient outcomes on motor function. The general understanding is that improvements in upper extremity occur mainly during the first month after the stroke incident and little if any, significant recovery can be gained after 3-6 months.

The purpose of this study is to describe the recovery of upper extremity function longitudinally in a non-selected sample initially admitted to a stroke unit with first ever stroke, living in Gothenburg urban area.

Methods: A sample of 120 participants with a first-ever stroke and impaired upper extremity function will be consecutively included from an acute stroke unit and followed longitudinally for one year. Assessments are performed at eight occasions: at day 3 and 10, week 3, 4 and 6, month 3, 6 and 12 after onset of stroke.

The primary clinical outcome measures are Action Research Arm Test and Fugl-Meyer Assessment for Upper Extremity. As additional measures, two new computer based objective methods with kinematic analysis of arm movements are used.

The ABILHAND questionnaire of manual ability, Stroke Impact Scale, grip strength, spasticity, pain, passive range of motion and cognitive function will be assessed as well. At one year follow up, two patient reported outcomes, Impact on Participation and Autonomy and EuroQol Quality of Life Scale, will be added to cover the status of participation and aspects of health related quality of life.DiscussionThis study comprises a non-selected population with first ever stroke and impaired arm function.

Measurements are performed both using traditional clinical assessments as well as computer based measurement systems providing objective kinematic data. The ICF classification of functioning, disability and health is used as framework for the selection of assessment measures.

The study design with several repeated measurements on motor function will give us more confident information about the recovery patterns after stroke. This knowledge is essential both for optimizing rehabilitation planning as well as providing important information to the patient about the recovery perspectives.Trial registrationClinicalTrials.gov NCT01115348

Author: Margit Alt MurphyHanna PerssonAnna DanielssonJurgen BroerenAsa Lundgren-NilssonKatharina Sunnerhagen
Credits/Source: BMC Neurology 2011, 11:56

Combining Confocal Laser Scanning Microscopy in the Study of Adult Neurogenesis

Another possibility in determining and watching neuroplasticity and neurogenesis. My earlier ones are listed here:
http://oc1dean.blogspot.com/2010/11/wiring-diagram-of-brain.html
http://oc1dean.blogspot.com/2010/11/array-tomography-and-stroke-research.html
http://oc1dean.blogspot.com/2011/04/ibrain-and-eegs-of-brain.html
http://oc1dean.blogspot.com/2011/04/brain-mapping-techniques-for-evaluating.html
The new possibility:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3097380/
Current advances in imaging techniques have extended the possibility of visualizing small structures within large volumes of both fixed and live specimens without sectioning. These techniques have contributed valuable information to study neuronal plasticity in the adult brain. However, technical limits still hamper the use of these approaches to investigate neurogenic regions located far from the ventricular surface such as parenchymal neurogenic niches, or the scattered neuroblasts induced by brain lesions. Here, we present a method to combine confocal laser scanning microscopy (CLSM) and serial section reconstruction in order to reconstruct large volumes of brain tissue at cellular resolution. In this method a series of thick sections are imaged with CLSM and the resulting stacks of images are registered and 3D reconstructed. This approach is based on existing freeware software and can be performed on ordinary laboratory personal computers. By using this technique we have investigated the morphology and spatial organization of a group of doublecortin (DCX)+ neuroblasts located in the lateral striatum of the late post-natal guinea pig. The 3D study unraveled a complex network of long and poorly ramified cell processes, often fascicled and mostly oriented along the internal capsule fiber bundles. These data support CLSM serial section reconstruction as a reliable alternative to the whole mount approaches to analyze cyto-architectural features of adult germinative niches.

Comparison Of Two Physiotherapy Approaches InAcute Stroke Rehabilitation: Motor RelearningProgram Versus Bobath Approach.

More nails in the coffin of Bobath/NDT.
http://www.indianjournals.com/ijor.aspx?target=ijor:jor&volume=1&issue=1&article=012
Objective

To evaluate the efficacy of two rehabilitative approaches to restore function in subjects with acute middle cerebral artery stroke.

Study design

Nonblinded, randomized clinical intervention trial

Method
22 subjects with first unilateral stroke (middle cerebral artery territory involvement) participated in the study. Group 1 (12 subjects) and group 2 (10 subjects) received Motor Relearning Program (MRP) and Bobath approach respectively for a period of six weeks.

Outcome measures
Fugl Meyer (FM), Motor assessment scale (MAS), Barthel index (BI), Functional independence measure (FIM), Functional ambulation category (FAC) and Dynamic gait index (DGI).

Results
The magnitude of change on all our primary outcome measures except FM, was greater in the MRP group as compared to Bobath group (p<0.05) & inclination of higher trend of change starting at 2weeks seen in MRP. Conclusion This study indicates that the physiotherapy treatment using MRP shows early & better improvement in functional mobility and activities of daily living than Bobath approach. Subject in MRP were able to walk early.

Automated measurement of proprioception following stroke

This is from 2007 but it takes forever to find documentation on stroke rehab. If I were a conspiracy person I would think someone is hiding this on purpose in order to take over the world. You know how smart stroke survivors are and their plans on world conquest.

I hope this got followed up and came to a therapy protocol that actually restores proprioception. My only earlier finding on this was here:
http://oc1dean.blogspot.com/2011/03/proprioception-and-stroke-rehab.html
The research paper here:
http://www.bgu.ac.il/~akarniel/pub/Leibowitz_etalDRinpress.pdf
ABSTRACT
Background: Proprioception provides feedback which is essential for adequate motor
control. Despite having detrimental functional implications, the assessment of proprioception
deficits in current clinical practice is mostly qualitative and inadequate for diagnosis and
longitudinal monitoring of subtle impairments and their effect on motor function.
Purpose: To evaluate a novel quantitative approach to the assessment of proprioception
deficits in stroke patients.
Method: We designed and implemented an automated protocol where a magnetic motion
tracking system and a sensor attached to each of the patient’s hands, enables registration of
trajectories in 3D coordinates. In this protocol the patient’s affected and healthy hands are
placed respectively below and above a square board. With vision blocked, the subject’s
affected hand is passively moved to one of four locations, and then the patient is instructed to
actively position the healthy hand directly above his/her perceived location of the affected
hand. The positional difference between the two hands is automatically recorded by the
system. This procedure is repeated several times and the magnitude and direction of errors
are used to quantify the proprioception deficit. The data for this pilot study was collected in a
sample of 22 stroke patients and an age-matched group of neurologically intact subjects.
Results: Stroke patients had significantly higher mean distance error compared with the control group (average values of 7.9 and 5.3 cm, respectively), and showed higher instability (variance) in repeated performance (average values of the standard deviation of errors 3.4 and 1.8 cm, respectively). Significant correlation was found between the mean distance error and the results of semi-quantitative clinical tests of proprioception.
Conclusion: The system provides a reliable quantitative measure of upper limb proprioception, offering considerable advantage over the traditional means applied in the clinic.

Automatic identification of gait events using an instrumented sock

And maybe we could put estim in there also to prevent
inversion.
http://www.jneuroengrehab.com/content/8/1/32/
Abstract (provisional)
Background
Textile-based transducers are an emerging technology in
which piezo-resistive properties of materials are used to
measure an applied strain. By incorporating these sensors
into a sock, this technology offers the potential to detect
critical events during the stance phase of the gait cycle.
This could prove useful in several applications, such as
functional electrical stimulation (FES) systems to assist
gait.
Methods
We investigated the output of a knitted resistive strain
sensor during walking and sought to determine the degree of
similarity between the sensor output and the ankle angle in
the sagittal plane. In addition, we investigated whether it
would be possible to predict three key gait events, heel
strike, heel lift and toe off, with a relatively straight-
forward algorithm. This worked by predicting gait events to
occur at fixed time offsets from specific peaks in the
sensor signal.
Results
Our results showed that, for all subjects, the sensor output
exhibited the same general characteristics as the ankle
joint angle. However, there were large between-subjects
differences in the degree of similarity between the two
curves. Despite this variability, it was possible to
accurately predict gait events using a simple algorithm.
This algorithm displayed high levels of trial-to-trial
repeatability.
Conclusions
This study demonstrates the potential of using textile-based
transducers in future devices that provide active gait
assistance

Facilitated Neurogenesis in the Developing Hippocampus After Intake of Theanine, an Amino Acid in Tea Leaves, and Object Recognition Memory

http://www.springerlink.com/content/32171505412q8817/

Abstract

Theanine, γ-glutamylethylamide, is one of the major amino acid components in green tea. In this study, cognitive function and the related mechanism were examined in theanine-administered young rats. Newborn rats were fed theanine through dams, which were fed water containing 0.3% theanine, and then fed water containing 0.3% theanine after weaning. Theanine level in the brain was under the detectable limit 6 weeks after the start of theanine administration. Theanine administration did not influence locomotor activity in the open-field test. However, rearing behavior was significantly increased in theanine-administered rats, suggesting that exploratory activity is increased by theanine intake. Furthermore, object recognition memory was enhanced in theanine-administered rats. The increase in exploratory activity in the open-field test seems to be associated with the enhanced object recognition memory after theanine administration. On the other hand, long-term potentiation (LTP) induction at the perforant path-granule cell synapse was not changed by theanine administration. To check hippocampal neurogenesis, BrdU was injected into rats 3 weeks after the start of theanine administration, and brain-derived neurotropic factor (BDNF) level was significantly increased at this time. Theanine intake significantly increased the number of BrdU-, Ki67-, and DCX-labeled cells in the granule cell layer 6 weeks after the start of theanine administration. This study indicates that 0.3% theanine administration facilitates neurogenesis in the developing hippocampus followed by enhanced recognition memory. Theanine intake may be of benefit to the postnatal development of hippocampal function.

Stem Cell Technology Enables New Disease in a dish

I like the brain in a dish comment, with that I would hope it makes it easier to determine what works and what doesn't for stroke rehab. I know this is for schizophrenia but the concept should work to determine behavior of brain cells trying to integrate into a damaged brain. Way above my pay grade but I can at least ask the questions. Ask your researcher about this possibility.
http://dana.org/uploadedFiles/News_and_Publications/BrainWork/bw_summer2011.pdf
The Neuroscience Newsletter BRAINWORK
THE DANA FOUNDATION’S
Vol. 19, No. 3 | Fall 2010 http://www.dana.org/
BrainWork / Fall 2010 / 1
For some brain diseases,laboratory models makes it hard for
researchers to understand disease-causes and develop
therapies. New stem cell technology offers a powerful solution.
By Jim Schnabe l
Stem cell therapies for disease are still mostly over the horizon. But stem
cell technology is already boosting scientists’ abilities to study diseases and
test drugs against them. The technology is proving particularly useful for brain disorders
that are hard to model in animals. Using an “induced pluripotent stem
cell” (iPS) technique first reported for human cells only in 2007, scientists now
can take skin cells from patients, convert them to iPS cells and then neurons in a lab
dish, and study the patient-derived neurons to gain insights into disease mechanisms
and therapies. Two recent reports show the power of the “brain-in-a-dish”
technique.
“We’re going to see a lot of these papers coming out,” says Clive Svendsen,
director of the Regenerative Medicine Institute at Cedars-Sinai Medical Center in
Los Angeles.

Modeling Schizophrenia
Schizophrenia features abnormalities in some of our more evolutionarily advanced
neural circuitry, including weak connectivity among the prefrontal and temporal
cortices and the hippocampus. The causes of schizophrenia are not well understood:
Although it is largely genetic, its known genetic risk factors are varied, and mostly
subtle. The disease is often described as being caused by “many rare mutations”
that somehow feed into a final common pathway of vulnerability. There is no good
animal model. In a study published online in Nature
on April 13, researchers led by senior investigator Fred H. Gage at the Salk
Institute took skin cells from four different people with schizophrenia. Using the
iPS technique, they reprogrammed the patients’ skin cells to act like fetal stem
cells—then used a biochemical recipe to “differentiate” these into neural progenitor
cells, which proliferated and produced mature neurons.
The technique produced a large supply of neurons per patient, and as newborn
neurons will, they spontaneously formed clusters that connected to each other.
Gage’s team thus was able study in detail how these schizophrenia-patient-derived
neurons were different from neurons that had been derived from healthy people
using the same iPS technique.
Comparing gene expression patterns, for example, they found in the schizophrenia
neurons 596 genes that, on average, were expressed at least 30 percent more
than normal or 30 percent less than normal. “When we looked at the categories
of functions for these genes, we found certain pathways that stood out quite
strongly, which gives us new leads about what may be going on in schizophrenia,”
says Gage, who also is a member of the Dana Alliance for Brain Initiatives. The
pathways disturbed in the schizophrenia neurons included those controlling
neuronal growth and the maintenance of synapses—the interfaces at which
neurons communicate. In one-quarter of cases, the gene expression changes in the
schizophrenia neurons confirmed changes known from previous research.
Gage’s team also was able to quantify how connected the neurons were to one
another. On average, the schizophrenia neurons had only about half the connectivity
of normal neurons, a difference that corresponded to some of the changes
seen in gene expression. When the researchers treated the
cells for 20 days each with five standard schizophrenia drugs, they found that each
drug improved connectivity and gene expression patterns—moving them in the
direction of normality—for at least some patients’ iPS-derived neurons. One drug,
loxapine, significantly boosted connectivity for all four sets of neurons. “And these
were all different and quote-unquote sporadic cases of schizophrenia,” Gage notes.
“The fact that one of the compounds could generally increase the connectivity
was quite impressive to us.”
Only three earlier studies of humaniPS-derived models have been published,
Stem Cell Technology Enables New ‘Disease in a Dish’ Models of Brain Disorders
Summer 2011
(Continued on page 2)
Summer 2011/ 1
BrainWork / Summer 2009 / 2
and each involved relatively simple comparisons of survival/degeneration
between patient-derived and control neurons. Gage’s group’s techniques had to
be more sophisticated to detect the more subtle neuronal disturbances at the heart
of schizophrenia. One such technique permitted the tracing of connections among
neurons using a modified rabies virus. Rabies viruses evolved to “swim” upstream
along nerve fibers and across synapses, hopping from neuron to neuron until they
get to the brain. In this case, Gage’s group, using a method developed elsewhere at
the Salk Institute, created a rabies virus that lacks a key protein, forcing it to stop
after a single hop. Because the modified rabies viruses expressed a fluorescent
tracer protein, their movements—and thus the neurons’ connections—could be
tracked.
Gage says the set of techniques used in this study could be applied to other
brain diseases in which researchers suspect abnormal connectivity. But he also
wants to refine the techniques to glean more insights about schizophrenia. “We’re
developing protocols to differentiate these cells specifically into hippocampal
neurons versus cortical neurons, so we can apply the same basic analysis using
more specific neuronal types,” he says. With these more sophisticated techniques
and a more diverse set of patient-derived neurons, he hopes the deep biology of
schizophrenia will eventually become much clearer. “We’re looking for a core
program that underlies the disease,” he says. “Perhaps not 596 gene expression
alterations, but some subset. This is not a single-gene disease.”
Modeling Spinal Muscular Atrophy One of the first clinical successes
enabled by the iPS-modeling technology could be for spinal muscular atrophy
(SMA). An iPS-derived model of SMA was reported in 2009 by Svendsen’s lab and
the lab of stem cell researcher James Thomson.
SMA is a childhood recessive genetic disease in which both parental genes
for the protein SMN are defective. The deficiency of SMN—for reasons that
haven’t been understood—causes spinal muscle-controlling neurons to degenerate.
In severe cases, SMA can proceed from the first symptoms at the age of about
six months to fatal paralysis a year and a half later. “It’s horrific for parents,” says
Svendsen. “There’s nothing they can do; there’s no cure for it.”
Svendsen’s and Thomson’s labs converted fibroblasts from a single SMA
patient into motor neurons like those affected in the disease, and were able to
show that the neurons underwent an SMA like process of degeneration, compared
with neurons generated from fibroblasts taken from the patient’s healthy mother.
“In effect we were able to replay the disease,”
says Svendsen. “The motor neurons were born and they were fine for a few
weeks, and then they underwent degeneration, so we actually watched them die.”
Since that initial demonstration, Svendsen and Thomson have developed
and studied neuronal lines from other SMA patients, and Svendsen says they
have found changes in the neurons that may account for their degeneration when
deprived of SMN. He and Thomson are about to submit their findings for publication.
“We’re also getting closer to thinking about rational drug design based on the
mechanism of these motor neuron deaths in the kids,” he says.
Tomorrow’s Must-Have Lab Tech Svendsen expects a flood of iPS-model
papers to be published in the next few years, particularly for the strongly genetic,
early-onset diseases like SMA that seem best suited to the technique. The iPS
induction process resets cells to something like a newborn state, and seems to erase
many of the cellular changes that occur with aging and environmental stresses. “I
always look at iPS models as developmental models essentially,” he says. “Because
you’re taking the cell back in time and then making it undergo development again.”
For this reason, he was surprised that Gage’s group found such clear connectivity
deficits in iPS-derived neurons from patients with schizophrenia—a disease
that normally doesn’t manifest until late childhood. “But if that [result] reproduces
in more neuron lines, it’ll be a very nice way of looking at the mechanism of cell
connections in schizophrenia,” he says. Later-onset diseases such as
Parkinson’s, Alzheimer’s, and Huntington’s could be more difficult to model in neurons generated by the iPS technique. But researchers might still generate useful
models for these disorders if they can find a way to artificially age or otherwise stress the cells, to see whether disease-derived neurons are more vulnerable than control neurons. “Many groups are looking at the possibility of adding toxins to the cell cultures, for example,” Svendsen says. He is mindful that these are only labdish models. “We’re not going to do away with whole-animal models,” he says. But
the technology is potentially valuable enough that he expects it to spread widely
in academic and commercial labs, replacing older cell-based disease modeling
techniques. “Eventually I think if you’re going to study a human disease or look
at a related pathway or a system, you’ll be expected to grab an iPS line from that disease
model if it’s available,” says Svendsen. Jim Schnabel is a science journalist and
author based in Florida.
Summer 2011
(stem cell tech, continued from page 1)
“I always look at iPS models as developmental models essentially, because you’re taking the cell back in time and then making it undergo development again.”
--Clive Svendsen, Regenerative Medicine Institute

Survival protein’ protects the brain against effects of stroke

http://www.kurzweilai.net/survival-protein-protects-the-brain-from-cell-death-in-stroke-and-heart-attack
‘Survival protein’ protects the brain against effects of stroke
May 25, 2011 by Editor
[+]
(Credit: iStockphoto)
A “survival protein” that protects the brain against the effects of stroke in rodent brain tissue has been discovered by scientists at Johns Hopkins University. The finding has implications for treating stroke as well as Parkinson’s Disease, diabetes, and heart attack.
When brain tissue is subjected to a stressful but not lethal insult, a defense response occurs that protects cells from subsequent insult. The scientists dissected this preconditioning pathway to identify the most critical molecular players, including the Iduna protein. This protein increased three- to four-fold in preconditioned mouse brain tissue following an insult to the tissue, the scientists said.
The team exposed mouse brain cells to short bursts of a toxic chemical, and then screened these “preconditioned” cells for genes that turned on as a result of the insult. Focusing on Iduna, the researchers turned up the gene’s activity in the cells during exposure to the toxic chemical, which induced preconditioning. Cells deficient in Iduna did not survive, but those with more Iduna did.
The scientists found that the Iduna protein interferes with a particular kind of cell death that’s implicated in complications from diabetes and heart attack as well as stroke. By binding with a molecule known as PAR polymer, Iduna prevents the movement of cell-death-inducing factor (AIF) into a cell’s nucleus.
“Apparently, what doesn’t kill you makes you stronger,” says Valina Dawson, Ph.D. “This protective response was broad in its defense of neurons and glia and blood vessels — the entire brain. It’s not just a delay of death, but real protection that lasts for about 72 hours.”
Ref: Shaida A Andrabi, Ho Chul Kang, et al., Iduna protects the brain from glutamate excitotoxicity and stroke by interfering with poly(ADP-ribose) polymer-induced cell death, Nature Medicine, 2011; DOI: 10.1038/nm.2387
Ref: Y. Wang, N. S. Kim, et al., Poly(ADP-Ribose) (PAR) Binding to Apoptosis-Inducing Factor Is Critical for PAR Polymerase-1-Dependent Cell Death (Parthanatos), Science Signaling, 2011; 4 (167): ra20 DOI: 10.1126/scisignal.2000902

Biomarker to tackle cardiovascular risk in older people?

http://www.barchester.com/Healthcare-News/Biomarker-to-tackle-cardiovascular-risk-in-older-people%3F/376/4438
A biomarker for cardiovascular conditions has identified a possible therapeutic target for heart failure.
Older patients, possible home care users, who have symptoms of heart failure and a certain biomarker in the blood have an associated increased risk of death, according to new findings.
A study published in journal JAMA found that increased concentrations in the blood of biomarker copeptin or a combination of high levels of copeptin concentrations and biomarker NT-proBNP, along with symptoms of heart failure, caused an increased risk of all-cause death.
Copeptin could be a potential surrogate marker for measurement of vasopressin - a cardiovascular disease marker - in the blood.
According to authors: "These data, together with our findings of the prognostic information provided by measurement of copeptin concentrations in elderly patients with symptoms of heart failure, suggest that vasopressin may be a potential target for therapeutic intervention."
This follows Johns Hopkins research which revealed that when a stroke occurs, a 'survival protein' is produced in the brain in order to protect cells
My next post refers to this survival protein

Epigenetics and the Human Brain

I covered this earlier here; but it bears more publicity, ask your researcher about it.
http://oc1dean.blogspot.com/2011/04/epigenics-of-stroke-rehabilitation.html
the new one here;
http://www.dana.org/news/cerebrum/detail.aspx?id=32670
Since the discovery of DNA in the 1950s, one of the primary goals of geneticists has been to understand how differences in the DNA sequence can influence human health and lead to diseases. After several decades of intense research, two conclusions are clear: (1) in most cases, it is difficult to establish a direct link between any specific gene(s) and specific biological processes or diseases, and (2) most traits and pathologies are associated with more than just one gene and have complex mechanisms. Discovering that such complexity is at play led researchers to acknowledge that the genome on its own is likely not sufficient to sustain all biological functions, and that another level of regulation is contributing. They proposed the epigenome as one of these additional levels.
Tightly associated with the genome, the epigenome represents an ensemble of biochemical marks present on the DNA itself. These marks modulate the DNA’s activity and functions, but occur without any change in the DNA sequence. Instead, various enzymes add epigenetic marks to the DNA. The marks stamp genes with a unique signature that signals the gene to be active or silent.
Unlike the DNA sequence, epigenetic processes are dynamic and not fixed, although some can persist for long periods of time, up to several years or a lifetime. Further, they are strongly influenced by the environment and by exposure to external factors like diet, living conditions, exercise, stress, chemicals, drugs, and toxins. Both positive and negative factors can modulate the epigenome. For instance, positive factors such as enriched living conditions, like social interactions, physical activity, and changing surroundings, can promote beneficial epigenetic marks, while severe stress or agricultural chemicals can permanently alter some marks.1,2 These modifications can impact various aspects of an organism’s life during any phase of development, and can increase the susceptibility to diseases. For example, traumatic events and severe chronic stress in early life can alter the epigenome in a persistent and sometimes heritable fashion.3-5 Many cancers are also associated with epigenetic alterations induced by factors such as poor diet and toxins.6,7

Deans' stroke rehabilitation outline

Once I got over 300 posts I knew I needed to put all of them together into an outline, not only for others but for myself. I was losing track of all the ideas generated. This is the result. Only 431 posts so far. I didn't realize I was so verbose.

If you are a newbie, you probably want to intelligently discuss next steps with your doctor, these two posts will help with that.
What my doctor should have told me about stroke recovery:
http://oc1dean.blogspot.com/2010/08/what-my-doctor-should-have-told-me.html
Interviewing your stroke rehab doctor:
http://oc1dean.blogspot.com/2010/11/interviewing-your-stroke-rehab-doctor.html
If you are working with a therapist ask about compensation vs. recovery:
http://oc1dean.blogspot.com/2010/10/compensation-vs-recovery.html
If you are a fact-based person and are able to read, stroke books listed here; I would get a piece or two of information from each one.
http://oc1dean.blogspot.com/2011/05/my-stroke-book-reading-list.html
http://oc1dean.blogspot.com/2010/10/book-reading-list.html
If you want to influence the future; letter to president, letters to NSA, ASA, WSO,NINDS;
http://oc1dean.blogspot.com/2010/09/letter-to-president.html
http://oc1dean.blogspot.com/2010/09/letter-to-international-jornal-of.html
http://oc1dean.blogspot.com/2010/11/emails-to-nsa-stroke-rehab-failures.html
Nothing to the ASA or NINDS yet

If you think I'm missing a section, let me know. Some posts are in multiple sections
Work in progress, when this line is gone it is complete.
General Brain and Stroke Knowledge.
http://oc1dean.blogspot.com/2011/06/suffolk-reports-damning-verdict-on.html
http://oc1dean.blogspot.com/2011/06/interest-and-costs-of.html
http://oc1dean.blogspot.com/2011/06/gold-seal-of-approval-from-joint.html
http://oc1dean.blogspot.com/2011/05/brain-basics.html
http://oc1dean.blogspot.com/2011/05/my-stroke-book-reading-list.html
http://oc1dean.blogspot.com/2010/11/my-take-on-stroke-rehab-forums.html
http://oc1dean.blogspot.com/2010/10/book-reading-list.html
http://oc1dean.blogspot.com/2011/05/stroke-recovery-statistics.html
http://oc1dean.blogspot.com/2011/05/paying-for-outcomes-of-health-care.html
http://oc1dean.blogspot.com/2011/05/four-out-of-five-families-will-be.html
http://oc1dean.blogspot.com/2011/05/how-long-will-you-live-blood-test-in-uk.html
http://oc1dean.blogspot.com/2011/06/what-are-long-term-outcomes-following.html%20
Research
http://oc1dean.blogspot.com/2011/06/what-are-long-term-outcomes-following.html

http://oc1dean.blogspot.com/2011/06/improved-stroke-treatment-problem-for.html


http://oc1dean.blogspot.com/2011/06/blocking-stress-related-cell-death.html

http://oc1dean.blogspot.com/2011/06/body-weightsupported-treadmill.html

http://oc1dean.blogspot.com/2011/06/what-happens-in-brain-as-it-loses.html

http://oc1dean.blogspot.com/2011/06/improved-stroke-treatment-problem-for.html%20

http://oc1dean.blogspot.com/2011/05/drugs-for-parkinsons-condition-may.html

http://oc1dean.blogspot.com/2011/05/epigenetics-and-human-brain.html

http://oc1dean.blogspot.com/2011/05/understand-explain-predict-stroke.html
http://oc1dean.blogspot.com/2011/05/stem-cell-technology-enables-new.html
http://oc1dean.blogspot.com/2011/05/stroke-arm-longitudinal-study-at.html
http://oc1dean.blogspot.com/2011/05/combining-confocal-laser-scanning.html
http://oc1dean.blogspot.com/2011/05/nanomagnetic-remote-control-of-animal.html
http://oc1dean.blogspot.com/2011/05/pediatric-strokes-more-common-than-most.html
http://oc1dean.blogspot.com/2011/05/when-all-you-have-is-hammer-everything.html
http://oc1dean.blogspot.com/2011/05/scientific-method-as-applied-to-stroke.html
http://oc1dean.blogspot.com/2011/05/50-important-clinical-studies-in-stroke.html
Prevention
http://oc1dean.blogspot.com/2011/06/atheronova-to-address-significant-unmet.html

http://oc1dean.blogspot.com/2011/06/atheronova-to-address-significant-unmet.html

http://oc1dean.blogspot.com/2011/06/fda-announces-new-safety.html

http://oc1dean.blogspot.com/2011/06/abcd2-score-not-accurate-enough-to.html

http://oc1dean.blogspot.com/2011/06/heart-can-repair-itself-new-basic.html

http://oc1dean.blogspot.com/2011/06/mercury-exposure-and-cvd-not-associated.html%20

http://oc1dean.blogspot.com/2011/05/europe-approves-pfizer-blood-thinner.html

http://oc1dean.blogspot.com/2011/05/boosting-good-cholesterol-with-niacin.html
http://oc1dean.blogspot.com/2011/05/biomarker-to-tackle-cardiovascular-risk.html
http://oc1dean.blogspot.com/2011/05/ninety-percent-of-stroke-risk-due-to-10.html
http://oc1dean.blogspot.com/2011/05/adhd-meds-dont-increase-cardiovascular.html
http://oc1dean.blogspot.com/2011/05/conjugated-linoleic-acid-cla-reduced.html
http://oc1dean.blogspot.com/2011/05/trigger-factors-and-their-attributable.html
http://oc1dean.blogspot.com/2011/05/tiny-turbine-inside-arteries-could.html
http://oc1dean.blogspot.com/2011/05/fda-panel-to-weigh-revoking-key-use-of.html
http://oc1dean.blogspot.com/2011/05/stroke-is-both-preventable-and.html
http://oc1dean.blogspot.com/2011/05/simple-fitness-test-may-predict-heart.html
http://oc1dean.blogspot.com/2011/05/how-long-will-you-live-blood-test-in-uk.html
http://oc1dean.blogspot.com/2011/05/pradaxa-bests-warfarin-for-atrial.html

http://oc1dean.blogspot.com/2011/05/fda-panel-to-weigh-revoking-key-use-of.html
http://oc1dean.blogspot.com/2011/05/trigger-factors-and-their-attributable.html
http://oc1dean.blogspot.com/2011/05/conjugated-linoleic-acid-cla-reduced.html
http://oc1dean.blogspot.com/2011/05/soy-may-benefit-stroke-patients.html
http://oc1dean.blogspot.com/2011/05/surgery-stenting-fare-equally-well-in.html
diagnosis
http://oc1dean.blogspot.com/2011/03/my-diagnosis-of-stroke.html
http://oc1dean.blogspot.com/2011/03/homunculus-and-stroke-rehab.html

http://oc1dean.blogspot.com/2011/05/i-heard-about-this-on-public-radio-this.html
http://oc1dean.blogspot.com/2011/05/automated-measurement-of-proprioception.html
http://oc1dean.blogspot.com/2011/05/multidisciplinary-stroke-units.html
http://oc1dean.blogspot.com/2011/05/diagnosing-stroke-via-iphone-app.html
http://oc1dean.blogspot.com/2011/05/brain-scan-for-parkinsons.html
http://oc1dean.blogspot.com/2011/05/i-heard-about-this-on-public-radio-this.html
http://oc1dean.blogspot.com/2011/04/ibrain-and-eegs-of-brain.html
Assessment
http://oc1dean.blogspot.com/2011/05/shopping-simulator-to-test-stroke.html
SubAcute
Mental therapy
http://oc1dean.blogspot.com/2011/04/keep-going-on-stroke-rehab.html

http://oc1dean.blogspot.com/2010/09/falling-from-top-of-mt-everest-to.html
http://oc1dean.blogspot.com/2011/04/when-bad-things-happen-to-good-people.html
http://oc1dean.blogspot.com/2011/04/are-you-paranoid.html
http://oc1dean.blogspot.com/2011/04/frogs-and-stroke-rehab.html
http://oc1dean.blogspot.com/2011/04/mindfulness-meditation-improves.html
http://oc1dean.blogspot.com/2010/11/instant-decrepitude-and-stroke-effects.html
http://oc1dean.blogspot.com/2010/11/no-boundary-stroke-rehab.html
http://oc1dean.blogspot.com/2010/11/is-your-stroke-rehab-half-full-or-half.html
http://oc1dean.blogspot.com/2010/10/depression-and-stroke-rehab.html
http://oc1dean.blogspot.com/2011/03/patients-subjective-experience-in.htmlRecovery
http://oc1dean.blogspot.com/2010/09/analysis-to-riding-two-wheeled-bike.html
Neurogenesis
http://oc1dean.blogspot.com/2011/05/facilitated-neurogenesis-in-developing.html

http://oc1dean.blogspot.com/2011/06/role-of-neurogenesis-in-stroke-recovery.html

http://oc1dean.blogspot.com/2011/05/increase-of-neurogenesis-induced-by.html
http://oc1dean.blogspot.com/2011/05/apoptosis-neurogenesis-favorably.html
http://oc1dean.blogspot.com/2011/05/cerebrospinal-fluid-control-of.html
http://oc1dean.blogspot.com/2011/05/new-insights-into-gpr40-creb.html
http://oc1dean.blogspot.com/2011/05/neurotransmitters-how-brain-cells-use.html
http://oc1dean.blogspot.com/2011/05/use-it-or-lose-it-how-neurogenesis.html
http://oc1dean.blogspot.com/2011/05/neuroplasticity-and-stroke-rehab-easy.html
http://oc1dean.blogspot.com/2011/04/acidic-fibroblast-growth-factor.html
http://oc1dean.blogspot.com/2011/04/regulation-of-neurogenesis-by.html
http://oc1dean.blogspot.com/2011/05/angiogenesis-and-stroke-rehab.html
http://oc1dean.blogspot.com/2011/04/new-brain-cells-in-highest-brain-area.html
http://oc1dean.blogspot.com/2011/04/stud-effect-on-neurogenesis.html
http://oc1dean.blogspot.com/2011/04/vascular-endothelial-growth-factor-vegf.html
http://oc1dean.blogspot.com/2011/03/sk3-channelnwaspabi-1-complex-and.html
http://oc1dean.blogspot.com/2011/03/sk3-channelnwaspabi-1-complex-and.html
http://oc1dean.blogspot.com/2011/03/astrocytes-in-central-nervous-system.html
http://oc1dean.blogspot.com/2011/01/deep-brain-neurons-andstroke-rehab.html
Neuroplasticity
http://oc1dean.blogspot.com/2011/05/optogenetics-control-desk-for-neural.html
http://oc1dean.blogspot.com/2011/05/reserve-pool-neuron-transmitter.html
http://oc1dean.blogspot.com/2011/05/brainstem-stroke-recovery.html
http://oc1dean.blogspot.com/2011/05/neuroplasticity-and-stroke-rehab-easy.html
Orthotics
http://oc1dean.blogspot.com/2011/06/mechatronic-design-and-characterization.html
http://oc1dean.blogspot.com/2011/06/hand-spring-operated-movement-enhancer.html
http://oc1dean.blogspot.com/2011/05/automatic-identification-of-gait-events.html

hyperacute - the first hours and days after onset

http://oc1dean.blogspot.com/2011/06/new-treatment-dissolves-blood-clots-in.html

http://oc1dean.blogspot.com/2011/06/endovascular-embolectomy-aids-minority.html

http://oc1dean.blogspot.com/2011/06/brain-cooling-and-stroke-recovery.html

http://oc1dean.blogspot.com/2011/06/new-understanding-of-brain-chemistry.html%20

http://oc1dean.blogspot.com/2011/05/tpa-maximum-dose-limit-in-heavier.html
http://oc1dean.blogspot.com/2011/05/survival-protein-protects-brain-against.html
http://oc1dean.blogspot.com/2011/05/ablation-in-ischemic-stroke.html
http://oc1dean.blogspot.com/2011/05/draculin-stroke-drug-from-vampire-bats.html
http://oc1dean.blogspot.com/2011/05/estimated-58000-wake-up-with-stroke.html
http://oc1dean.blogspot.com/2011/05/prompt-stroke-therapy-will-cut-disease.html
http://oc1dean.blogspot.com/2011/05/survival-protein-protects-brain-against.html
http://oc1dean.blogspot.com/2011/05/when-all-you-have-is-hammer-everything.html
http://oc1dean.blogspot.com/2011/05/estimated-58000-wake-up-with-stroke.html
http://oc1dean.blogspot.com/2011/05/prompt-stroke-therapy-will-cut-disease.html
http://oc1dean.blogspot.com/2011/05/blood-clots-made-visible-by.html
http://oc1dean.blogspot.com/2011/05/snake-venom-and-stroke-rehab.html
http://oc1dean.blogspot.com/2011/04/apoptosis-target-for-neuroprotection.html
http://oc1dean.blogspot.com/2011/04/iron-deposition-and-acute-stroke-rehab.html
http://oc1dean.blogspot.com/2011/04/injection-to-limit-heart-attacks-and.html
http://oc1dean.blogspot.com/2011/04/nicotine-and-stroke-rehab-part-2.html
http://oc1dean.blogspot.com/2011/04/most-stroke-patients-not-getting-clot.html
http://oc1dean.blogspot.com/2011/03/science-of-stroke-mechanisms-in-search.html
http://oc1dean.blogspot.com/2011/03/new-zealand-stroke-research.html
http://oc1dean.blogspot.com/2011/03/nasal-spray-against-alzheimers-disease.html
http://oc1dean.blogspot.com/2011/03/xenon-gas-and-stroke-rehab.html
http://oc1dean.blogspot.com/2011/03/bubbles-with-ultrasound-stroke-drugs.html
http://oc1dean.blogspot.com/2010/12/nanoparticles-and-stroke-rehab.html
Acute
http://oc1dean.blogspot.com/2011/06/home-based-stroke-rehab-is-as.html

http://oc1dean.blogspot.com/2011/06/body-weightsupported-treadmill.html

http://oc1dean.blogspot.com/2011/06/which-neurorehabilitation-for-stroke-or.html

http://oc1dean.blogspot.com/2011/06/next-generation-gamers-computer-games.html%20

http://oc1dean.blogspot.com/2011/05/convection-enhanced-drug-delivery-ced.html

http://oc1dean.blogspot.com/2011/05/computer-games-that-improve-stroke.html
http://oc1dean.blogspot.com/2011/05/comparison-of-two-physiotherapy.html
http://oc1dean.blogspot.com/2011/03/patients-subjective-experience-in.html Chronic
http://oc1dean.blogspot.com/2011/05/spider-silk-constructs-enhance-axonal.html
http://oc1dean.blogspot.com/2011/05/impressionable-brain-and-mirror-neurons.html
http://oc1dean.blogspot.com/2011/05/hormone-improves-long-term-recovery.html
http://oc1dean.blogspot.com/2011/05/stroke-assessments-and-scales.html
http://oc1dean.blogspot.com/2011/05/angiogenesis-and-stroke-rehab.html
http://oc1dean.blogspot.com/2011/05/what-are-liposomes-good-for-in-stroke.html
http://oc1dean.blogspot.com/2011/04/mental-practice-with-motor-imagery-does.html
http://oc1dean.blogspot.com/2011/04/molecular-therapy-for-improved-post.html
http://oc1dean.blogspot.com/2011/03/mirror-therapy-promotes-recovery-from.html
http://oc1dean.blogspot.com/2011/03/viagara-and-stroke-rehab.html
http://oc1dean.blogspot.com/2011/03/neurotransmitter-reboxetine-could.html
http://oc1dean.blogspot.com/2011/03/tgf-alpha-and-stroke-rehab.html
http://oc1dean.blogspot.com/2010/10/dead-brain-recovery-options.html
http://oc1dean.blogspot.com/2011/05/hormone-improves-long-term-recovery.html
Therapies
http://oc1dean.blogspot.com/2011/05/onehanded-problems.html
http://oc1dean.blogspot.com/2011/05/comparison-of-two-physiotherapy.html
http://oc1dean.blogspot.com/2011/06/sunburn-and-stroke-rehab.html
stem cells
http://oc1dean.blogspot.com/2011/06/generating-functional-neurons-directly.html

http://oc1dean.blogspot.com/2011/05/stem-cell-technology-enables-new.html

http://oc1dean.blogspot.com/2011/04/clinical-trial-of-cell-therapy-for.html
http://oc1dean.blogspot.com/2011/04/stemgevity-and-stroke-rehab.html
http://oc1dean.blogspot.com/2011/04/stemedica-treats-stroke-patient-with.html
http://oc1dean.blogspot.com/2011/04/nutraceuticals-synergistically-promote.html
http://oc1dean.blogspot.com/2011/05/why-do-stroke-survivors-believe-in-stem.html

fatigue
http://oc1dean.blogspot.com/2011/03/post-stroke-fatigue-treatment-protocol.html
http://oc1dean.blogspot.com/2010/12/rem-sleep-and-stroke-fatigue.html
spasticity
http://oc1dean.blogspot.com/2011/04/whats-reason-for-spasticity-drugs.html
http://oc1dean.blogspot.com/2011/04/froomsplint-and-hand-anti-spasticity.html
http://oc1dean.blogspot.com/2011/04/prolonged-muscle-stretch-on-spastic.html
http://oc1dean.blogspot.com/2011/03/spasticity-intervention-for-stroke.html
http://oc1dean.blogspot.com/2011/03/spasticity-during-sleep-does-it-exist.html
http://oc1dean.blogspot.com/2011/03/sleeping-and-necessary-therapy.html
http://oc1dean.blogspot.com/2011/03/sleeping-and-necessary-therapy.html
http://oc1dean.blogspot.com/2011/03/finger-gloves-and-stroke-rehab.html
http://oc1dean.blogspot.com/2011/03/eversion-of-ankle-stroke-rehab.html
http://oc1dean.blogspot.com/2011/03/post-stroke-spasticity-ask-experts.html
http://oc1dean.blogspot.com/2011/02/marijuana-and-stroke-rehab.html
http://oc1dean.blogspot.com/2011/02/quantitative-measure-of-muscle.html
http://oc1dean.blogspot.com/2011/02/spasticity-exercise.html
http://oc1dean.blogspot.com/2011/02/brunnstroms-stages-of-recovery.html
http://oc1dean.blogspot.com/2011/02/spasticity-rant-and-stroke-rehab.html
http://oc1dean.blogspot.com/2010/10/fingerprinting-and-stroke-rehab.html
http://oc1dean.blogspot.com/2010/09/obstacles-to-my-stroke-recovery.html
http://oc1dean.blogspot.com/2010/08/stroke-rehabilitation-during-sleep.html
http://oc1dean.blogspot.com/2010/08/what-my-doctor-should-have-told-me.html
Therapists
Doctors
quackery?
http://oc1dean.blogspot.com/2011/06/stroke-stroke-damage-treatment.html

http://oc1dean.blogspot.com/2011/06/xing-nao-kai-qiao-stroke-rehabilitation.html

http://oc1dean.blogspot.com/2011/05/future-has-arrived-heart-attack-and.html
http://oc1dean.blogspot.com/2011/04/periodic-whole-body-acceleration.html
http://oc1dean.blogspot.com/2011/04/stemgevity-and-stroke-rehab.html
http://oc1dean.blogspot.com/2011/04/reflexology-and-stroke-rehab.html
http://oc1dean.blogspot.com/2011/04/spect-scan-brain-and-soul-work-together.html
http://oc1dean.blogspot.com/2011/04/neuro-infrah-stroke-therapy.html
http://oc1dean.blogspot.com/2011/04/shak-stroke-therapy-really.html
http://oc1dean.blogspot.com/2011/04/alzheimers-helmet-stimulates-growth-of.html
http://oc1dean.blogspot.com/2011/03/hbot-as-stroke-therapy.html
http://oc1dean.blogspot.com/2011/03/apoplexy-rehabilitation-instrument.html
http://oc1dean.blogspot.com/2011/03/nostrums-for-apoplexy-rehab.html
http://oc1dean.blogspot.com/2010/10/neuroaid-and-stroke-rehab.html
Humor

http://oc1dean.blogspot.com/2011/03/caveperson-stroke-rehab.html
http://oc1dean.blogspot.com/2011/04/online-shoppers-unknowingly-sold-their.html
http://oc1dean.blogspot.com/2011/02/annual-senior-citizan-test.html
http://oc1dean.blogspot.com/2011/01/canoe-race-as-stroke-rehab.html
http://oc1dean.blogspot.com/2010/11/men-and-drinking-nothing-on-stroke.html
http://oc1dean.blogspot.com/2010/10/plane-rides-and-stroke-rehab.html
http://oc1dean.blogspot.com/2010/10/hospital-vampires.html
http://oc1dean.blogspot.com/2011/06/sunburn-and-stroke-rehab.html
History

Boosting Good Cholesterol With Niacin Did Not Cut Heart Risks

I have been on this research trial for the last three years. I was taking the Niaspan, extended release niacin, I wasn't supposed to know the dose but they had us go to the max dose at first to validate that we could stand the side effects, flushing and itching. So based on the same effects I got when on the research trial I got the maximmum dose of 2000 something. Just this past month I decided I was going to quit the trial because of itching on my arms and legs, I had an old patch of excema on my leg that completely flared up and was close to driving me to scratch until it bled.

http://www.vpr.net/npr/136678665/
In a surprising setback, a big federal study testing prescription-strength niacin as an add-on to cholesterol-lowering statins to prevent heart disease was stopped early because the niacin didn't work.
Plus, more patients taking the drug Niaspan had strokes than those who got a placebo. That potential safety issue was another factor in the decision to halt the study 18 months early, doctors involved with the research said in a media conference call Thursday.
Niacin is the most effective treatment for raising HDL, or good cholesterol. And the study aimed to find out if raising HDL and lowering triglycerides (another consequence of niacin treatment) in addition to using a statin to control LDL, or bad cholesterol, would lead to better outcomes for patients.
The answer: Niaspan didn't reduce the risk of cardiovascular events, including heart attacks and strokes. There were 5.6 such events per year for the group that got placebo — compared with 5.8 per year for those who got Niaspan.

All of the more than 3,400 patients in the study took simvastatin, the cholesterol-lowering medicine sold under the brand-name Zocor. Some also got Zetia, another cholesterol-reducer.
The federally funded trial, called AIM-HIGH, was stopped because a scheduled review by an independent safety committee in April concluded the chances that the trial, started in early 2006, would ever show the expected benefit from niacin was less than 1 in 10,000. There was also that small but significant increase in stroke.
The results deal a blow to the so-called HDL hypothesis, which holds that raising good cholesterol should lower risk of heart disease. Epidemiological studies have suggested that's the case, but this test didn't bear it out.
Dr. William Boden, one of the lead investigators on the study, conceded the researchers were unable to show any additional benefit from raising HDL in patients whose bad cholesterol was controlled so well. Still, he didn't rule out the possibility of a positive HDL effect for different types of patients.
The Food and Drug Administration recommended no changes, for now, in the instructions or use of Niaspan. But the agency will analyze the data further.

Increase of Neurogenesis Induced by Pyridoxine and Increase of Neural Proliferation in the Mouse Dentate Gyrus

I like the increased cell proliferation and neuroblast differentiation and it does refer to epigenetics
http://www.springerlink.com/content/p02n818q4xm8q2x5/
Abstract
We previously observed that pyridoxine (vitamin B6) significantly increased cell proliferation and neuroblast differentiation without any neuronal damage in the hippocampus. In this study, we investigated the effects of sodium butyrate, a histone deacetylase (HDAC) inhibitor which serves as an epigenetic regulator of gene expression, on pyridoxine-induced neural proliferation and neurogenesis induced by the increase of neural proliferation in the mouse dentate gyrus. Sodium butyrate (300 mg/kg, subcutaneously), pyridoxine (350 mg/kg, intraperitoneally), or combination with sodium butyrate were administered to 8-week-old mice twice a day and once a day, respectively, for 14 days. The administration of sodium butyrate significantly increased acetyl-histone H3 levels in the dentate gyrus. Sodium butyrate alone did not show the significant increase of cell proliferation in the dentate gyrus. But, pyridoxine alone significantly increased cell proliferation. Sodium butyrate in combination with pyridoxine robustly enhanced cell proliferation and neurogenesis induced by the increase of neural proliferation in the dentate gyrus, showing that sodium butyrate treatment distinctively enhanced development of neuroblast dendrites. These results indicate that an inhibition of HDAC synergistically promotes neurogenesis induced by a pyridoxine and increase of neural proliferation.

Apoptosis-Neurogenesis Favorably Informs Memory Development

Not sure why apoptosis is in the title, its not even referred to in the article but if you want to know about it read this post;
http://oc1dean.blogspot.com/2011/04/apoptosis-target-for-neuroprotection.html
This is hard to understand and I'm not sure how a therapy protocol could be gleaned from this.
http://www.cs.yale.edu/publications/techreports/tr1284.pdf

Cerebrospinal fluid control of neurogenesis induced by retinoic acid during early brain development

More proof of the usefulness of CSF, I know it talks about early brain development but that just means someone has to research how to recreate that in the adult brain. I talked about this in an earlier post;
http://oc1dean.blogspot.com/2011/03/role-of-cerebrospinal-fluid-in-brain.html

The new article:
http://onlinelibrary.wiley.com/doi/10.1002/dvdy.22657/full
Keywords:CSF;brain development;retinol binding protein;neural precursors;neural tube;neurogenesis
Abstract
Embryonic-cerebrospinal fluid (E-CSF) plays crucial roles in early brain development including the control of neurogenesis. Although FGF2 and lipoproteins present in the E-CSF have previously been shown to be involved in neurogenesis, the main factor triggering this process remains unknown. E-CSF contains all-trans-retinol and retinol-binding protein involved in the synthesis of retinoic acid (RA), a neurogenesis inducer. In early chick embryo brain, only the mesencephalic-rombencephalic isthmus (IsO) is able to synthesize RA. Here we show that in chick embryo brain development: (1) E-CSF helps to control RA synthesis in the IsO by means of the RBP and all-trans-retinol it contains; (2) E-CSF has retinoic acid activity, which suggests it may act as a diffusion pathway for RA; and (3) the influence of E-CSF on embryonic brain neurogenesis is to a large extent due to its involvement in RA synthesis. These data help to understand neurogenesis from neural progenitor cells. Developmental Dynamics, 2011. © 2011 Wiley-Liss, Inc

New insights into GPR40-CREB interaction in adult neurogenesis specific for primates

I don't quite know what this might mean for a therapy protocol, so ask your researcher/doctor what it means.
It mentions polyunsaturated fat which can be found mostly in nuts, seeds, fish, algae, leafy greens, and krill. And it seems to create BDNF. But I like the neurogenesis part.
http://onlinelibrary.wiley.com/doi/10.1002/hipo.20951/full
Keywords:PUFA;pCREB;hippocampus;brain ischemia
Abstract
Polyunsaturated fatty acids (PUFA), such as docosahexaenoic (DHA) and arachidonic acids (ARA) are known to be closely related to the brain development and also have beneficial effects on adult neurogenesis, learning, and mental disorders. Although PUFA were demonstrated as ligands for G protein-coupled receptor 40 (GPR40), their signaling mechanism in the brain, especially in the neurogenic niche, remains unknown. Using a monkey model of ischemia-enhanced hippocampal neurogenesis, we studied the spatial correlation between GPR40 and the phosphorylated cAMP response element-binding protein (pCREB), a transcription factor involved in adult neurogenesis, learning and memory. Furthermore, the brain-derived neurotrophic factor (BDNF) and its receptor tropomyosin receptor kinase B (TrkB), both being downstream gene transcripts of pCREB, were studied. Similar to the dynamic change of GPR40 as the authors reported previously, pCREB was up-regulated significantly after transient global brain ischemia on Western blots, and this was associated with an enhanced hippocampal neurogenesis. Immunofluorescence microscopic analysis showed that GPR40 and pCREB expression patterns were completely identical, and they were coexpressed in both mature and newborn neurons as well as in the astrocytes residing in the subgranular zone (SGZ). GPR40/pCREB double-positive cells significantly increased in the SGZ on day 15 after ischemia. The mature form of BDNF (mBDNF) and TrkB receptor showed no remarkable changes on Western blots, although proBDNF (precursor of mBDNF) was maximal on day 9. Immunofluorescence microscopy showed that the newborn neurons expressed BDNF, but not TrkB. These results altogether suggest that PUFA, GPR40, pCREB, and BDNF may be engaged in the same signaling pathway to promote neurogenesis in the adult primate hippocampus. © 2011 Wiley-Liss, Inc.

Pradaxa bests warfarin for atrial fibrillation stroke risk

And I so liked taking rat poison when I was on Warfarin, wonder what the basis of this drug is.
http://www.usatoday.com/yourlife/health/medical/heartdisease/2010-10-21-a-fib-stroke_N.htm
Posted 10/21/2010

The drug Pradaxa has been approved by the U.S. Food and Drug Administration to help prevent stroke in people with a type of abnormal heart rhythm called atrial fibrillation.

The drug may prove a new option for patients who now use standard blood thinners such as warfarin to control the heart condition.

More than 2 million Americans have atrial fibrillation, which occurs when the heart's two upper chambers beat quickly and out of sync, the FDA said Wednesday in a news release.

Pradaxa (dabigatran) is an anti-clotting drug that inhibits an enzyme involved in blood clotting. Clinical studies of the drug found that when compared with warfarin, people with atrial fibrillation had fewer strokes on Pradaxa than those on warfarin, the FDA said.

One such trial was presented in February at the American Stroke Association annual meeting in San Antonio. It included more than 3,600 patients with atrial fibrillation and a previous stroke who were randomly chosen to receive warfarin, a low dose of Pradaxa (110 milligrams) twice a day or a higher dose (150 mg) of Pradaxa twice a day for about two years.

The rate of stroke or transient ischemic attack (TIA, often called "mini- stroke") in those taking warfarin was about 2.7% a year and 2.3% a year for those taking Pradaxa, not a significant difference.

However, the lower dose of Pradaxa caused less bleeding and was easier to manage than warfarin, a famously difficult drug to administer and monitor.

"In contrast to warfarin, dabigatran is given in a fixed dose twice daily independent of body weight, sex, food, whatever, and you don't need to monitor the coagulation system," study author Dr. Hans-Christoph Diener, chairman of neurology at University Hospital in Essen, Germany, said during a news conference held during the meeting.

"In patients who already had a transient ischemic attack or stroke and suffer from atrial fibrillation, dabigatran is as effective as warfarin," he added. "And it's much easier to handle."

Patients receiving Pradaxa had more heart attacks than those taking warfarin, but the absolute difference was small, the authors stated. Also, Pradaxa patients had higher rates of gastrointestinal bleeding.

The study was funded by Boehringer-Ingelheim GmbH, which makes the drug.

Those findings were echoed by a study published last year in the New England Journal of Medicine. In that trial, also funded by the drugmaker, Pradaxa proved equal to warfarin in preventing dangerous venous clots, but much easier for doctors and patients to manage.

"For patients and health-care providers, dabigatran is a far more convenient drug than warfarin because it has no known interactions with foods and minimal interactions with other drugs and therefore does not require routine blood-coagulation testing," wrote the international team of researchers led by Dr. Sam Schulman of McMaster University and the Henderson Research Center in Hamilton, Ontario.

And last November, two other promising reports on Pradaxa were presented at the American Heart Association meeting in Orlando. Those studies found the drug to be safe and effective in preventing blood clots when patients were treated for acute coronary syndrome, a cluster of symptoms that might indicate a heart attack. It was also found superior to warfarin in preventing strokes in patients with atrial fibrillation.

Pradaxa, which is produced in 75 milligram and 150 milligram strengths, is not without side effects or risk, however. According to the FDA, as with other anti-clotting drugs, a potential side effect is life-threatening bleeding. Other potential adverse reactions include stomach discomfort or pain, nausea, heartburn and bloating.

"It's premature to say that a drug like dabigatran will take the place of warfarin," Dr. Bernard Gersh, a professor of medicine at the Mayo Clinic College of Medicine in Rochester, Minn., said at the time of last November's conference. "There will be a lot of discussion about cost and convenience. It's a twice-daily dose and there are some questions about a possible higher rate of heart attack. I don't think this is truly resolved yet, but I think we can say that for the first time we have seen a drug that certainly has the potential to be an alternative to warfarin, and maybe even superior."

Understand, explain, predict stroke rehabilitation

I know this has become obsessive with me but someone has to point out the stupidity of it all. I heard about this again listening to a scientist on the radio. So right now we don't understand anywhere enough about the brain to explain what is going on when damaged, until that occurs we won't be able to make predictions. This once again points out the need for a longitudinal research study and a repository of all the case studies.
But first we need a valid stroke damage diagnosis.

Theories are analytical tools for understanding, explaining, and making predictions about a given subject matter.
http://en.wikipedia.org/wiki/Theory

Europe approves Pfizer blood thinner

http://www.wane.com/dpps/health/healthy_living/europe-approves-pfizer-blood-thinner_3817521
I'm wondering if this does not require the INR blood test.

Will be available in all EU countries

Updated: Friday, 20 May 2011, 3:54 PM EDT
Published : Friday, 20 May 2011, 3:54 PM EDT

NEW YORK (AP) - Drugmaker Pfizer said Friday that European regulators have approved its highly-anticipated blood thinner Eliquis to prevent blood clots in patients who have had hip or knee replacement surgery.
The approval by the European commission means the drug, known as apixaban, will be available in the 27 countries of the European Union. Pfizer Inc. co-developed the drug with Bristol-Myers Squibb, which will share the profits.
The drug was approved based on two studies that showed better outcomes for patients taking twice-daily Eliquis rather than receiving an injection of the typical current treatment. Bleeding side effects were approximately the same between the two groups. All patients studied had undergone orthopedic surgery to replace a knee or hip, a procedure that raises the risk of blood clots.
Eliquis has been touted as a potential blockbuster drug for its ability to prevent blood clots without the bleeding side effects of older drugs like warfarin. However, last year the companies had to halt a 10,000-patient study of the drug in people with a history of heart disease after an unexpected number of bleeding side effects.
Apixaban works by blocking a clotting protein called factor Xa, which is part of the clotting reaction. That is in contrast to other blood thinners, which work by preventing platelets from sticking together.
The drug is not available in the U.S., though Pfizer and Bristol-Myers plan to submit it to the Food and Drug Administration later this year. The companies are seeking approval to prevent stroke in patients with a type of heart defect.

How long will you live? Blood test in the UK

http://www.popsci.com/science/article/2011-05/new-blood-test-will-tell-you-how-long-you-will-live
A new test set to hit the market in Britain in the next year aims to tell patients how long they have to live, and naturally that’s not happening without controversy. The test measures a person’s telomeres, those structures found on the tips of chromosomes. The length of telomeres apparently correlates with how fast a person is aging biologically, and hence researchers want to offer individuals some insight into just how much longer their bodies can hold up.
Well, some researchers do. Others aren’t so sure it’s a great idea. The test, developed at the Spanish National Cancer Research Centre, will be marketed via the company Life Length, which is in talks with medical diagnostics companies across Europe. When it goes on sale next year it will cost roughly $700.

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Tags

Science, Clay Dillow, chromosomes, diagnostics, health, medical diagnostics, telomeres

It works pretty simply: provide a blood sample, and the test checks the length of your telomeres, which are basically used to determine your biological age. Research has shown that those with shorter than normal telomeres have shorter average life spans than those with longer telomeres. They also might have a severe case of telomere anxiety that they didn’t know they had previously.

Critics see that as a problem. Aside from the fact that insurance companies might start requiring telomere testing and using it to determine life insurance and health insurance rates, it might also stoke peoples’ fears of death--and open them up to scams and bad medicine purporting to extend their telomeres/lives.
That all sounds like an interesting backdrop for a novel (perhaps one set in a not too distant future dystopian New York and written by Gary Shteyngart), but some are afraid that such a test would open a Pandora’s Box that we couldn’t put the lid back on. The price might be the more controversial part; $700, and let’s face it: no one’s telomeres are going to be quite long enough.

This blogger has some good points about this test.
http://theness.com/neurologicablog/index.php/how-long-will-you-live/

Convection-enhanced drug delivery (CED) to directly deliver drugs into brain tissue

http://cancerres.aacrjournals.org/content/65/15/6858.abstract
Abstract
Convection-enhanced drug delivery (CED) is a novel approach to directly deliver drugs into brain tissue and brain tumors. It is based on delivering a continuous infusion of drugs via intracranial catheters, enabling convective distribution of high drug concentrations over large volumes of the target tissue while avoiding systemic toxicity. Efficient formation of convection depends on various physical and physiologic variables. Previous convection-based clinical trials showed significant diversity in the extent of convection among patients and drugs. Monitoring convection has proven to be an essential, yet difficult task. The current study describes the application of magnetic resonance imaging for immediate assessment of convection efficiency and early assessment of cytotoxic tissue response in a rat brain model. Immediate assessment of infusate distribution was obtained by mixing Gd-diethylenetriaminepentaacetic acid in the infusate prior to infusion. Early assessment of cytotoxic tissue response was obtained by subsequent diffusion-weighted magnetic resonance imaging. In addition, the latter imaging methodologies were used to establish the correlation between CED extent and infusate's viscosity. It was found that low-viscosity infusates tend to backflow along the catheter track, whereas high-viscosity infusates tend to form efficient convection. These results suggest that CED formation and extent may be significantly improved by increasing the infusate's viscosities, thus increasing treatment effects.
from May 2005
This should be able to be used to deliver tPA and other acute therapies that stop neuron death.

Drugs For Parkinson’s condition may possibly Ease Stroke-related Disability

Poorly written, never could figure out the meaning.

Drugs For Parkinson’s condition may possibly Ease Stroke-related Disability

— researchers have untangled two equivalent disabilities that frequently afflict stroke sufferers, inside the practice revealing that a single may possibly be treatable with drug treatments for Parkinson’s condition. Researchers at Washington college college of medication in St. Louis confirmed that stroke injury in a very brain location recognised because the putamen is strongly connected to motor neglect, a ailment that can make sufferers sluggish to transfer towards the left facet. Like stroke sufferers with motor neglect, Parkinson’s sufferers are also sluggish to initiate responses involving motion. researchers attribute this deficit in Parkinson’s condition to reduction of neurons that utilize the neurotransmitter dopamine to regulate exercise inside the putamen. "Earlier attempts to deal with stroke sufferers with neglect with dopamine-like compounds have made combined benefits," says lead writer Ayelet Sapir, Ph.D., postdoctoral researcher in neurology. "It’s doable, even though, that all those unfavorable results resulted from an inability to recognize the sufferers most very likely to advantage through the intervention. Our information point out that sufferers with injury on the putamen may possibly reply in a different way to this remedy than sufferers who’ve neglect from stroke injury to other components of brain." Sapir describes the exploration, which seems inside the Journal of Neuroscience, as element of the broader hard work to exactly figure out how strokes in various components in the brain’s correct hemisphere have an effect on sufferers. She and other folks would like to intently website link injury in a very presented correct brain location to a selected set of signs or symptoms. "This tactic has long been used to strokes impacting the left hemisphere, exactly where injury to a variety of brain places is connected to unique types of language deficits," Sapir says. "Taking the similar tactic to learning lesions in the correct hemisphere need to support boost affected person remedy by letting us to produce therapeutic ways targeted to unique brain circuits and neurochemical methods." Many issues just after a right-brain stroke fall underneath the broad heading of neglect: inability to detect a stimulus or do a thing about this. Neglect is hugely disabling seeing that it interferes with many simple pursuits this kind of as dressing, self-care and driving, Sapir notes. Every 12 months, around three to five million folks with strokes in the correct facet in the brain among the ear as well as temple produce a ailment recognised as spatial neglect that hampers their capacity to detect points on their left facet. sufferers may possibly seem to be to become unaware of their left arm, for instance, or could fall short to consume through the left facet of the meals tray. The ailment is most significant inside the initially several months subsequent a stroke, but in some sufferers it gets to be a persistent dilemma. Some sufferers with strokes on this place produce a somewhat various ailment recognised as motor neglect. This leads to them to become sluggish to act towards the left facet of their surroundings. It could, for instance, make them sluggish to swat at a bug that lands on their left facet. How to separate slowness to detect a stimulus (spatial neglect) from slowness to act on the stimulus (motor neglect) has long been a persistent dilemma for neuroscientists. in a very popular laboratory check of neglect’s outcomes, sufferers observe a video clip display for your look of the stimulus, typically a image or form, on both the left or even the correct facet in the display. after they see a stimulus, they report which facet it absolutely was on to scientists. The problem for scientists was that spatial neglect and motor neglect made the similar results–a affected person who was sluggish to report stimuli appearing in the left facet in the video clip display. This was genuine for spatial neglect sufferers due to the fact they have been sluggish to discover the stimulus; motor neglect sufferers could see it but have been sluggish to generate the movements essential to report they had viewed it. To defeat this dilemma, Sapir had sufferers start out the check with their hand on the button positioned on the left in the video clip display. after they noticed a stimulus, they attained towards the video clip display and touched it in the facet exactly where the stimulus appeared. Slowness to reply to stimuli appearing in the left facet in the video clip display, she theorized, would necessarily mean the affected person had spatial neglect and was owning difficulty noticing the stimuli. Patients who promptly observed left-side stimuli could report that perception by reaching to their unimpaired correct facet. Of 29 sufferers examined, 6 have been capable to reply promptly to left-side stimuli, suggesting that they had motor neglect. When Sapir in contrast high-resolution magnetic resonance imaging brain scans through the two teams, she observed a starkly regular pattern: each of the sufferers determined as owning motor neglect had injury on the putamen, whilst all those who however responded bit by bit to left-side stimuli didn’t. Although the putamen isn’t really broken in Parkinson’s condition, researchers have determined it as being a brain location that processes dopamine, the neurotransmitter that drops to reduced stages in Parkinson’s sufferers. Scientists method even more examine of how other kinds of neglect may possibly be linked to injury to various brain places. for example, Sapir notes that when clinicians give recovering stroke sufferers a straightforward drawing to duplicate, some will depart out the left facet in the drawing, whilst other folks will duplicate objects from throughout the drawing, but depart out the left sides of person objects. irrespective of whether this represents various types of neglect stemming from injury to various brain places is simply not nonetheless distinct. "Another doable type of neglect needs to do with placing a affected person’s very good hand on their terrible facet," Sapir says. "When you do that to some sufferers, their capacity to reply with their very good hand decreases. it is like a postural deficit." Sapir and her colleagues hope to sooner or later produce a battery of checks which will let clinicians to dissociate the various types of neglect and produce new solutions. Sapir A, Kaplan JB, He BJ, Corbetta M. Anatomical correlates of directional hypokinesia in sufferers with hemispatial neglect. The Journal of Neuroscience, April four, 2007.