Blood from umbilical cord may help fix your brain after a stroke

You'll have to ask your doctor to find the research that reported this.
https://www.newscientist.com/article/2169547-blood-from-umbilical-cord-may-help-fix-your-brain-after-a-stroke/

By Alice Klein

A healing balm for the brain? Infusions of umbilical cord blood seem to help people recover better after a stroke.

Strokes occur when blood can’t reach brain cells because of a blocked or burst blood vessel, causing them to rapidly starve and die. Joanne Kurtzberg at Duke University, North Carolina, and her colleagues wondered if young blood might help heal brains that have been damaged in this way.

Blood from babies and teenagers has previously been shown to reverse brain ageing in older mice, and there are …

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Aging Research: Plasma Protein Revitalizes the Brain

If they can get it down to a manufactured protein you won't have to get blood transfusions from your grandchildren.
https://directorsblog.nih.gov/2017/04/25/aging-research-plasma-protein-revitalizes-the-brain/

Posted on April 25, 2017 by Dr. Francis Collins

For centuries, people have yearned for an elixir capable of restoring youth to their aging bodies and minds. It sounds like pure fantasy, but, in recent years, researchers have shown that the blood of young mice can exert a regenerative effect when transfused into older animals. Now, one of the NIH-funded teams that brought us those exciting findings has taken an early step toward extending them to humans.
In their latest work published in Nature, the researchers showed that blood plasma collected from the umbilical cords of newborn infants possesses some impressive rejuvenating effects [1]. When the human plasma was infused into the bloodstream of old mice, it produced marked improvements in learning and memory. Additional experiments traced many of those cognitive benefits to a specific protein called TIMP2—an unexpected discovery that could pave the way for the development of brain-boosting drugs to slow the effects of aging.
When babies are born, a teaspoon or so of blood plasma remains in their umbilical cords that often gets discarded as medical waste. For the team led by Joseph Castellano and Tony Wyss-Coray of Stanford University, Palo Alto, CA, that youthful plasma seemed an obvious place to look for human proteins that might rejuvenate the aging brain.
At four-day intervals over the next two weeks, the team infused the human cord plasma into older mice. They wanted to see if it could revitalize the hippocampus, a part of the brain involved in learning and memory, in much the same way that blood from young mice had done in previous experiments [2]. (By the way, the strain of mice used in these studies had compromised immune systems that prevented their bodies from rejecting the human material.)
To help them gauge the effects of the cord plasma, the researchers also infused similar older mice with human plasma from either young adults (aged 19-24) or elderly donors (aged 61-82). The mice that received plasma from the elderly donors showed little change in gene expression. But those given cord and young adult plasma had a boost in the activity of genes that encourage neurons to grow and form new connections for learning.
Where things got real intriguing was that the cord plasma alone specifically increased the activity of genes playing important roles in memory formation. Most notable was an increase in a gene called c-Fos, which is linked to long-term memory storage and declines with age.
But did this interesting genetic profile translate to improved memories and learning? Sure enough, it did.  Mice given the cord plasma outperformed the other mice in a battery of learning and memory tests, and impressively so.
The researchers compiled a long list of human plasma proteins that vary with age and might explain the cord plasma’s rejuvenating power. To narrow it down further, they searched for proteins on the list that shift in mice with age and also when older mice are infused with young mouse blood. That yielded about 30 proteins. At the top of the list was a total surprise called TIMP2. While the protein has been studied in other contexts, next to nothing was known about its role in the aging brain.
Further study confirmed a decline in TIMP2 with age in the hippocampus. The researchers also found that injections of TIMP2 into mice led to improvements in learning and memory similar to those seen with the cord plasma. And when the researchers treated aged mice with cord plasma that had the TIMP2 protein removed, the treatment lost its brain-rejuvenating effects.
These findings help to confirm that proteins naturally present early in life could help to revitalize aged tissue. Based on these latest findings, TIMP2 holds promise for further study and perhaps even therapeutic development. Such a treatment might ultimately benefit people experiencing normal aging, as well as those with neurodegenerative conditions such as Alzheimer’s disease. We need not get too far ahead of ourselves here. But might the elusive elixir of youth that people have long pined for been inside us all along?
References:
[1] Human umbilical cord plasma proteins revitalize hippocampal function in aged mice. Castellano JM, Mosher KI, Abbey RJ, McBride AA, James ML, Berdnik D, Shen JC, Zou B, Xie XS, Tingle M, Hinkson IV, Angst MS, Wyss-Coray T. Nature. 2017 April 19. [Epub ahead of print]
[2] Young blood reverses age-related impairments in cognitive function and synaptic plasticity in mice. Villeda SA, Plambeck KE, Middeldorp J, Castellano JM, Mosher KI, Luo J, Smith LK, Bieri G, Lin K, Berdnik D, Wabl R, Udeochu J, Wheatley EG, Zou B, Simmons DA, Xie XS, Longo FM, Wyss-Coray T. Nat Med. 2014 May 4.
Links:
Cognitive Health and Older Adults (NIA/NIH)
Understanding Memory Loss (National Institute on Aging/NIH)
Wyss-Coray Lab (Stanford University, Palo Alto, CA)
NIH Support: National Institute on Aging

Saneron and Henry Ford Health: Cell Therapy Combo Aids Stroke

This might be difficult for your doctor to acquire the day you have a stroke so you better tell your doctor to stock up.
http://www.newswise.com/articles/saneron-and-henry-ford-health-cell-therapy-combo-aids-stroke
Researchers at the Henry Ford Health System (Detroit, MI) and colleagues at Saneron CCEL Therapeutics, Inc. of Tampa, Florida, have found that when human umbilical cord blood cells (HUCBCs) were transplanted into test rats modeled with stroke, the addition of Simvastatin to the HUCBCs significantly increased the therapeutic benefit of the HUCBCs.
The study was published in a recent issue of Neuroscience (227:223-231)
According to N. Kuzmin-Nichols, Saneron president and COO, the combination treatment, delivered 24 hours after the test animals were subjected to simulated stroke, showed an interactive effect in improving neurological outcome. When compared with monotherapy, the combination therapy increased densities of key blood vessels, arteries, and smooth muscle cells in vascular walls.
“HUCBCs are a source for blood stem cells, endothelial cell precursors, mensenchymal cell progenitors, and other multipotent and pluripotent stem cells,” said Kuzmin-Nichols. “They offer a promising therapy for stroke. However, when HUCBCs are used alone, and injected via a vascular route for brain repair, success has been limited.”
Because the drug Simvastatin has been demonstrated to be a neurorestorative and neuroprotective agent in ischemic brain injury, the research team hypothesized that the combination of therapeutic doses of Simvastatin and HUCBCs would increase the expression of Angiopoietin-1(Ang-1, a protein with important roles in vascular development and blood vessel growth) and its receptor Tie2 (a cell-surface receptor that binds with Ang-1). Both Ang-1 and Tie2 promote vascular stabilization and artery growth and could enhance blood vessel remodeling (angiogenesis) after stroke, said the researchers.
According to the researchers, HUCBCs contain a “ready supply” of neurotrophic and angiogenic factors that induce neurogenesis (neural cell repair) and angiogenesis (blood vessel growth), both of which are critical to promoting neurological recovery post stroke. While transplanted HUCBCs have been found to selectively migrate to the injured brain, past and recent research has discovered that few transplanted HUCBCs express neural cell characteristics, and few find their way to the ischemic region of the brain.
“Our study using subtherapeutic monotherapy doses did not show significant improvement in either vasculogenesis or functional outcome,” said Dr. Jieli Chen of Henry Ford Hospital and the study corresponding author. “However, the combination of HUCBCs and Simvastatin did show an interactive effect with a significant improvement in neurological outcome. The combination also amplified endogenous angiogenesis and arteriogenesis, and enhanced vascular remodeling.”
Their in vitro experiments showed that combination treatment and Ang-1 significantly increased capillary-like tube formation and arterial cell migration while anti-Ang-1 significantly reduced combination treatment-induced tube formation and artery cell migration.
Dr. Chen noted that combination treatment likely increases the signaling between the brain vasculature and parenchymal cells that facilitate the migration of HUCBCs into the injured cerebral tissue. This signaling may be attributed to the increased expression of stromal derived factor (SDF-1) in brain vascular and parenchymal cells and its receptor (CXCR4) in HUCBCs.
The researchers concluded that their findings “indicate that the combination of sub-therapeutic doses of Simvastatin and HUCBCs increases Ang1/Tie2 and thereby enhances vascular remodeling that contribute to improved functional outcome after stroke.”
“Our results in this preclincial study support further exploration of the use of combination therapies - such as those combining Simvastatin and HUCBCs - for stroke treatment,” said Kuzmin-Nichols.
Funding for the study came from grants from the National Institute on Aging, RO1 AG031811,National Institute of Neurological Disorder and Stroke, PO1 NS23393 and 1R41NS064708, and from the American Heart Association, grant 09GRNT2300151.