Showing posts with label doctor question. Show all posts
Showing posts with label doctor question. Show all posts
Tuesday, July 28, 2026
Friday, July 17, 2026
Scientists expected one result from alcohol and Alzheimer’s—they found another
I couldn't tell if this was a good thing or not and there is no point in asking a doctor.
Scientists expected one result from alcohol and Alzheimer’s—they found another
Alcohol may not affect the Alzheimer’s-damaged brain in one single way—instead, its impact appears to depend on which type of brain change is already present, according to new research from Texas A&M University.
The findings complicate the widely held assumption that alcohol simply worsens Alzheimer’s-related decline across the board. Instead, the study found that alcohol interacted with two of the disease’s hallmark features—amyloid-beta plaques and tau tangles—in opposite ways.
Two Proteins, Two Different Reactions
Alzheimer’s disease is marked by two main types of abnormal protein buildup in the brain: amyloid-beta, which forms sticky plaques between brain cells, and tau, which forms tangles inside them. Scientists have long studied both, but rarely examined how alcohol interacts with each separately.
The research team set out to do exactly that. They focused on the corticostriatal circuit, a brain pathway that helps control decision-making and behavioral flexibility—the ability to adjust behavior when circumstances change. This function is often impaired in both addiction and Alzheimer’s disease.
Using animal models representing amyloid-beta pathology and tau pathology separately, the researchers tracked how chronic alcohol exposure changed communication within this circuit.
An Unexpected Reversal
Scientists initially expected alcohol to push each model further in the direction its existing pathology was already headed. Amyloid-beta pathology is typically linked to abnormal increases in brain cell activity, while tau pathology is usually linked to reduced communication between cells. The researchers therefore predicted alcohol would increase circuit activity in the amyloid-beta model and decrease it in the tau model.
Instead, they found the opposite. In animals with amyloid-beta pathology, alcohol reduced communication in the corticostriatal circuit. In animals with tau pathology, alcohol increased it. The same substance produced reversed effects depending on which type of pathology was present.
“The key point for non-experts is not that our study proves alcohol causes Alzheimer’s disease,” the researchers told Newsweek, in a joint statement. “Rather, it suggests that alcohol can meaningfully affect vulnerable brain circuits, and that those effects depend on which Alzheimer’s-related changes are already present. People who are concerned about their brain health or Alzheimer’s risk may wish to be cautious about alcohol and follow their doctor’s advice.
(This will be your doctor's advice; NO thinking required!
Safest level of alcohol consumption is none, worldwide study shows)
“More broadly, our findings raise new questions about how alcohol, Alzheimer’s-related brain changes, and the brain’s immune responses influence one another—and how alcohol might shape brain-circuit function and the progression of the disease.”
Why It Matters
The findings add to growing evidence that Alzheimer’s disease is not one uniform condition. Differences in disease stage, the specific pathology involved, genetics and lifestyle factors may all shape how a person’s brain responds to outside influences such as alcohol.
That distinction could eventually matter for how doctors think about risk. A blanket warning about alcohol and dementia may be too simple, the researchers suggest, if the underlying brain pathology changes how alcohol acts on neural circuits in the first place.
Dr. Amy Swift, psychiatrist and deputy chief medical officer at Silver Hill Hospital, told Newsweek: “Integrating these nuanced insights into clinical decision-making may be particularly valuable for patients who continue to struggle with alcohol use after receiving a diagnosis of Alzheimer’s disease and related dementia. As our understanding of the underlying mechanisms evolves, treatment approaches should likewise adapt to reflect these biological and phenotypic differences, ultimately supporting more individualized, evidence-informed patient care.”
Reference
Huang, Y., Xie, X., Huang, Z., Gangal, H., Chen, R., Wang, X., Li, J., Wang, J. (2026). Chronic alcohol exposure produces pathology-dependent corticostriatal circuit remodeling in Aβ- and tau-based mouse models of Alzheimer’s disease. Neuropharmacology. Chronic alcohol exposure produces pathology-dependent corticostriatal circuit remodeling in Aβ- and tau-based mouse models of Alzheimer’s disease – ScienceDirect
Contact Newsweek editors on this story: Kara Dolman and Emma Lee-Sang
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Sunday, July 12, 2026
Mental tasks induce common modulations of oscillations in cortex and spinal cord
Ask your competent? doctor if this creates the proper waves and oscillations for these interventions. Your doctor better know of all of these and the answer IF COMPETENT AT ALL!
- alpha oscillations
(3 posts to December 2019)
- beta oscillations
(2 posts to August 2021)
- brain oscillation
(4 posts to September 2021)
- gamma oscillations
(27 posts to May 2012)
- Low-frequency oscillations
(4 posts to June 2018)
- neural oscillations
(1 post to November 2013)
- sleep oscillations
(1 post to January 2025)
- theta oscillations
(1 post to September 2024)
- beta waves
(1 post to October 2015)
- brain waves
(31 posts to May 2012)
- electrical waves
(1 post to December 2024)
- gamma waves
(4 posts to November 2017)
- theta waves
(1 post to December 2017)
Mental tasks induce common modulations of oscillations in cortex and spinal cord
Abstract
Background
Spike trains from spinal motor neurons contain low-frequency components that modulate muscle force, and higher-frequency components (above 10 Hz) that do not. The functional role of these higher-frequency components in motor control is still debated. We investigated whether mental tasks that modulate the power of cortical oscillations produce corresponding modulations in spinal motor neuron activity above 10 Hz without affecting force output. Such coupling would indicate that some higher-frequency components are not merely arising as a byproduct of force generation nor indirectly contributing to motor control, but simply reflect cortical oscillations propagating to spinal motor neurons. If voluntary power modulations of these higher-frequency oscillations do not affect force output, they could potentially serve as control signals for neural interface applications such as movement augmentation or motor neuroprostheses.
Methods
We recruited 15 human participants and recorded high-density electromyography signals (HD-EMG) from the tibialis anterior muscle, as well as electroencephalography (EEG) signals. The cumulative spike train (CST) was computed from the activity of spinal motor neurons decoded from HD-EMG signals. The participants performed sustained dorsiflexion concurrent with foot motor imagery, hand motor imagery, mental arithmetic, or no specific mental task. We analysed the bandpower correlation between EEG and CST signals as well as evaluated the task discriminability of CST bandpower signals with a linear classifier.
Results
At the intra-muscular coherence peak, we found statistically significant power correlations between CST and EEG in two separate analyses: first, when correlating across individual trials regardless of the mental task, and second, when correlating across the four mental tasks (Kendall’s coefficient , respectively; mean ± std. dev.). To evaluate the potential of the CST as a control signal, we classified the mental tasks based on CST bandpower and obtained classification accuracies slightly but significantly above chance level (; chance level = 25%).
Conclusion
These results show that mental tasks can simultaneously modulate the power of cortical and spinal oscillations. This supports the notion that cortical oscillations not contributing to ongoing force control can propagate to the spinal level. We further demonstrate that mental tasks can be classified from CST bandpower, but classification performance is limited by the low signal-to-noise ratio.
Thursday, July 9, 2026
Researchers Discover Biological Mechanism Behind Exercise and Healthier Aging Muscles
More reasons for your competent? doctor to have EXACT 100% RECOVERY PROTOCOLS! You don't want sarcopenia or muscle atrophy to occur.
Ask your doctor if 'Exercise-in-a-pill' (9 posts to May 2017) will also produce this benefit.
Researchers Discover Biological Mechanism Behind Exercise and Healthier Aging Muscles
And another article here:
Scientists discover why exercise reverses muscle aging
Wednesday, June 17, 2026
New exoskeleton therapy could redefine how stroke survivors relearn to walk
So, you've proven all these others aren't worth trying?
Ask your doctor which of these walking exoskeletons will get you 100% recovered, meaning walking without the exoskeleton.
There are many more exoskeletons out there. Which ones has your hospital tested?
Maybe these?
5-Link model based gait trajectory adaption control strategies of the gait rehabilitation exoskeleton for post-stroke patients August 2020
A Control Framework of Lower Extremity Rehabilitation Exoskeleton based on Neuro-Muscular-Skeletal Model.pdf August 2020
Passive-elastic knee-ankle exoskeleton reduces the metabolic cost of walking July 2020
Effects of a wearable exoskeleton stride management assist system (SMA®) on spatiotemporal gait characteristics in individuals after stroke: a randomized controlled trial June 2020
The H2 robotic exoskeleton for gait rehabilitation after stroke: early findings from a clinical study May 2020
Gait training early after stroke with a new exoskeleton--the hybrid assistive limb: a study of safety and feasibility April 2020
Gait training early after stroke with a new exoskeleton--the hybrid assistive limb: a study of safety and feasibility January 2020
I gave up listing them all, it is your doctor's job to know this.
Your doctor can analyze the intersection of these multiple sets of data.
No knowledge of ALL OF THESE IS COMPLETE FUCKING INCOMPETENCE!
LOPES was first written up in Sept. 2007.
LOPES researchers hope to get the device into rehabilitation clinics by early 2012, with a mid-2012 target for introduction into the market. Is it available and does your hospital know about it? Have they been following this for the past 13 years? Or are they completely incompetent? But then it doesn't seem to work that well.
The latest here:
New exoskeleton therapy could redefine how stroke survivors relearn to walk
First-of-its-kind intervention improved range of motion and muscle activation
- Link to: Northwestern Now Story
- Study used lower-limb exoskeletons to facilitate therapist-patient interactions while performing functional tasks
- Therapist’s and stroke survivor’s exoskeletons were virtually connected at the hips and knees
- Patients reported high levels of motivation and enjoyment from new therapy
EVANSTON, Ill. — Physical therapists have long walked alongside stroke survivors during recovery. Now, they are walking with them.
Scientists at Northwestern University and Shirley Ryan AbilityLab have developed a first-of-its-kind rehabilitation system that virtually connects therapists and patients through robotic exoskeletons. The real-time connection allows therapists to respond to a patient’s movements, continuously adapting support and assistance as the patient’s performance evolves.
Tuesday, June 16, 2026
Popular Joint Supplement Tied to Faster AD Progression - Glucosamine
FYI. Ask your doctors what this means. They have had 11 years to figure this out. How incompetent are they to have done nothing in 11 years?
glucosamine (4 posts to March 2015)
This research comes to a different conclusion than the latest one below so ask your doctor for EXACTNESS! Maybe age 60 is the cutoff point
The latest here:
Popular Joint Supplement Tied to Faster AD Progression
Glucosamine, a popular joint-pain supplement, may worsen outcomes in people with mild cognitive impairment (MCI), and a newly identified metabolic pathway involving excessive protein glycosylation could help explain why, new research suggests.
In a large electronic health record analysis, glucosamine use was associated with a 25% higher likelihood of progression from MCI to dementia over 5 years. Experiments in human brain tissue and mouse models suggested that excessive protein glycosylation may contribute to Alzheimer’s disease (AD) progression and that glucosamine supplementation could exacerbate the process by fueling glycan production.
Although preliminary, researchers said the findings point to glycan metabolism as a possible therapeutic target and raise questions about the safety of glucosamine use among patients with established dementia.
“In the United States, there are about 7 million people living with Alzheimer’s and millions more with related dementias such as Lewy body or frontotemporal dementia. A lot of these people actively take an over-the-counter supplement that could be making their disease progression worse,” senior investigator Ramon Sun, PhD, director of the Center for Advanced Spatial Biomolecule Research and associate director for innovation at the McKnight Brain Institute at the University of Florida, Gainesville, Florida, said in a statement.
The study was published online on June 9 in Nature Metabolism.
Friday, May 29, 2026
Scientists Develop Enhanced Vitamin K Compound That May Help Repair Brain Damage
Ask your competent? doctor how to eat healthy if on warfarin and can't consume Vitamin K foods. You do want good cognition and no inflammation, right? That requires a diet protocol and I bet your incompetent doctor doesn't have one for you! Is your doctor also FUCKING INCOMPETENT in not getting human testing going?
Scientists Develop Enhanced Vitamin K Compound That May Help Repair Brain Damage
Wednesday, May 27, 2026
Dopamine Cell Replacement Therapy: A New Frontier in Parkinson Disease Treatment
Ask your competent? doctor if you should be getting this NOW, as a preventative to your Parkinsons' risk post stroke!
Parkinson’s Disease May Have Link to Stroke March 2017
The latest here:
Dopamine Cell Replacement Therapy: A New Frontier in Parkinson Disease Treatment
Dopaminergic cell replacement therapy is re-emerging as an investigational strategy for Parkinson disease (PD), supported by a growing number of early-phase clinical trials reporting favorable preliminary safety findings and early motor improvements.1
Evolution of Dopamine Cell Replacement in PD
Early efforts to replace dopaminergic neurons in PD began in the 1980s, but were limited by several challenges.1
“Initial human fetal ventral mesencephalon cell transplantation showed some encouraging results with graft survival and striatal dopamine synthesis,” said Jacob Yomtoob, MD, a movement disorders fellow at Northwestern Feinberg School of Medicine in Chicago, Illinois, and co-author of a 2026 review describing cell therapies and other advanced therapeutics in PD.2
When [pluripotent stem cell] technology became accessible, it was almost a no-brainer to develop strategies to derive dopaminergic neurons in the lab with a plan to eventually implant them in the brain.
“However, concerns arose about variable efficacy and graft-induced dyskinesias, and there were also significant supply concerns regarding sourcing fetal stem cells,” Dr Yomtoob continued.
More recently, the open-label TransEuro trial failed to show improvement in the primary outcome – the Movement Disorder Society Unified Parkinson’s Disease Rating Scale (MDS-UPDRS) Part III OFF score – at 36 months among patients with PD who were treated with human fetal ventral mesencephalic transplantation.3
Those results “largely confirmed the limitations and highlighted the need for alternative pluripotent stem cell sources informed by decades of laboratory studies and in-human trials,” Dr Yomtoob noted.
Together, these limitations have driven a shift toward stem cell-based strategies as a more scalable and standardized approach to dopaminergic replacement.
With advances in cell technology, it is now feasible to generate dopaminergic progenitor cells from sources such as human embryonic stem cells (hESCs), induced pluripotent stem cells (iPSCs), and parthenogenetic stem cells (hpSCs), Dr Yomtoob explained.2
“When [pluripotent stem cell] technology became accessible, it was almost a no-brainer to develop strategies to derive dopaminergic neurons in the lab with a plan to eventually implant them in the brain,” said Viviane Tabar, MD, chair of the department of neurosurgery and the Theresa Feng Chair in Neurosurgical Oncology at Memorial Sloan Kettering Cancer Center in New York, New York.
Dr Tabar cited multiple advantages of pluripotent stem cells (PSCs) compared with fetal stem cells. “They can be expanded on a large scale, and they can be directed to differentiate into very specific neuron types,” she said.1 “Importantly, it was possible to direct differentiation of PSC into authentic midbrain neurons with no serotonergic neuron contamination.”
Serotonergic neurons may have been the cause of dyskinesia in those earlier trials of fetal tissue grafts in PD, Dr Tabar noted.
Among other benefits, PSC-derived products “can be subjected to rigorous quality assurance testing to make sure they have the correct phenotype and are devoid of unwanted contaminants,” Dr Tabar added.1
Building on this preclinical and translational rationale, several early-phase clinical trials have now begun evaluating PSC–derived dopaminergic progenitors in patients with PD.
Recent Early-Phase Trials
In an open-label phase 1 clinical trial (ClinicalTrials.gov Identifier: NCT04802733) published in Nature in May 2025, Dr Tabar and colleagues assessed the safety and tolerability of bilateral putaminal transplantation of a cryopreserved, off-the-shelf hESC-derived dopaminergic neuron progenitor cell product (bemdaneprocel) in 12 patients with PD. Participants were sequentially enrolled in low-dose and high-dose cohorts.4
The trial met its primary endpoints of safety and tolerability at 12 months, and no cases of graft-induced dyskinesia were observed. In addition, no adverse events (AEs) related to the cell product were reported.
Dr Tabar noted that, at 18 months, the data showed continued safety and “no serious adverse events, including no dyskinesias and no tumor formation.”
Among the trial’s secondary endpoints, the MDS-UPDRS Part III OFF scores demonstrated a mean improvement of 8.6 points in the low-dose cohort and 23.0 points in the high-dose cohort. This change is “consistent with a moderate and large ‘clinically important difference’ in motor score,” the authors wrote.4
Additional clinical evidence is emerging from parallel phase 1 and 2 studies using alternative pluripotent stem cell-derived products and manufacturing approaches.
In an open-label dose-escalation phase 1/2a trial (ClinicalTrials.gov Identifier: NCT05887466) published in Cell in December 2025, investigators in Korea evaluated the safety and exploratory efficacy of bilateral putaminal transplantation of freshly cultured hESC-derived dopaminergic progenitors (A9 subtype) among 12 patients with PD. This trial also included a low-dose and a high-dose cohort.5
The study met its primary endpoints at 12 months, with no observed dose-limiting toxicities or graft-related AEs. Exploratory outcomes showed greater MDS-UPDRS Part III OFF score improvements in the high-dose group compared with the low-dose group (15.5 vs 12.7), along with improvements in activities of daily living, motor function, and quality of life.5
Further, a phase 1/2 trial in Japan evaluated bilateral putaminal transplantation of freshly cultured iPSC-derived dopaminergic progenitor cells in 7 patients with PD. The study reported no serious adverse events or graft overgrowth, with mean improvements of 9.5 points in MDS-UPDRS Part III OFF scores and 4.3 points in ON scores.6
Currently, a phase 1 multisite, open-label trial (ClinicalTrials.gov Identifier: NCT06687837)is evaluating autologous iPSC-derived dopaminergic progenitor cells in 12 patients with PD in the United States.7 Xenos Mason, MD, a co-principal investigator on the study and neurologist at Keck Medicine at the University of Southern California in Los Angeles, explained that his team is “conducting studies using neuroimaging and wearable sensors to understand, for example, how stem cells integrate into brain circuits.” Dr Mason added that these methods may elucidate “how the presence of these cells and the dopamine that they produce modifies the intrinsic neurophysiology and the pathophysiology of different forms of [PD].”
Future Directions
As early clinical data continue to accumulate, attention is now shifting toward larger confirmatory trials and longer-term outcome assessment.
The future trajectory of dopamine cell replacement therapy in PD will become more defined in the coming years as larger trials continue to test this approach, according to Dr Tabar.
In addition to ongoing early-phase studies, a phase 3 randomized sham surgery-controlled trial (ClinicalTrials.gov Identifier: NCT06944522) of bemdaneprocel is being conducted at Memorial Sloan Kettering Cancer Center and other sites.
“With more patients receiving the treatment, we expect to learn a lot more about the profile of those who benefit the most, so the indications will become more refined with growing input from patients and their neurologists,” Dr Tabar stated.
While the optimal timing for dopamine cell replacement therapy in the course of PD remains to be determined, Dr Mason suggested some possibilities: “If we think of stem cells as analogous to other procedural therapies for PD, it may be best to use them when medications start to lose efficacy, which tends to occur 3 to 10 years into the course of the disease.”
“However, it may be that stem cells offer a very safe and durable symptomatic improvement, in which case it may be most appropriate to offer the therapy earlier – perhaps soon after diagnostic confirmation,” Dr Mason continued.
According to Dr Yomtoob, dopamine cell replacement therapies in PD will initially be compared with deep brain stimulation (DBS) and magnetic resonance imaging-guided focused ultrasound. “Time will tell if cell therapies have proven benefits over DBS – such as potential for slowing or delaying disease progression and no need for an implanted device or battery replacement – that overcome downsides such as the need for immunosuppression with most dopamine cell therapies, a lack of adjustability over time, and the risk [for] graft-induced side effects.”
Along with long-term safety and efficacy and identification of the optimal patient population, additional questions to be resolved in ongoing research include the optimal dopaminergic progenitor cell source, the need for immunosuppression, and the role of these therapies in the PD treatment landscape, Dr Yomtoob said.
Dr Tabar and other scientists are continuing to explore ideas regarding future versions of cell products, including “development of a better specified dopaminergic neuron subtype, methods to improve graft survival, variations on where exactly in the brain the cells should be grafted, the design of better devices for delivery of the cells, and the possibility of combining cell therapy with novel small molecules or other approaches such as genetically modified cells that impact disease progression or are more resistant to the disease,” she explained.
“Importantly, the success of cell therapy in PD will open the door for similar strategies for other CNS disorders,” Dr Tabar said.
Sunday, May 17, 2026
Paradigm Change Coming in Secondary Stroke Prevention: OCEANIC-STROKE
What is your competent? doctors current secondary stroke prevention? Will this replace the current protocol? Or don't you even have a protocol?
Paradigm Change Coming in Secondary Stroke Prevention: OCEANIC-STROKE
This transcript has been edited for clarity.
Dear colleagues, I am Christoph Diener, from the Faculty of Medicine at the University of Duisburg-Essen. In this month's video, I would like to concentrate on new developments in secondary stroke prevention, in particular, the OCEANIC-STROKE trial.
From Aspirin to Factor Xa Inhibitors
Until about 20 years ago, for secondary stroke prevention, we only had aspirin, which was not terribly effective. Then it turned out that we had much more effective drugs in stroke prevention in people with atrial fibrillation. On one side, dabigatran, and on the other side, the factor Xa inhibitors, for example, apixaban, rivaroxaban, and edoxaban.
The big difference was that stroke prevention in atrial fibrillation with aspirin had a risk reduction of about 15%, but with new anticoagulants, we had risk reductions compared to placebo of 60%-70%. New anticoagulants were more effective, but they also had bleeding, so there is a need to develop new antithrombotic drugs that have lower bleeding risk and similar efficacy.
Suggested for you
This is why factor XI came into play. There are people who have a genetic disorder and they have no factor XI. Clinically, they have a reduced risk of ischemic stroke and myocardial infarction, and they have only a very small increase in the risk of bleeding, particularly in the urogenital tract and oropharyngeal tract if they have to undergo surgery.
Factor XIa Inhibitors
This is why factor XIa inhibitors were developed. There are small molecules, and I will talk today about asundexian, and there are monoclonal antibodies against factor XI, and one of them is abelacimab.
Let me start with asundexian. The first trial was done in atrial fibrillation. The OCEANIC-AF study compared asundexian with apixaban. This trial was terminated prematurely because the drug was inferior to apixaban and had a similar bleeding risk.
The next approach was to study this drug in secondary stroke prevention in people without cardioembolic strokes, and also in people who have high-risk transient ischemic attack (TIA). This is the OCEANIC-STROKE trial. This trial used asundexian as a factor XIa inhibitor, and following a dose-finding study, the final dose was selected. This was a placebo-controlled, international trial, and asundexian was given on top of antiplatelet therapy, which was initially the combination of aspirin and clopidogrel followed by long-term aspirin.
The primary endpoint was ischemic stroke — recurrent ischemic stroke in people who had a stroke or first ischemic stroke in people who had a high-risk TIA. The primary safety endpoint was International Society on Thrombosis and Haemostasis (ISTH) major bleeding. The key inclusion criteria were non-cardioembolic strokes and a history of atherosclerosis, either by imaging, ultrasound, or they could have a non-lacunar stroke on imaging; and they had to have antiplatelet therapy.
This trial had 6150 patients who received asundexian 50 mg once daily compared to placebo, and they were followed between 3 and 31 months. At baseline, they were on average 67 years old, about one-third were females, they had typical risk factors like diabetes and hypertension, and 25% were current smokers. The index event in the majority: 95% was an ischemic stroke.
If we look at the cumulative incidence of ischemic stroke, there was a clear benefit of asundexian 50 mg compared to placebo, with a hazard ratio of 0.74, which translates into a 25% risk reduction, which was highly significant. The study was also positive for all the secondary outcomes. For example, all strokes or cardiovascular deaths or all-cause mortality, myocardial infarction, and stroke, and so on.
Very importantly, in terms of safety, there were no differences in ISTH major bleeding events and there were also no statistically significant differences in the other bleeding events. The cumulative incidence of major bleeding had a hazard ratio of 1.10, which was not statistically significant. The benefit of this drug was shown in all subgroups.
Ladies and gentlemen, this is a major step forward. For the first time in 50 years, we have a new drug, which is superior to aspirin or the initial antiplatelet therapy with clopidogrel and aspirin, and has no increased bleeding risk. This will change clinical practice.
AF vs Stroke Results
Now, you will ask, why was this drug not effective in people with atrial fibrillation? Why was it effective in people with atherosclerosis and ischemic stroke and high-risk TIA? We don't know, but there is a difference, obviously, compared with the monoclonal antibody abelacimab because abelacimab was effective in people with atrial fibrillation compared to rivaroxaban — not in terms of efficacy, but it had a significantly lower bleeding risk. This monoclonal antibody at present will undergo a study with secondary stroke prevention.
Dear colleagues, ladies and gentlemen, our clinical practice will change once asundexian is approved. In future, this patient group who has ischemic stroke or high-risk TIA and has non-cardioembolic stroke and has atherosclerosis somewhere in the body will clearly benefit from this drug on top of long-term aspirin therapy. This is a change in the paradigm how secondary stroke prevention is performed.
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