Use the labels in the right column to find what you want. Or you can go thru them one by one, there are only 34,278 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 neuronsthatDIEeach day because there areNOeffective 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.
New Scientist magazine has this to say about this research:
Giving mice antibiotics can protect them from brain damage caused by stroke. Antibiotics change the make-up of the mice's gut bacteria, which in turn alters the immune cells that travel to the brain and would normally cause inflammation. The treatment appears to reduce cell destruction by around 60 percent.
What is your doctor and hospital doing to ensure human testing gets done? Being incompetent like usual and doing nothing?
Commensal
gut bacteria impact the host immune system and can influence disease
processes in several organs, including the brain. However, it remains
unclear whether the microbiota has an impact on the outcome of acute
brain injury. Here we show that antibiotic-induced alterations in the
intestinal flora reduce ischemic brain injury in mice, an effect
transmissible by fecal transplants. Intestinal dysbiosis alters immune
homeostasis in the small intestine, leading to an increase in regulatory
T cells and a reduction in interleukin (IL)-17–positive γδ T cells
through altered dendritic cell activity. Dysbiosis suppresses
trafficking of effector T cells from the gut to the leptomeninges after
stroke. Additionally, IL-10 and IL-17 are required for the
neuroprotection afforded by intestinal dysbiosis. The findings reveal a
previously unrecognized gut-brain axis and an impact of the intestinal
flora and meningeal IL-17+ γδ T cells on ischemic injury.
This installment of Pipeline Pulse focuses on a single cardiovascular
risk factor, lipoprotein(a), and examines two CV outcomes trials aimed
at reducing CV events through Lp(a) reduction.
Lipoprotein(a), or Lp(a), is produced in the liver and contains two
units connected by a covalent disulfide bond, a small LDL-like component
and a single apolipoprotein(a) molecule. The apo(a) part of Lp(a) is
almost entirely genetically determined, and its highly variable length
is generally inversely proportional to Lp(a) concentration. Lp(a)
increases CV risk through three pathways — atherogenic, inflammatory and
thrombotic — making it a CV triple threat. Copious oxidized
phospholipids augment inflammation, thrombosis and atherogenicity;
apolipoprotein(a)’s homology to plasminogen increases thrombosis; and
the cholesterol content of Lp(a) causes atherosclerosis.
Seth J. Baum
Emerging focus on Lp(a)
We know from many lines of evidence that elevated Lp(a) levels
increase risk for CV events. Epidemiologic, genome-wide association and
Mendelian randomization studies consistently demonstrate this, and
evidence from PCSK9 inhibitor studies lends further support.
Being more than 90% dependent on genetics, Lp(a) levels are typically
highly stable throughout one’s life. Though some conditions, such as
liver disease, hypothyroidism, nephrotic syndrome and hormonal changes
during menopause can impact levels, therapeutic lifestyle changes
cannot. And although some medications, such as the PCSK9 inhibitors and
niacin, can reduce Lp(a) levels up to 30%, none has been given an FDA
indication to do so. In fact, the only currently approved FDA treatment
for Lp(a) is lipoprotein apheresis, specifically in the setting of Lp(a)
> 60 mg/dL and LDL >100 mg/dL and with either documented CAD or
peripheral artery disease. Additionally, although Lp(a) varies
significantly by race/ethnicity, high levels are decidedly prevalent
across all populations, with significantly elevated levels in 20% of
white individuals, 15% of Latin American individuals, 10% of East Asian
individuals, 25% of South Asian individuals and 30% of Black
individuals.
In view of Lp(a)’s high prevalence, genetically disparate risk and
apparent causal role in atherosclerotic CVD, there has been enhanced
focus worldwide on better identifying this risk factor in clinical
practice. In the U.S., Lp(a) has been highlighted in guidelines as a
valuable “risk enhancer,” while in Europe and Canada, guidelines now
mandate universal screening. Along with the recent shift to more broadly
identifying Lp(a) levels, there is now a recognized urgency to better
understand its pathologic attributes and more rapidly identify effective
risk-reducing therapies.
CV outcome trials
Consequently, multiple therapeutics are in early development,
including an oral small molecule and potential gene editing approaches,
but two later-stage drugs are already being studied in large phase 3 CV
outcome trials.
Pelacarsen (Novartis/Ionis), a second-generation antisense
oligonucleotide, is being studied in the HORIZON trial, and olpasiran
(Amgen), a small interfering (or silencing) RNA, is being evaluated in
OCEAN(a)-Outcomes. The studies have some key differences.
HORIZON has two co-primary endpoints, the time to first occurrence of
expanded major adverse CV events (CV death, nonfatal MI, nonfatal
stroke and urgent coronary revascularization requiring hospitalization)
in two populations of patients, those with Lp(a) 70 mg/dL and those
with Lp(a) > 90 mg/dL. The trial first enrolled participants in
December 2019 with the key inclusion criteria for the 8,324 participants
being an Lp(a) > 70 mg/dL (approximately 175 nmol/L), and history of
spontaneous MI or ischemic stroke within 10 years of screening or
symptomatic PAD. The agent is given monthly via subcutaneous injection.
Prior studies using the same dose of pelacarsen produced an
approximately 80% reduction in Lp(a).
OCEAN(a)-Outcomes has as its primary composite endpoint the time to
CHD death, MI, or urgent coronary revascularization, whichever occurs
first. It began enrollment in December 2022 with an ultimate goal of
6,000 participants and the key inclusion criteria being a screening
Lp(a) > 200 nmol/L, a history of ASCVD, defined as either a prior
type 1 MI or prior revascularization with PCI plus at least one
specified risk-enhancing feature. The study drug is administered once
every 12 weeks via subcutaneous injection. Prior studies with the same
dose of olpasiran produced > 95% reduction in Lp(a).
There are a few key distinctions between the studies. HORIZON
included ischemic stroke and PAD as qualifying events, while
OCEAN(a)-Outcomes did not. Stroke is less consistently associated with
elevated Lp(a) than is MI. Still, it is important to understand the
relationship of Lp(a) and stroke and whether reducing Lp(a) effectively
diminishes risk for stroke, and HORIZON will provide these insights.
Similarly, HORIZON will enhance our understanding of Lp(a)’s
relationship to PAD, a high-risk and vastly undertreated condition.
OCEAN(a)-Outcomes, however, did include PCI as a qualifying event.
Evaluating the response to Lp(a) reduction in patients with prior PCI
will potentially greatly broaden the utility of Lp(a) reducing therapies
if the study is positive. On balance, HORZION enrolled higher-risk
patients than did OCEAN(a), but interestingly, HORIZON’s cutpoint for
Lp(a) was lower than OCEAN(a)-Outcome’s, 175 nmol/L vs. 200 nmol/L. So,
from an Lp(a) standpoint, the OCEAN(a)-Outcomes participants are at
somewhat higher risk than HORIZON’s. Regarding endpoints, both studies
included urgent coronary revascularization, CHD death and nonfatal MI,
but HORIZON included nonfatal stroke and OCEAN(a)-Outcomes did not.
Including stroke as an endpoint will not only be informative, but it may
also provide a new therapy to mitigate the risk of this highly
prevalent and often devastating CV event.
Editor’s Note: Information in this article was up to date at the
time of publication. The next installment of Pipeline Pulse will focus
on the Inflation Reduction Act (IRA). In this column, Baum will examine
the potential impact of this legislation on the CVD drug pipeline.
References:
Clinicaltrials.gov. clinicaltrials.gov/ct2/show/NCT04023552. Published July 17, 2019. Accessed April 26, 2023.
Clinicaltrials.gov. clinicaltrials.gov/ct2/show/NCT05581303. Published Oct. 14, 2022. Accessed April 26, 2023.
Grundy SM, et al. Circulation. 2019;doi:10.1161/CIR.0000000000000625.
Tsimikas S, et al. J Am Coll Cardiol. 2018;doi:10.1016/j.jacc.2017.11.014.
For more information:
Seth J. Baum, MD, is chief scientific officer at
Flourish Research and clinical affiliate professor of cardiology at the
Florida Atlantic University Charles E. Schmidt College of Medicine. He
is also a member of the Cardiology Today Editorial Board. Baum can be reached at sjbaum@fpim.org; Twitter: @sethjbaummd.
If we had anything other than fucking failures of stroke associations we would be assured that they would be getting human testing done for all of these to find the best one. Stroke survivors have to guess on what might work and the amounts because the stroke medical world is completely failing at their job.
How the hell do we get stroke researchers to focus on the only reason for stroke research? 100% recovery for all.
The latest here in which nothing will be done because WE HAVE NO STROKE LEADERSHIP.No one in stroke is doing a fucking thing to solve stroke, everyone is just beating around the edges or doing prediction, awareness or compensation crapola.
In a new study, researchers found the traditional psychoactive drug ayahuasca stimulates the growth of new brain cells
in the hippocampi of research mice. The hippocampus is responsible for
many memory functions, and the mice dosed with ayahuasca also performed
better in a battery of memory tests.
While ayahuasca, a hallucinogenic and often purgative tea
brewed from leaves of a shrub that grows in South America, contains the
psychoactive compound N, N-dimethyltryptamine (DMT), it also packs
harmine and tetrahydoharmine, two compounds that form new neurons from
stem cells in a petri dish, per IFL Science.
Ayahuasca is used in spiritual practices across different belief systems, and Healthline explains
that the plant’s naturally occurring DMT—which can produce powerful
hallucinations and visions—works in tandem with another compound that
makes it more “bioavailable.” That means it’s absorbed better by the
body, with less flushed out as waste afterward. Think about how calcium
and vitamin D work together to increase absorption.
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DMT is the secret agent in this research,
literally—besides ayahuasca, DMT is found in a variety of contexts in
humans and animals. Scientists believe DMT’s chemical role is to boost
and trigger certain chemical reactions in the body. And because it
naturally occurs in ayahuasca, too, scientists wonder if this outside
application could work inside the body the same way.
