Use the labels in the right column to find what you want. Or you can go thru them one by one, there are only 34,264 posts. Searching is done in the search box in upper left corner. I blog on anything to do with stroke. DO NOT DO ANYTHING SUGGESTED HERE AS I AM NOT MEDICALLY TRAINED, YOUR DOCTOR IS, LISTEN TO THEM. BUT I BET THEY DON'T KNOW HOW TO GET YOU 100% RECOVERED. I DON'T EITHER BUT HAVE PLENTY OF QUESTIONS FOR YOUR DOCTOR TO ANSWER.
Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of 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.
Showing posts with label spermidine. Show all posts
Showing posts with label spermidine. Show all posts
Thursday, August 27, 2026
Could a Little-Known Nutrient Be the Key to Healthier Immune Aging? by Super Age
How long has your doctor been incompetent?
Wednesday, July 23, 2025
Spermidine: A Predictor for Neurological Outcome and Infarct Size in Focal Cerebral Ischemia?
Did your competent? doctor and hospital DO ANYTHING with this from 2001? NO? So, incompetence reigned! And the board of directors is so incompetent that they allow doing nothing to continue for decades!
Found spermidine this from this article: How to get the anti-ageing benefits of fasting without having to give up eating
Spermidine: A Predictor for Neurological Outcome and Infarct Size in Focal Cerebral Ischemia?
Originally Published 1 January 2001
Th. Els, J. Bruckmann, G. Röhn, M. Daffertshofer, J. Schulte Mönting, R.-I. Ernestus, and M. HennericiAuthor Info & Affiliations
5,52824Abstract
Background and Purpose—Polyamines
are mainly restricted to the intracellular space. During focal cerebral
ischemia, polyamines are released from the intracellular compartment.
Experimental studies have implicated a marked elevation in brain tissue
and blood. The aim of our study was to investigate whether the elevation
of polyamines in the blood of patients with focal cerebral ischemia
correlates with the clinical outcome and the infarct volume.
Methods—Polyamines
were measured in 16 patients with focal cerebral ischemia and in 8
healthy control subjects. Blood samples for polyamine measurement were
taken at admission and at fixed time points for the next 28 days.
Polyamines were analyzed in red blood cells by a high-pressure liquid
chromatography system. Clinical findings were recorded with the NIH
Stroke Scale score. Volume of infarction was analyzed from cranial CT at
admission and on days 4 to 6 after ischemia.
Results—A
significant increase of the spermidine level in the peripheral blood
could be observed in all patients with focal cerebral ischemia as
compared with control subjects (P<0.01), starting with the
admission. Spermidine values correlated positively with the clinical
outcome at several time points in the first 48 hours (r=0.90 to 0.40; P<0.01) and with the infarct volume in cranial CT on days 4 to 6 (r=0.91; P<0.01).
Conclusions—As
hypothesized from experimental data, polyamine levels in blood increase
in patients after focal cerebral ischemia. The results indicate that
the peripheral spermidine level is closely associated with the clinical
outcome as well as with the infarction volume. Therefore, polyamines may
be used as a novel predictor for the prognosis of patients with focal
cerebral ischemia.
The
endogenous polyamines putrescine, spermidine, and spermine are
low-molecular-weight aliphatic amines that are found in high
concentrations in the brain.1 Polyamine metabolism is regulated by the activity of the first key enzyme ornithine decarboxylase (ODC).2
Polyamines are predominantly found intracellularly, whereas only
smaller amounts could be observed in the extracellular space or in the
peripheral blood.3 Animal studies have shown that polyamines play an important role in the ischemic cascade.4 5 Polyamines activate N-methyl-d-aspartate (NMDA) receptors,6 7 8 9 followed by a calcium influx. Other possible mechanisms are calcium-related events at the cell membrane10 11 and release of neurotransmitters from nerve endings.11
However, polyamines have not been determined in clinical studies of
cerebral ischemia, and their clinical significance is thus unknown.
Because
polyamines are released from the intracellular compartment during focal
cerebral ischemia, the aim of our study was to analyze their value as a
marker of neuronal tissue destruction in the peripheral blood and a
potential predictor for clinical outcome in the acute stage of stroke.
Subjects and Methods
Patients
The
polyamine level was determined in 16 patients (6 women and 10 men; mean
age±SD, 70.4±8.3 years) with a first-ever acute focal cerebral ischemia
(<6 hours) of the middle cerebral artery (MCA) as determined by
clinical signs and cranial CT. Adults of any age were included, and
informed consent was obtained according to the Helsinki Declaration of
Ethical Requirements. CT as well as blood samples were part of the
routine workup.
Exclusion criteria were (1)
brain stem or lacunar stroke, (2) a transient neurological deficit with
rapid recovery during workup, (3) a previous ischemia in the same
territory, and (4) primary or secondary cerebral hemorrhage with
preexisting disability.
All patients
underwent a complete cerebrovascular workup, including extracranial and
transcranial Doppler ultrasound, electrocardiography, echocardiography,
and serum investigations for exclusion of coagulation disorders.
An
age-matched healthy group (68.8±15.3, n=8) with no previous
neurological disorder or severe general disease served as control
subjects. The level of polyamines was determined at the same time points
as in the patient group.
More at link.
Tuesday, May 28, 2019
Ragweed compounds could protect nerve cells from Alzheimer’s
You likely will need this.
1. A documented 33% dementia chance post-stroke from an Australian study? May 2012.
2. Then this study came out and seems to have a range from 17-66%. December 2013.
3. A 20% chance in this research. July 2013.
4. Dementia Risk Doubled in Patients Following Stroke September 2018
What is your stroke hospital doing to ensure this is tested out on humans?
Ragweed compounds could protect nerve cells from Alzheimer’s
Source: ACS
As spring arrives in the northern hemisphere, many people are cursing ragweed, a primary culprit in seasonal allergies. But scientists might have discovered a promising new use for some substances produced by the pesky weed. In ACS’ Journal of Natural Products, researchers have identified and characterized ragweed compounds that could help nerve cells survive in the presence of Alzheimer’s disease (AD) peptides.
Those with AD, a neurodegenerative disorder, often have impaired judgment, cognition, memory and behavior. Scientists have linked AD to the accumulation of amyloid-β (Aβ) peptides in the brain, which form plaques that kill nerve cells. Unfortunately, the five drugs currently approved for AD treatment only delay disease progression for a short time. When Won Keun Oh and colleagues screened 300 natural plant extracts for activity against AD in a preliminary study, they found a surprising candidate: Ambrosia artemisiifolia (common ragweed). This invasive weed, native to North America, has now spread to South America, Asia and much of Europe. Oh and colleagues decided to isolate and characterize the structures of ragweed compounds responsible for this neuroprotective activity.

When
Won Keun Oh and colleagues screened 300 natural plant extracts for
activity against AD in a preliminary study, they found a surprising
candidate: Ambrosia artemisiifolia (common ragweed). The image is in the
public domain.
Funding: The authors acknowledge funding from the National Research Foundation of Korea.
About this neuroscience research article
Source:ACS
Media Contacts:
Katie Cottingham – ACS
Image Source:
The image is in the public domain.
Original Research: Closed access
“Eudesmane Glycosides from Ambrosia artemisiifolia (Common Ragweed) as Potential Neuroprotective Agents”. Jin-Pyo An, Thi Kim Quy Ha, Hyun Woo Kim, Byeol Ryu, Jinwoong Kim, Junsoo Park, Chul Ho Lee, and Won Keun Oh.
Journal of Natural Products. doi:10.1021/acs.jnatprod.8b00841
Abstract
Eudesmane Glycosides from Ambrosia artemisiifolia (Common Ragweed) as Potential Neuroprotective Agents
In Alzheimer’s disease, amyloid-β (Aβ) accumulation in the brain results in neuronal cell death and is one of the major causes of dementia. Because the current therapeutic agents are not yet sufficiently effective or safe, there have been attempts to find new neuroprotective chemicals against Aβ-induced cytotoxicity. A 70% EtOH extract of whole plants of Ambrosia artemisiifolia (common ragweed) was selected after the screening of a natural extract library. Seven new eudesmane-type glycosides and seven known compounds were obtained through bioactivity-guided fractionation from the aerial parts of this plant. Their structures were determined on the basis of their nuclear magnetic resonance spectra, high-resolution electrospray ionization mass spectrometry analysis, and electronic circular dichroism calculations. Among them, compounds showed protective effects against Aβ-induced cytotoxicity in Aβ42-transfected HT22 cells. The most active compounds, exhibited moderate protective activity dose-dependently (10, 20, and 40 μM
Monday, October 3, 2016
Keeping your synapses sharp: How spermidine reverses age-related memory decline
If true, how many decades before your doctor finds out about this? And how many decades after that will a stroke protocol be written? I'm betting never. You are fucking screwed along with all future stroke survivors. We have got fucking idiots in charge of stroke.
And look, already 3 years have passed;
Administering Natural Substance Spermidin Stopped Dementia Sept. 2013
http://medicalxpress.com/news/2016-10-synapses-sharp-spermidine-reverses-age-related.html
Synapses, connecting the neurons in our brains, continuously encode new memories, but the ability to form new memories ("learning") diminishes drastically for many of us as we get older.
Just like humans, the fruit fly Drosophila melanogaster - a leading model for aging research - suffers from memory impairment with advancing age. The same team of researchers previously observed that Drosophila exhibits an age-induced decline in levels of spermidine, and that these memory deficits can be suppressed by feeding with a diet supplemented by spermidine. They now describe an unexpected scenario that convincingly explains the suppression of memory deficits by spermidine feeding. In a nutshell, synapses within the Drosophila brain seem to narrow their operational space, and thus become increasingly unable to form new memories with age.
Dietary supplementation with spermidine, however, prevented these changes. Importantly, when the authors mimicked these age-associated changes by genetic means, learning suffered even in young flies, providing a causal link between generic synaptic mechanisms and age-induced memory impairment. This work promises to open up a new avenue when searching for new therapeutic strategies to fight age-associated dementia, a major health threat of our times.
More information: Varun K. Gupta et al, Spermidine Suppresses Age-Associated Memory Impairment by Preventing Adverse Increase of Presynaptic Active Zone Size and Release, PLOS Biology (2016). DOI: 10.1371/journal.pbio.1002563
Monday, September 2, 2013
Administering Natural Substance Spermidin Stopped Dementia
What does your doctor have to say about the similarity of your brain to a fruit fly? What else is your doctor doing to prevent your dementia? ANYTHING AT ALL?
http://www.alphagalileo.org/ViewItem.aspx?ItemId=134030&CultureCode=enScientists from Freie Universität Berlin and the University of Graz Have Shown That Feeding Fruit Flies with Spermidin Suppresses Age-dependent Memory Impairment
Age-induced memory impairment can be suppressed by administration of the natural substance spermidin. This was found in a recent study conducted by Prof. Dr. Stephan Sigrist from Freie Universität Berlin and the Neurocure Cluster of Excellence and Prof. Dr. Frank Madeo from Karl-Franzens-Universität Graz. Both biologists, they were able to show that the endogenous substance spermidine triggers a cellular cleansing process, which is followed by an improvement in the memory performance of older fruit flies. At the molecular level, memory processes in animal organisms such as fruit flies and mice are similar to those in humans. The work by Sigrist and Madeo has potential for developing substances for treating age-related memory impairment. The study was first published in the online version of Nature Neuroscience.
Aggregated proteins are potential candidates for causing age-related dementia. With increasing age, the proteins accumulate in the brains of fruit flies, mice, and humans. In 2009 Madeo’s group in Graz already found that the spermidin molecule has an anti-aging effect by setting off autophagy, a cleaning process at the cellular level. Protein aggregates and other cellular waste are delivered to lysosomes, the digestive apparatus in cells, and degraded.
Feeding the fruit flies spermidin significantly reduced the amount of protein aggregates in their brains, and their memories improved to juvenile levels. This can be measured because flies can learn under classical Pavovian conditioning and adjust their behavior accordingly.
In humans, memory capacity decreases beginnning around the age of 50. This loss accelerates with increasing age. Due to increasing life expectancy, age-related memory impairment is expected to increase drastically. The spermidine concentration increases with age in flies as in humans. If it were possible to delay the onset of age-related dementia by giving individuals spermidin as a food supplement, it would be a great breakthrough for individuals and for society. Patient studies are the next step for Sigrist and Madeo.
NeuroCure is a Cluster of Excellence in the neurosciences at Charité ‑ Universitätsmedizin Berlin working in collaboration with the departments of biology and biochemistry at Freie Universität Berlin and Humboldt-Universität zu Berlin as well as with three independent research institutions.
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