Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective 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.

Wednesday, September 9, 2020

The neuroplasticity marker PSA-NCAM: Insights into new therapeutic avenues for promoting neuroregeneration

You want neuroplasticity to work for you. So DEMAND YOUR DOCTOR GIVES YOU EXACT PROTOCOLS to do that. Guidelines don't count, if your doctor doesn't know the difference between guidelines and protocols they need to be fired.

The neuroplasticity marker PSA-NCAM: Insights into new therapeutic avenues for promoting neuroregeneration

 

TaranjeetKaurShikhaKalotraGurcharanKaur

Highlights

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PSA-NCAM as a modulator of adult brain plasticity.

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PSA-NCAM in promoting repair/regeneration after nervous system injury.

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PSA as a novel candidate for neurotherapeutics.

Abstract

Neuroplastic alterations are the key processes involved in adaptation and rehabilitation after all neurological injuries and pathologies. Being the central contributor to the developmental and adult neuroplasticity, the polysialylated form of Neural Cell Adhesion Molecule (PSA-NCAM) may prove to be a potential target to facilitate repair/regeneration after CNS injury and disease. Over the years, several experimental approaches have been developed to exploit the therapeutic potential of PSA-NCAM. Broadly, the studies focused on cell-transplantation strategies to alter PSA-NCAM properties at the injury site, injection of peptide based as well as synthetic PSA mimetics directly into the injury site or the application of PSA containing hydrogels and scaffolds as biomaterials. A comprehensive understanding of the PSA-based experimental approaches, as well as their pros and cons, is urgently required for successful implementation of this molecule in therapeutics. The current review, therefore, has been designed to give the readers a thorough account of all the diverse roles of PSA in the adult nervous system and the recent progress that has been made in developing PSA-based therapeutic approaches for neuroregeneration.

Graphical abstract

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Graphical Abstract represents Structure and Function of polysialated NCAM:(A)Schematic structure represents post translation synthesis of polysialic acid(PSA) on the fifth immunoglobin domain of NCAM at two asparagine amino acid residue.This post translational mechanism regulated by two Golgi associated polysialyl transferases:ST8SiaIV(PST)andST8SiaII(STX).(B)represents the underlying molecular pathway activated by polysialated NCAM resulted in regulation of synaptic plasticity, axonal growth, migration, remyelination etc in the cell.

Chemical compounds studied in this article

γ-aminobutyric acid (PubChem CID: 119)
N-methyl-d-aspartate (PubChem CID: 22880)
N-acetylneuraminic acid (PubChem CID: 439197)
5-hydroxytryptamine oxalate (PubChem CID: 9943249)
5-hydroxytryptamine (PubChem CID: 528728)
5‐nonyloxytryptamine oxalate (PubChem CID: 10126593)
6-hydroxydopamine (PubChem CID: 4624)
Phenoxybenzamine (PubChem CID: 4768)
2-deoxy-2,3-dehydro-N-acetylneuraminic acid (PubChem CID: 65309)
6’-sialyllactose (PubChem CID: 643987)
7-chloro-4-(phenylselanyl) quinoline (PubChem CID: 71521341)

Abbreviations

5-NOT
5‐nonyloxytryptamine oxalate
Akt
protein kinase B
Arc
activity-regulated cytoskeleton-associated protein
BDNF
brain-derived neurotrophic factor
CNS
central nervous system
CREB
cAMP-response element binding protein
ELISA
enzyme-linked immunoassay
ERK
extracellular signal-regulated protein kinases
mTOR
mechanistic target of rapamycin
NCAM
neural cell adhesion molecule
NIH
national institutes of health
PNS
peripheral nervous system
PSA
polysialic acid
PST
polysialyltransferases
STX
siayltransferase
TSD
50 % ethanolic extract of Tinospora cordifolia fed sleep deprived
VSD
vehicle-sleep deprived
VUD
vehicle-undisturbed sleep
WSD
ashwagandha water extract fed sleep deprived
WT
wild type

Keywords

PSA-NCAM
Neuroregeneration
PSA-mimetics
PSA-based biomaterials
Neuroplasticity
Learning and memory
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© 2020 Elsevier Ltd. All rights reserved.
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