Deans' stroke musings

Changing stroke rehab and research worldwide now.Time is Brain!Just think of all the trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 493 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It's quite disgusting that this information is not available from every stroke association and doctors group.
My back ground story is here:

Sunday, February 26, 2017

Peptide regulation of cofilin activity in the CNS: A novel therapeutic approach for treatment of multiple neurological disorders

Sounds pretty good. You will need to hire your own researcher to follow this up and see where is might be useful for humans.


Cofilin is a ubiquitous protein which cooperates with many other actin-binding proteins in regulating actin dynamics. Cofilin has essential functions in nervous system development including neuritogenesis, neurite elongation, growth cone pathfinding, dendritic spine formation, and the regulation of neurotransmission and spine function, components of synaptic plasticity essential for learning and memory. Cofilin's phosphoregulation is a downstream target of many transmembrane signaling processes, and its misregulation in neurons has been linked in rodent models to many different neurodegenerative and neurological disorders including Alzheimer disease (AD), aggression due to neonatal isolation, autism, manic/bipolar disorder, and sleep deprivation. Cognitive and behavioral deficits of these rodent models have been largely abrogated by modulation of cofilin activity using viral-mediated, genetic, and/or small molecule or peptide therapeutic approaches. Neuropathic pain in rats from sciatic nerve compression has also been reduced by modulating the cofilin pathway within neurons of the dorsal root ganglia. Neuroinflammation, which occurs following cerebral ischemia/reperfusion, but which also accompanies many other neurodegenerative syndromes, is markedly reduced by peptides targeting specific chemokine receptors, which also modulate cofilin activity. Thus, peptide therapeutics offer potential for cost-effective treatment of a wide variety of neurological disorders. Here we discuss some recent results from rodent models using therapeutic peptides with a surprising ability to cross the rodent blood brain barrier and alter cofilin activity in brain. We also offer suggestions as to how neuronal-specific cofilin regulation might be achieved.


  • , β-amyloid peptide produced from amyloid precursor protein in AD;
  • AD, Alzheimer disease;
  • ADF, actin depolymerizing factor;
  • AMPA, α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid;
  • APP, amyloid precursor protein;
  • APPsw, human APP with Swedish mutation;
  • Arp2/3 complex, actin-related proteins 2/3 complex;
  • CCR2 and CCR5, G-protein coupled chemokine receptors;
  • CIN, chronophin, a cofilin phosphatase (aka pyridoxal-5′-phosphate phosphatase);
  • CNS, central nervous system;
  • CPP, cell penetrating peptide;
  • CTD, C-terminal domain;
  • DAPTA, d-ala peptide T-amide (d-ala-STTTNYT-amide);
  • DOCK, dedicator of cytokinesis;
  • DS, Down syndrome;
  • F-actin, filamentous actin;
  • G-actin, globular actin (monomeric);
  • HIV, human immunodeficiency virus;
  • LIMK, a cofilin kinase with a LIM domain;
  • LTD, long-term depression;
  • LTP, long-term potentiation;
  • nArgBP2, neural Abelson-related gene-binding protein 2, product of the Sorbs2 gene NLG1: neuroligin 1;
  • NMDA, N-methyl-d-aspartate;
  • NOX, NADPH oxidase;
  • Pak, p21-activated kinase;
  • PDZ, a structural domain first identified in the proteins PSD-95, Dlg1 and ZO-1;
  • PKCα, protein kinase C alpha;
  • PP2B, protein phosphatase 2B (aka calcineurin);
  • PrPC, cellular prion protein;
  • PS12, presenilin 1 with M146L and L286V mutations;
  • PS1ΔE9, human presenilin 1 missing exon 9;
  • pS3 peptide, the S3 peptide phosphorylated on serine 3;
  • RanBP9, Ran binding protein 9;
  • RAP-310, an all D-amino acid version of DAPTA;
  • ROCK, Rho kinase;
  • ROS, reactive oxygen species;
  • S3 peptide, The N-terminal 16 amino acids of mammalian cofilin;
  • Shank3, SH3 and multiple Ankyrin repeat domains 3, also known as ProSAP2;
  • SPAR, spine-associated Rap GTPase-activating protein;
  • Srv2, named for suppressor of RAS2-val19 allele 2. Also known as cyclase associated protein (CAP or Srv2/CAP);
  • SSH, slingshot phosphatase;
  • TAT, transactivator of transcription from the human immunodeficiency virus;
  • Tβ4, thymosin β4;
  • Tpm, tropomyosin;
  • WAVE1, Wiskott-Aldrich Syndrome protein-family verprolin homologous protein 1


  • Dendritic spines;
  • Cofilin phosphoregulation;
  • Cognitive disorders;
  • Psychiatric disorders;
  • Neuropathic pain;
  • Sleep deprivation;
  • Rodent models
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Corresponding author at: Department of Biochemistry and Molecular Biology, Colorado State University, Fort Collins, CO 80523-1870, United States.

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