New Study Discovers Fat-Trapping Green Tea Beads for Safe Weight Loss

 Interesting. Ask your doctor to followup and tell you when approved.

New Study Discovers Fat-Trapping Green Tea Beads for Safe Weight Loss

Host‐Microbial Cometabolite Ursodeoxycholic Acid Protects Against Poststroke Cognitive Impairment

 If your competent? doctor isn't actively researching cognitive impairment fixes; you DON'T have a functioning stroke doctor! Don't know what it is, but it's NOT a doctor! Proof that you don't have a doctor is NO followup with human testing!

cognitive impairment (110 posts to January 2019)

cognitive decline (315 posts to December 2011)

50% cognitive impairment (2 posts to September 2021)

24 to 70% post-stroke cognitive impairment (2 posts to November 2019)

Host‐Microbial Cometabolite Ursodeoxycholic Acid Protects Against Poststroke Cognitive Impairment

Xuxuan Gao, MD https://orcid.org/0009-0007-5558-7012, Feng Zhang, MD, Jiafeng Zhang, MSc, Yu Ma, MSc, Yiting Deng, MD https://orcid.org/0009-0001-4927-6003, Jiaying Chen, MD, Yueran Ren, MD, Huidi Wang, MD, Boxin Zhao, PhD https://orcid.org/0000-0003-3574-0511 zhaobx@smu.edu.cn, Yan He, PhD https://orcid.org/0000-0002-6611-2959 yanhe@smu.edu.cn, and Jia Yin, MD https://orcid.org/0000-0001-8944-6604 yinj@smu.edu.cnAuthor Info & Affiliations

Journal of the American Heart Association

New online

https://doi.org/10.1161/JAHA.124.038862

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Abstract

Background

Poststroke cognitive impairment (PSCI) is a common residual disability after stroke, often underestimated and underdiagnosed. We previously found that ursodeoxycholic acid (UDCA), a host‐microbiota cometabolite, ameliorates brain damage in stroke mice. Based on these findings, we aimed to evaluate the predictive value of UDCA for PSCI risk in a prospective cohort study.

Methods and Results

We recruited 202 patients with mild acute ischemic stroke and 63 patients with symptomatic large‐artery atherosclerotic stenosis as the modeling and external validation cohorts, respectively. Mice were subjected to transient middle cerebral artery occlusion, and cognitive function was assessed using the Morris water maze test. Patients with mild acute ischemic stroke who developed PSCI exhibited significant alterations in gut microbiota and plasma bile acid profiles during the acute stroke phase, including a notable reduction in UDCA level. Through feature selection and machine learning, we constructed a predictive model for PSCI incorporating plasma UDCA level, the relative abundance of Clostridia, Bacilli, and Bacteroides, as well as age, educational level, and the presence of moderate to severe white matter lesions. This model exhibited robust predictive performance in both internal (area under the curve, 0.904 [95% CI, 0.808–1.000]) and external (area under the curve, 0.838 [95% CI, 0.742–0.934]) validations. Animal studies in mice also showed reduced UDCA levels in plasma and brain tissue following stroke. UDCA administration improved cognitive function in stroke mice by reducing hippocampal microglial activation and neuronal apoptosis.

Conclusions

Our findings indicate that UDCA has potential as a biomarker for predicting PSCI risk and plays a neuroprotective role in the progression of PSCI. This suggests that early identification and intervention targeting UDCA could represent a promising strategy for the prevention and treatment of PSCI.

Graphical Abstract

Scientists discover how to 'upload knowledge to your brain'

Maybe you want your doctor to followup and see if your missing movements can be uploaded. In my case I don't know where they would go since I have lots of dead brain. 171 million dead neurons in the first 90 minutes, who knows how much died in the next week. My estimate is another 5.4 billion dead neurons.

Scientists discover how to 'upload knowledge to your brain'

01:5704:56

• Mark Molloy

1 March 2016 • 7:45pm

Feeding knowledge directly into your brain, just like in sci-fi classic The Matrix, could soon take as much effort as falling asleep, scientists believe.
Researchers claim to have developed a simulator which can feed information directly into a person’s brain and teach them new skills in a shorter amount of time, comparing it to “life imitating art”.
They believe it could be the first steps in developing advanced software that will make Matrix-style instant learning a reality.

In the neo-noir sci-fi classic, protagonist Neo is able to learn kung fu in seconds after the martial art is ‘uploaded’ straight to his brain.

Glutathione in Brain: Overview of Its Conformations, Functions, Biochemical Characteristics, Quantitation and Potential Therapeutic Role in Brain Disorders

You just might want your doctor and hospital to contact researchers to follow this up with human testing for the improvement of cognitive decline possibility. Up to you, YOUR HOSPITAL WILL DO NOTHING WITHOUT YOUR PRODDING. 

Glutathione in Brain: Overview of Its Conformations, Functions, Biochemical Characteristics, Quantitation and Potential Therapeutic Role in Brain Disorders

Dwivedi D¹,

Megha K¹,

Mishra R¹,

Mandal PK¹

Author information

Neurochemical Research, 14 Apr 2020,
DOI: 10.1007/s11064-020-03030-1 PMID: 32297027 

Review

Abstract 

---

Glutathione (GSH) is an important antioxidant found abundantly and synthesized intracellularly in the cytosol in a tightly regulated fashion. It has diverse physiological functions, including protection against reactive oxygen species and nitrogen species, antioxidant defense as well as maintenance of cellular thiol status. The human brain due to the high oxygen consumption is extremely susceptible to the generation of reactive oxygen species. GSH plays a paramount role in brain antioxidant defense, maintaining redox homeostasis. The depletion of brain GSH has also been observed from both autopsies as well as in vivo MRS studies with aging and varied neurological disorders (Alzheimer's disease, Parkinson's disease, etc.). Therefore, GSH enrichment using supplementation is a promising avenue in the therapeutic development for these neurological disorders. This review will enrich the information on the importance of GSH synthesis, metabolism, functions, compartmentation and inter-organ transport, structural conformations and its quantitation via different techniques. The transportation of GSH in the brain via different interventional routes and its potential role in the development of therapeutic strategies for various brain disorders is also addressed. Very recent study found significant improvement of behavioral deficits including cognitive decline, depressive-like behaviors, in APP (NL-G-F/NL-G-FG-) mice due to oral GSH administration. This animal model study put an emergent need to complete GSH supplementation trial in MCI and AD patients for cognitive improvement as proposed earlier.

Intermittent fasting increases adult hippocampal neurogenesis

Now you need your doctors and hospital to initiate human research in this and specify how these newly created neurons will migrate to needed areas.  

Maybe these might help:

• Interkinetic nuclear migration (1)
• migration (41)
• transendothelial migration (1)

Intermittent fasting increases adult hippocampal neurogenesis

Sang‐Ha Baik, ¹ Vismitha Rajeev, ¹ David Yang‐Wei Fann, ¹ Dong‐Gyu Jo, ² and Thiruma V. Arumugam ^{1 , 2 , 3}

Author information Article notes Copyright and License information Disclaimer

Associated Data

Data Availability Statement

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Abstract

Introduction

Intermittent fasting (IF) has been suggested to have neuroprotective effects through the activation of multiple signaling pathways. Rodents fasted intermittently exhibit enhanced hippocampal neurogenesis and long‐term potentiation (LTP) at hippocampal synapses compared with sedentary animals fed an ad libitum (AL) diet. However, the underlying mechanisms have not been studied. In this study, we evaluated the mechanistic gap in understanding IF‐induced neurogenesis.

Methods

We evaluated the impact of 3 months of IF (12, 16, and 24 hr of food deprivation on a daily basis) on hippocampal neurogenesis in C57BL/6NTac mice using immunoblot analysis.

Results

Three‐month IF significantly increased activation of the Notch signaling pathway (Notch 1, NICD1, and HES5), neurotrophic factor BDNF, and downstream cellular transcription factor, cAMP response element‐binding protein (p‐CREB). The expression of postsynaptic marker, PSD95, and neuronal stem cell marker, Nestin, was also increased in the hippocampus in response to 3‐month IF.

Conclusions

These findings suggest that IF may increase hippocampal neurogenesis involving the Notch 1 pathway.

Keywords: brain‐derived neurotrophic factor, hippocampus, intermittent fasting, neurogenesis, Notch

Go to:

Abstract

Intermittent fasting (IF) is a dietary protocol where energy restriction is induced by alternate periods of ad libitum feeding and fasting. The present study has sought to investigate the relationship between IF and hippocampal neurogenesis. Our findings suggest that IF may increase hippocampal neurogenesis involving the Notch 1 pathway.

Go to:

1. INTRODUCTION

Dietary restriction (DR) is defined as a decrease in energy consumption without reducing nutritional value. This simple dietary intervention has been shown in a wide range of experimental animals to extend lifespan and decrease the incidence of several age‐related diseases. The definition of DR has been expanded from an alternative description of caloric restriction (CR) to also encompass a broader scope of interventions, including short‐term starvation, periodic fasting, fasting‐mimetic diets, and intermittent fasting (IF; Mattson & Arumugam, 2018). IF has been proven to be advantageous to various organ systems in the body and acts as a mild metabolic stressor. It has been postulated that IF is able to cause powerful changes in the metabolic pathways in the brain via an increase in stress resistance, and breakdown of ketogenic amino acids and fatty acids (Bruce‐Keller, Umberger, McFall, & Mattson, 1999; Kim et al., 2018). Experimental studies have also shown that IF is neuroprotective against acute brain injuries such as stroke, and neurodegenerative diseases (Arumugam et al., 2010; Halagappa et al., 2007; Manzanero et al., 2014). In addition, recent studies have also shown that IF can lead to an increase in neurogenesis levels in the hippocampus (Manzanero et al., 2014).

In the adult brain, the niches of neuronal stem cells (NSCs) are located specifically at the subventricular zone (SVZ) of the lateral ventricles, and in the subgranular zone (SGZ) of the hippocampus. The ability of NSCs to maintain cerebral neurogenesis is controlled by the tight regulation of balanced events commencing from stem cell maintenance, to stem cell division and proliferation, to its differentiation into mature neurons, and finally their survival and functional integration into the brain parenchyma (Lathia, Mattson, & Cheng, 2008; Lledo, Alonso, & Grubb, 2006). The process of adult neurogenesis is highly regulated and is adaptable to environmental, morphological, and physiological cues, whereby cerebral performance is suited to function at optimal levels for a given environment. Studies have demonstrated that the proliferation of neural stem cells can be modified through metabolic perturbations experienced during high temperatures (Matsuzaki et al., 2009), physical activity (Niwa et al., 2016), and a high‐fat diet (Kokoeva, Yin, & Flier, 2005). Experimental studies from our group have also shown that IF increases neurogenesis in the hippocampus as a form of neuroprotection following acute brain injury such as ischemic stroke. Moreover, we established that the number of BrdU‐labeled cells in the dentate gyrus of IF mice was elevated (Manzanero et al., 2014). To measure cell proliferation without the confound availability of an exogenous marker BrdU, we established increases in the number of Ki67‐labeled cells in the dentate gyrus of mice on the IF diet, indicating enhancement of cell proliferation in these mice (Manzanero et al., 2014). In addition to our findings, previous work similarly demonstrated that using the every other day (EOD) IF regimen also increased BrdU‐labeled cell number in the hippocampus (Lee, Duan, & Mattson, 2002).

However, the molecular process involved in IF‐induced neurogenesis is not well understood. The Notch signaling pathway that is intricately involved in the determination of cell fate during brain development and adult neurogenesis may be a possible molecular process involved in IF‐induced neurogenesis (Lathia et al., 2008). In this study, we investigated the expression levels of molecular and cellular components of the hippocampal region, focusing specifically on Notch activation and associated proteins that are known to promote hippocampal neurogenesis such as brain‐derived neurotrophic factor (BDNF) and cAMP response element‐binding protein (CREB).

More at link.

Facilitation of Auditory Comprehension After Theta Burst Stimulation of Wernicke's Area in Stroke Patients: A Pilot Study

Since the effect is transitory you will need to have your doctor and stroke hospital followup with researchers to ensure research on how to make this permanent is done.

Facilitation of Auditory Comprehension After Theta Burst Stimulation of Wernicke's Area in Stroke Patients: A Pilot Study

Viviana Versace^1,2*, Kerstin Schwenker^3,4, Patrick B. Langthaler³, Stefan Golaszewski^3,4, Luca Sebastianelli^1,2, Francesco Brigo^5,6, Elke Pucks-Faes⁷, Leopold Saltuari^2,7 and Raffaele Nardone^3,4,5

• ¹Department of Neurorehabilitation, Hopsital of Vipiteno-Sterzing, Vipiteno-Sterzing, Italy
• ²Research Unit for Neurorehabilitation of South Tyrol, Bolzano, Italy
• ³Department of Neurology, Christian Doppler Klinik, Paracelsus Medical University, Salzburg, Austria
• ⁴Karl Landsteiner Institut für Neurorehabilitation und Raumfahrtneurologie, Salzburg, Austria
• ⁵Department of Neurology, Franz Tappeiner Hospital, Merano, Italy
• ⁶Department of Neuroscience, Biomedicine and Movement Science, University of Verona, Verona, Italy
• ⁷Department of Neurology, Hochzirl Hospital, Zirl, Austria

Introduction: 

Single-pulse transcranial magnetic stimulation (TMS) and high-frequency repetitive TMS (rTMS) over Wernicke's area were found to facilitate language functions in right-handed healthy subjects. We aimed at investigating the effects of excitatory rTMS, given as intermittent theta burst stimulation (iTBS) over left Wernicke's area, on auditory comprehension in patients suffering from fluent aphasia after stroke of the left temporal lobe.

Methods: 

We studied 13 patients with chronic fluent aphasia after an ischemic stroke involving Wernicke's area. iTBS was applied in random order to Wernicke's area, the right-hemisphere homologous of Wernicke's area, and the primary visual cortex. Auditory comprehension was blind assessed using the Token test before (T0), 5 (T1), and 40 min (T2) after a single session of iTBS.

Results: 

At the first evaluation (T1) after iTBS on left Wernike's area, but not on the contralateral homologous area nor on the primary visual cortex, the scores on the Token test were significantly increased. No significant effects were observed at T2.

Conclusion: 

We demonstrated that a single session of excitatory iTBS over Wernicke's area was safe and led to a transient facilitation of auditory comprehension in chronic stroke patients with lesions in the same area. Further studies are needed to establish whether TBS-induced modulation can be enhanced and transformed into longer-lasting effects by means of repeated TBS sessions and by combining TBS with speech and language therapy.

Researchers successfully reverse Alzheimer's disease in mouse model

Did your doctor followup on this with researchers to get this tested in humans? If not, incompetence reigns in your stroke hospital, beginning at the top with the stroke president and board of directors. Have them all fired.  Only 20 months old.

Researchers successfully reverse Alzheimer's disease in mouse model

by Rockefeller University Press

The brain of a 10-month-old mouse with Alzheimer's disease (left) is full of amyloid plaques (red) surrounded by activated microglial cells (green). But these hallmarks of Alzheimer's disease are reversed in animals that have gradually lost the BACE1 enzyme (right). Credit: Hu et al., 2018

A team of researchers from the Cleveland Clinic Lerner Research Institute have found that gradually depleting an enzyme called BACE1 completely reverses the formation of amyloid plaques in the brains of mice with Alzheimer's disease, thereby improving the animals' cognitive function. The study, which will be published February 14 in the Journal of Experimental Medicine, raises hopes that drugs targeting this enzyme will be able to successfully treat Alzheimer's disease in humans.

One of the earliest events in Alzheimer's disease is an abnormal buildup of beta-amyloid peptide, which can form large, amyloid plaques in the brain and disrupt the function of neuronal synapses. Also known as beta-secretase, BACE1 helps produce beta-amyloid peptide by cleaving amyloid precursor protein (APP). Drugs that inhibit BACE1 are therefore being developed as potential Alzheimer's disease treatments but, because BACE1 controls many important processes by cleaving proteins other than APP, these drugs could have serious side effects.
Mice completely lacking BACE1 suffer severe neurodevelopmental defects. To investigate whether inhibiting BACE1 in adults might be less harmful, Riqiang Yan and colleagues generated mice that gradually lose this enzyme as they grow older. These mice developed normally and appeared to remain perfectly healthy over time.
The researchers then bred these rodents with mice that start to develop amyloid plaques and Alzheimer's disease when they are 75 days old. The resulting offspring also formed plaques at this age, even though their BACE1 levels were approximately 50% lower than normal. Remarkably, however, the plaques began to disappear as the mice continued to age and lose BACE1 activity, until, at 10 months old, the mice had no plaques in their brains at all.
"To our knowledge, this is the first observation of such a dramatic reversal of amyloid deposition in any study of Alzheimer's disease mouse models," says Yan, who will be moving to become chair of the department of neuroscience at the University of Connecticut this spring.
Decreasing BACE1 activity also resulted in lower beta-amyloid peptide levels and reversed other hallmarks of Alzheimer's disease, such as the activation of microglial cells and the formation of abnormal neuronal processes.
Loss of BACE1 also improved the learning and memory of mice with Alzheimer's disease. However, when the researchers made electrophysiological recordings of neurons from these animals, they found that depletion of BACE1 only partially restored synaptic function, suggesting that BACE1 may be required for optimal synaptic activity and cognition.
"Our study provides genetic evidence that preformed amyloid deposition can be completely reversed after sequential and increased deletion of BACE1 in the adult," says Yan. "Our data show that BACE1 inhibitors have the potential to treat Alzheimer's disease patients without unwanted toxicity. Future studies should develop strategies to minimize the synaptic impairments arising from significant inhibition of BACE1 to achieve maximal and optimal benefits for Alzheimer's patients."

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Explore further

PET tracer gauges effectiveness of promising Alzheimer's treatment

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More information: Hu et al., 2018. J. Exp. Med. DOI: 10.1084/jem.20171831

Journal information: Journal of Experimental Medicine

Provided by Rockefeller University Press

Pharmacological Enhancement of Stroke Rehabilitation

Just when the fuck will your stroke doctor and hospital help get this research to the level of an interventional drug? It has already been tested in primates here. 

Stroke Recovery Drug Found Effective In Rewiring Brains Of Mice And Monkeys  April 2018

 NEVER? They are that fucking lazy AND incompetent?

You may want your doctor to ensure human testing followup is done. 

Pharmacological Enhancement of Stroke Rehabilitation

Sphenopalatine Ganglion Stimulation to Augment Cerebral Blood Flow

The takeaway from this is that your doctor and hospital have the responsibility  to followup, contact researchers and get further trials done. No followup, contact the board of directors and have those doctors, directors and president responsible fired.  Why not do this for all stroke patients? Better cerebral blood flow would probably save more of the penumbra from dying.

Sphenopalatine Ganglion Stimulation to Augment Cerebral Blood Flow

A Randomized, Sham-Controlled Trial

Natan M. Bornstein

,

Jeffrey L. Saver

,

Hans-Christoph Diener

,

Philip B. Gorelick

,

Ashfaq Shuaib

,

Yoram Solberg

,

Thomas Devlin

,

Thomas Leung

,

Carlos A. Molina

, … Show all Authors

and The ImpACT-24A Investigators include the Site Principal Investigators, DSMB members, and the Site Co-Investigators listed

Originally publishedhttps://doi.org/10.1161/STROKEAHA.118.024582Stroke. ;0

Abstract

Background and Purpose—

Many patients with acute ischemic stroke are not eligible for thrombolysis or mechanical reperfusion therapies due to contraindications, inaccessible vascular occlusions, late presentation, or large infarct core. Sphenopalatine ganglion (SPG) stimulation to enhance collateral flow and stabilize the blood-brain barrier offers an alternative, potentially more widely deliverable, therapy.

Methods—

In a randomized, sham-controlled, double-masked trial at 41 centers in 7 countries, patients with anterior circulation ischemic stroke not treated with reperfusion therapies within 24 hours of onset were randomly allocated to active SPG stimulation or sham control. The primary efficacy outcome was improvement beyond expectations on the modified Rankin Scale of global disability at 90 days (sliding dichotomy), assessed in the modified intention-to-treat population. The initial planned sample size was 660 patients, but the trial was stopped early when technical improvements in device placement occurred, so that analysis of accumulated experience could be conducted to inform a successor trial.

Results—

Among 303 enrolled patients, 253 received at least one active SPG or sham stimulation, constituting the modified intention-to-treat population (153 SPG stimulation and 100 sham control). Age was median 73 years (interquartile range, 64–79), 52.6% were female, deficit severity on the National Institutes of Health Stroke Scale was median 11 (interquartile range, 9–15), and time from last known well median 18.6 hours (interquartile range, 14.5–22.5). For the primary outcome, improved 3-month disability beyond expectations, rates in the SPG versus sham treatment groups were 49.7% versus 40.0%; odds ratio, 1.48 (95% CI, 0.89–2.47); P=0.13. A significant treatment interaction with stroke location (cortical versus noncortical) was noted, P=0.04. In the 87 patients with confirmed cortical involvement, rates of improvement beyond expectations were 50.0% versus 27.0%; odds ratio, 2.70 (95% CI, 1.08–6.73); P=0.03. Similar response patterns were observed for all prespecified secondary efficacy outcomes. No differences in mortality or serious adverse event safety end points were observed.

Conclusions—

SPG stimulation within 24 hours of onset is safe in acute ischemic stroke. SPG stimulation was not shown to statistically significantly improve 3-month disability above expectations, though favorable outcomes were nominally higher with SPG stimulation. Beneficial effects may distinctively be conferred in patients with confirmed cortical involvement. The results of this study need to be confirmed in a larger pivotal study.

Clinical Trial Registration—

URL: https://www.clinicaltrials.gov. Unique identifier: NCT03767192.

Blood test may predict cardiovascular disease

You can tell the competency of your doctor and hospital if they do nothing to ensure further research is done. Hope you are ok with such incompetency. I bet they did nothing with these earlier posts and of course our fucking failures of stroke associations did nothing either.

• elevated troponin (2 posts from Nov. 2018)
• troponin T (1 post from June 2013) 

 

 

Blood test may predict cardiovascular disease

Healthline/Medical News Today | May 01, 2019

Advertisement

New research suggests that a simple blood test, which doctors currently use to diagnose heart attacks, may be useful in predicting the risk of cardiovascular disease.
According to the latest statistics from the American Heart Association (AHA), almost half of the people living in the United States have some form of cardiovascular disease. In fact, according to 2016 figures, 121.5 million US adults, or 48% of the entire population, have cardiovascular disease (CVD), which is a cluster of conditions that includes hypertension. Doctors often call hypertension the "silent killer" because it does not show any visible symptoms until it is too late.
The same AHA report predicts that by 2035, over 130 million adults will have a form of CVD that could bring costs in the United States to 1.1 trillion dollars. Currently, heart disease is the leading cause of death in the United States, while stroke is the fifth.
But what if there was a blood test that could accurately predict whether a person will have heart disease or a stroke? New research suggests that such a test may already exist. By detecting the blood levels of specific proteins that heart muscles release when they are injured, scientists may be able to predict a person's risk of eventually developing CVD.
Dr. Christie Ballantyne, who is the cardiology chief at Baylor College of Medicine in Houston, TX, and his team, detail this idea in a new study that appears in the AHA journal Circulation.

Troponin levels can predict CVD risk

Troponins are proteins that signal heart muscle damage, and in the new research, Dr. Ballantyne and his colleagues wanted to see if detecting troponin in the blood of healthy middle-aged adults or seniors could predict CVD risk.
Dr. Ballantyne and colleagues analyzed a group of 8,121 people aged 54–74 who participated in the "Atherosclerosis Risk in Communities" study. None of the participants had a history of cardiovascular disease. The scientists identified troponin levels in 85% of the participants and applied Cox proportional hazards models to examine the links between these levels and cardiovascular disease. Namely, they studied correlations with coronary heart disease, myocardial infarction, ischemic stroke, atherosclerotic cardiovascular disease, heart failure hospitalization, global cardiovascular disease, and all-cause mortality.

• See Also: Study questions long-term heart benefits of tight blood sugar control

The research found that high levels of troponin correlated strongly with "increased global CVD incidence in the general population independent of traditional risk factors." High-sensitivity troponin tests, therefore, proved to be an accurate way of predicting CVD risk, especially when combined with a standard method of calculating a person's 10-year cardiovascular risk.
"What we're finding out is that these tests can be used in the general population to give us information as to who is most likely to have a future problem, whether it be a heart attack, stroke, or heart failure," says Dr. Ballantyne. "If you can treat someone much earlier, before [they] have symptoms, you will be far more effective in preventing events," continues the researcher, who adds, "Our major problem is that we do too little, too late."

"If the first time you find out that you're at risk for heart failure is when you actually start getting short of breath and you end up in the hospital, you probably have advanced heart disease already, and it is going to be harder to treat than if that person took steps years earlier."
—Dr. Ballantyne

Instead, knowing the risk in advance can prompt people to take preventive measures, such as exercising more and watching their blood pressure. However, the scientists explain that although doctors currently use troponin tests to diagnose a heart attack, they do not yet accept them as a tool for predicting risk. Scientists need to do more research before using these tests to evaluate risk.
"Research in this area is leading us toward individualized care more and more, so we can better predict who's at risk for developing adverse cardiovascular outcomes," comments Dr. Rebecca Vigen, an assistant professor of internal medicine at the University of Texas Southwestern Medical Center in Dallas, who did not participate in the research. "This study is a step in the direction of personalizing care," Dr. Vigen says.

• See Also: Intensive glucose control in patients with type 2 diabetes — 15-year follow-up

Read the full article on Healthline/Medical News Today

With grit and gratitude, stroke survivor plays on

Recovery should not require grit. Your doctor should have all the skills and stroke protocols that get you 100% recovered. Starting with stoppingthe 5 causes of the neuronal cascade of death in the first week. This is what is wrong with stroke, the doctor has NO responsibility for getting you recovered, everything is put on your shoulders with NO PROTOCOLS to guide you.  If your doctor assumed responsibility every survivor that didn't get recovered would have an analysis as to why and a plan developed to solve that for next time. But that isn't what occurs. My opinion is that this is massive incompetence on the part of any part of the stroke medical world that doesn't do followup and initiate research to solve stroke. The status quo is a complete failure.

Not getting you 100% recovered is failure on your doctor and stroke hospitals part.

 

With grit and gratitude, stroke survivor plays on

By American Heart Association News

Stroke survivor Dave Kim at the Red Cross Gala in San Francisco. (Photo courtesy of Dave Kim)

Dave Kim can hardly remember a time he wasn't making music. He plays three instruments – most notably the electric violin – and has performed at countless weddings and in concerts around the world, opening for such acts as Hootie and the Blowfish.
So after having a stroke in August 2016 at age 42, he called upon his music training to help him recover.
While in intensive care, Kim used what strength he had to focus, not on the proper notes or certain chords or harmonies, but on his right thumb. He willed that thumb to move. On Day Five, it did.
Then came research, including the discovery that the way musicians' brains were formatted could help aid stroke recovery.
"When communication cuts off from the brain to the limbs," he said, "the brain finds other ways to communicate with the limbs." That ability is called neuroplasticity. Reading about it gave Kim impetus to work on each finger, each arm, each leg.
"I found that everything I've done in my life is therapy," he said.

Dave Kim recuperates in the hospital after his stroke. (Photo courtesy of Dave Kim)

Kim had his stroke while recording a music video in his California home. While playing, his right arm gave way. Then his right leg went limp. He was able to call a doctor friend. A neighbor drove him to the hospital. Kim's blood pressure was measured at a dangerous 230/130. An MRI showed a blood clot in the brain.
The stroke left him unable to stand, much less play his beloved instruments. He felt trapped in his body and, he said, "buried alive." He feared being in the hospital forever and nobody remembering him.
But when Kim shared his plight on social media, dozens and dozens of fans and friends came to visit. They posted well wishes. Their support overwhelmed his spirits.
"I do matter," Kim realized.
Longtime friend Will O'Brien said that when he visited Kim in the hospital, he could sense a change. Not in the obvious physical way, but more deeply. The stroke, he said, gave Kim "a new lease on life. It was one of those tragic events he turned into a true blessing."
After leaving the hospital, Kim spent three weeks in rehab, working to regain the ability to walk, to play music, to do everyday tasks often taken for granted. He also learned about strokes – which he, like many people, thought only happen to the elderly.
Looking back, he sees signs that pointed the way to his stroke. Each of his parents had had one. He was overweight and not eating a healthy diet. He didn't exercise. His cholesterol level and his blood pressure were high. And while he cherished time with his two young sons, raising them as a single parent was stressful.

Dave Kim, with his sons Brandon (left) and Christian, before his stroke. (Photo courtesy of Dave Kim)

Kim is now on medications that have helped lower his blood pressure and reduce his cholesterol. He's eating better. He's lost weight and has a lot more energy. And he's changed for the better in another way, too, because of something he gleaned while at the hospital: Acceptance.
"Once I had acceptance, I kind of had some gratitude," he said. "I've had a tremendous life."
When something tragic happens to people, O'Brien said, it brings out their true character. They ask, "Who am I at the core?" And, "Is this a chance to be a victim or to bring a message of positivity?"
Kim chose positivity.
He now uses his experience and his talent to help others in such ways as speaking out on stroke awareness. And though he made his name by recording popular music, his life mission now is to inspire people through mindful and meditative music.
"For sure I've learned about myself," he said. "I just have a lot of grit, a lot of gratitude, and confidence to believe in myself."
Stories From the Heart chronicles the inspiring journeys of heart disease and stroke survivors, caregivers and advocates.
If you have questions or comments about this story, please email editor@heart.org.

Neural stem cells harvested from live brains by antibody-conjugated magnetic nanoparticles

Well, now for some followup from your doctor, your stroke hospital, your

fucking failures of stroke associations.  I have billions of neurons needed. But nothing will occur since we have NO STROKE LEADERSHIP to ask them to followup and execute the stroke strategy.  This might be the only way I ever fully recover.

Neural stem cells harvested from live brains by antibody-conjugated magnetic nanoparticles

Lui CN¹, Tsui YP, Ho AS, Shum DK, Chan YS, Wu CT, Li HW, Tsang SC, Yung KK.

Author information

Abstract

It stems from the magnetism: The extraction of stem/progenitor cells from the brain of live animals is possible using antibodies conjugated to magnetic nanoparticles (Ab-MNPs). The Ab-MNPs are introduced to a rat's brain with a superfine micro-syringe. The stem cells attach to the Ab-MNPs and are magnetically isolated and removed. They can develop into neurospheres and differentiate into different types of cells outside the subject body. The rat remains alive and healthy.

Copyright © 2013 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.

KEYWORDS:

antibodies; magnetic nanoparticles; nanoparticles; regenerative medicine; stem cells

PMID:

24108547

DOI:

10.1002/anie.201305482

[Indexed for MEDLINE]

Blood test may predict cardiovascular disease

You can tell the competency of your doctor and hospital if they do nothing to ensure further research is done. Hope you are ok with such incompetency. I bet they did nothing with these earlier posts and of course our fucking failures of stroke associations did nothing either.

• elevated troponin (1post from Nov. 2018)
• troponin T (1 post from June 2013) 

 

Blood test may predict cardiovascular disease

Healthline/Medical News Today | May 01, 2019

New research suggests that a simple blood test, which doctors currently use to diagnose heart attacks, may be useful in predicting the risk of cardiovascular disease.

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According to the latest statistics from the American Heart Association (AHA), almost half of the people living in the United States have some form of cardiovascular disease. In fact, according to 2016 figures, 121.5 million
US adults, or 48% of the entire population, have cardiovascular disease (CVD), which is a cluster of conditions that includes hypertension. Doctors often call hypertension the "silent killer" because it does not show any visible symptoms until it is too late. The same AHA report predicts that by 2035, over 130 million adults will have a form of CVD that could bring costs in the United States to 1.1 trillion dollars. Currently, heart disease is the leading cause of death in the United States, while stroke is the fifth.
But what if there was a blood test that could accurately predict whether a person will have heart disease or a stroke? New research suggests that such a test may already exist. By detecting the blood levels of specific proteins that heart muscles release when they are injured, scientists may be able to predict a person's risk of eventually developing CVD.

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Dr. Christie Ballantyne, who is the cardiology chief at Baylor College of Medicine in Houston, TX, and his team, detail this idea in a new study that appears in the AHA journal Circulation.

Troponin levels can predict CVD risk

Troponins are proteins that signal heart muscle damage, and in the new research, Dr. Ballantyne and his colleagues wanted to see if detecting troponin in the blood of healthy middle-aged adults or seniors could predict CVD risk.
Dr. Ballantyne and colleagues analyzed a group of 8,121 people aged 54–74 who participated in the "Atherosclerosis Risk in Communities" study. None of the participants had a history of cardiovascular disease. The scientists identified troponin levels in 85% of the participants and applied Cox proportional hazards models to examine the links between these levels and cardiovascular disease. Namely, they studied correlations with coronary heart disease, myocardial infarction, ischemic stroke, atherosclerotic cardiovascular disease, heart failure hospitalization, global cardiovascular disease, and all-cause mortality.
The research found that high levels of troponin correlated strongly with "increased global CVD incidence in the general population independent of traditional risk factors." High-sensitivity troponin tests, therefore, proved to be an accurate way of predicting CVD risk, especially when combined with a standard method of calculating a person's 10-year cardiovascular risk.
"What we're finding out is that these tests can be used in the general population to give us information as to who is most likely to have a future problem, whether it be a heart attack, stroke, or heart failure," says Dr. Ballantyne. "If you can treat someone much earlier, before [they] have symptoms, you will be far more effective in preventing events," continues the researcher, who adds, "Our major problem is that we do too little, too late."

"If the first time you find out that you're at risk for heart failure is when you actually start getting short of breath and you end up in the hospital, you probably have advanced heart disease already, and it is going to be harder to treat than if that person took steps years earlier."
—Dr. Ballantyne

Instead, knowing the risk in advance can prompt people to take preventive measures, such as exercising more and watching their blood pressure. However, the scientists explain that although doctors currently use troponin tests to diagnose a heart attack, they do not yet accept them as a tool for predicting risk. Scientists need to do more research before using these tests to evaluate risk.
"Research in this area is leading us toward individualized care more and more, so we can better predict who's at risk for developing adverse cardiovascular outcomes," comments Dr. Rebecca Vigen, an assistant professor of internal medicine at the University of Texas Southwestern Medical Center in Dallas, who did not participate in the research. "This study is a step in the direction of personalizing care," Dr. Vigen says.

• See Also: Common oral infections in childhood may increase the risk of atherosclerosis in adulthood

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One Day There May Be a Drug to Turbocharge the Brain. Who Should Get It?

Ask your doctor and stroke hospital to followup and see how close to regular use this is. Survivors should be able to benefit. 

One Day There May Be a Drug to Turbocharge the Brain. Who Should Get It?

By Carl Zimmer

• April 2, 2019

In 2011, Dr. Dena Dubal was hired by the University of California, San Francisco, as an assistant professor of neurology. She set up a new lab with one chief goal: to understand a mysterious hormone called Klotho.

Dr. Dubal wondered if it might be the key to finding effective treatments for dementia and other disorders of the aging brain. At the time, scientists only knew enough about Klotho to be fascinated by it.

Mice bred to make extra Klotho lived 30 percent longer, for instance. But scientists also had found Klotho in the brain, and so Dr. Dubal launched experiments to see whether it had any effect on how mice learn and remember.

The results were startling. In one study, she and her colleagues found that extra Klotho protects mice with symptoms of Alzheimer’s disease from cognitive decline. “Their thinking, in every way that we could measure them, was preserved,” said Dr. Dubal.

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She and her colleagues also bred healthy mice to make extra Klotho. They did better than their fellow rodents on learning mazes and other cognitive tests.

Klotho didn’t just protect their brains, the researchers concluded — it enhanced them. Experiments on more mice turned up similar results.

“I just couldn’t believe it — was it true, or was it just a false positive?” Dr. Dubal recalled. “But here it is. It enhances of cognition even in a young mouse. It makes them smarter.”

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Five years have passed since Dr. Dubal and her colleagues began publishing these extraordinary results. Other researchers have discovered tantalizing findings of their own, suggesting that Klotho may protect against other neurological disorders, including multiple sclerosis and Parkinson’s disease.

Now Dr. Dubal and other researchers are trying to build treatments based on these results. Either by injecting Klotho into the body or by stimulating the brain to make more of the hormone, they hope to treat diseases like Alzheimer’s.

The researchers developing these treatments readily acknowledge that they may fail. And other Klotho experts think there’s a huge amount of work left to do first to figure out how Klotho affects the brain.

“You’ve got all of this amazing stuff showing a really major impact, but we can’t really explain why,” said Gwendalyn D. King, a neuroscientist at the University of Alabama at Birmingham. “That’s where we’re stuck.”

But what happens if scientists get unstuck? What if a drug that enhances cognition really were possible?

Eric Juengst, the director of the University of North Carolina Center for Bioethics, has been thinking about these questions for two decades — back when such drugs were little more than thought experiments.

We tend to think of drugs that enhance performance — say, sports doping — as bad. Drugs that cure or prevent diseases are good. “The scientific community and the public all draw that line,” said Dr. Juengst.

When it comes to Klotho, there may be no such line. In theory, such a drug might offer both a way to prevent diseases of the brain and to enhance it.

Recent research is giving these questions a sudden urgency, according to Dr. Juengst.

“It’s exciting for someone who’s been doing armchair work on this for a long time to see it happening in the real world,” he said. “But it also makes it all the more pressing that this conversation get started in earnest.”

The rest is behind the NYTimes paywall unless it is one of the free articles you can get. 

Flashing Light, Sound Restore Memory in Alzheimer's Mice

Is your stroke hospital and doctors going to do one damn thing to see this gets tested in humans? Or will they sit with their heads up their asses sucking on their thumbs waiting for SOMEONE ELSE TO SOLVE THE PROBLEM? 

 

Flashing Light, Sound Restore Memory in Alzheimer's Mice Flashing Light, Sound Restore Memory in Alzheimer's Mice

 

An innovative light and sound stimulation therapy reduced the number of amyloid plaques found in the brains of laboratory mice with Alzheimer's disease, improving memory and cognitive function. Could an hour of light and sound a day keep Alzheimer's at bay in people?
Alzheimer's disease is a type of degenerative brain disease that causes memory loss and language problems. Over 5.8 million Americans are currently living with Alzheimer's disease, including one in 10 people age 65 or older, according to the Alzheimer's Association.
The disease is caused by the buildup of two proteins in the brain—amyloid beta and tau—that clump together to form plaques or neurofibrillary tangles that impair memory function.
The research was published March 14 in Cell.
The noninvasive treatment induces brain waves called gamma oscillations.
Alzheimer's patients have impairments in gamma-frequency oscillations. Although the exact function of these oscillations, which range from 25-90 hertz, is unknown, it's believed to contribute to attention perception and memory in the brain.
In 2016, Li-Huei Tsai, director of MIT's Picower Institute for Learning and Memory, and her team exposed laboratory mice that genetically predisposed to Alzheimer's disease to a light flickering at 40 hertz for one hour a day. They found that this treatment reduced the levels of tau and amyloid beta in visual cortex of the brain and stimulated the activity of debris-clearing immune cells.
For the current study, Tsai and her team sought to improve on these results. By adding sound stimuli, they hoped the treatment would be able to reach other brain regions.
They played a 40-hertz tone one hour a day for seven hours for laboratory mice predisposed to Alzheimer's disease. At the conclusion of the study, the mice had dramatically lowered levels of beta amyloid in the auditory cortex, which process sound, and the brain's memory center, the hippocampus.
The treated mice also displayed improvements in cognition when navigating a maze that required them to remember key landmarks.
Next, the researchers administered both light and sound together. This had an even greater effect than either one given alone. Amyloid plaques reduced throughout a greater part of the brain, including teh prefrontal cortex, where higher cognitive functions take place.
Preliminary safety tests for this type of brain stimulation have already been performed in healthy human subjects, although more research is needed to determine if the treatment will work in people with Alzheimer's disease.
"As our intervention is completely non-invasive, there is minimal safety concerns. We still need to conduct human trials to determine if this is effective," Tsai said.