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.My back ground story is here:http://oc1dean.blogspot.com/2010/11/my-background-story_8.html

Friday, October 15, 2021

High intake of fatty acid in nuts, seeds and plant oils linked to lower risk of death

 Just maybe your doctor can find out what high means.

High intake of fatty acid in nuts, seeds and plant oils linked to lower risk of death

 
MedicalXpress Breaking News-and-Events|October 14, 2021

A high intake of alpha linolenic acid (ALA)—found mainly in nuts, seeds, and plant oils—is associated with a lower risk of death from all causes, and specifically from diseases of the heart and blood vessels, finds a study published by The BMJ today.

Higher ALA intake was associated with a slightly higher risk of death from cancer, but the researchers say further studies are needed to confirm this.

Alpha-linolenic acid (ALA) is a type of omega-3 polyunsaturated fatty acid found in plants, such as soybean, nuts, canola oils and flaxseed.

Previous studies have shown that a high ALA intake is associated with a lower risk of fatal coronary heart disease, but findings from other studies on ALA and risk of death have been inconclusive.

To address this uncertainty, an international team of researchers analyzed the results of 41 studies published between 1991 and 2021 on the associations between ALA and risk of death from all causes, cardiovascular disease and cancer.

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Together, these studies involved around 120,000 participants aged between 18 and 98 years who were monitored for between two and 32 years, and they accounted for factors such as age, weight, smoking status, alcohol consumption, and physical activity.

After thoroughly assessing each study for bias, the researchers found that a high intake of ALA was associated with a 10%, 8%, and 11% lower risk of mortality from all causes, cardiovascular disease, and coronary heart disease, respectively.

This is equivalent to 113 fewer deaths per 10,000 person years for all causes, 33 fewer cardiovascular disease deaths, and 23 fewer coronary heart disease deaths.

A higher intake of ALA, however, was associated with a slightly higher risk of cancer mortality, equivalent to 63 extra cancer deaths for the highest compared with lowest levels of ALA intake.

A dose-response effect was found for dietary ALA intake and cardiovascular disease mortality, such that a 1g per day increase in ALA intake (equivalent to one tablespoon of canola oil or 0.5 ounces of walnut oil) was associated with a 5% lower risk of cardiovascular disease mortality.

Higher blood levels of ALA were also associated with lower risks of mortality.

Due to the observational design of included studies, causality cannot be established, nor can the researchers rule out the possibility that other unknown factors or measurement errors of food and nutrient intakes might have affected their results.

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Nevertheless, use of stringent study inclusion criteria together with rigorous and systematic evaluation of study quality suggests their conclusions are robust.

As such, they say their study adds to evidence of the potential health benefits of polyunsaturated fatty acids.

And they conclude: "Further studies should examine the association between ALA and a wider range of causes of death to provide a more comprehensive assessment of the potential health effects of ALA as well as to examine whether specific foods rich in ALA are differentially associated with mortality from cancer and other causes."

A linked article summarizes the current evidence on dietary intakes of different types of fatty acids and death.

Despite the beneficial effects of omega 3 fatty acids, it suggests that recommendations for intakes should be made cautiously because ALA intake might slightly increase the risk of cancer mortality. Further studies are, however, needed to confirm the increased risk.

To read more, click here

External Validation of Risk Prediction Models to Improve Selection of Patients for Carotid Endarterectomy

With zero medical training I would say; if the Circle of Willis is complete then just close up the offending artery.

My problems with stents has to do with putting an inflexible medical implement into flexible arteries. But I obviously know nothing.

This is why I would never consider a carotid endarterectomy as long as the Circle of Willis is complete. Didn't your doctor tell you of these possible complications?

Cognitive Dysfunction and Mortality After Carotid Endarterectomy

The latest here:

 

External Validation of Risk Prediction Models to Improve Selection of Patients for Carotid Endarterectomy

Originally publishedhttps://doi.org/10.1161/STROKEAHA.120.032527Stroke. 2021;0:STROKEAHA.120.032527

Background and Purpose:

The net benefit of carotid endarterectomy (CEA) is determined partly by the risk of procedural stroke or death. Current guidelines recommend CEA if 30-day risks are <6% for symptomatic stenosis and <3% for asymptomatic stenosis. We aimed to identify prediction models for procedural stroke or death after CEA and to externally validate these models in a large registry of patients from the United States.

Methods:

We conducted a systematic search in MEDLINE and EMBASE for prediction models of procedural outcomes after CEA. We validated these models with data from patients who underwent CEA in the American College of Surgeons National Surgical Quality Improvement Program (2011–2017). We assessed discrimination using C statistics and calibration graphically. We determined the number of patients with predicted risks that exceeded recommended thresholds of procedural risks to perform CEA.

Results:

After screening 788 reports, 15 studies describing 17 prediction models were included. Nine were developed in populations including both asymptomatic and symptomatic patients, 2 in symptomatic and 5 in asymptomatic populations. In the external validation cohort of 26 293 patients who underwent CEA, 702 (2.7%) developed a stroke or died within 30-days. C statistics varied between 0.52 and 0.64 using all patients, between 0.51 and 0.59 using symptomatic patients, and between 0.49 to 0.58 using asymptomatic patients. The Ontario Carotid Endarterectomy Registry model that included symptomatic status, diabetes, heart failure, and contralateral occlusion as predictors, had C statistic of 0.64 and the best concordance between predicted and observed risks. This model identified 4.5% of symptomatic and 2.1% of asymptomatic patients with procedural risks that exceeded recommended thresholds.

Conclusions:

Of the 17 externally validated prediction models, the Ontario Carotid Endarterectomy Registry risk model had most reliable predictions of procedural stroke or death after CEA and can inform patients about procedural hazards and help focus CEA toward patients who would benefit most from it.

 

Thursday, October 14, 2021

ReGear: an upper and lower limb simultaneous system for stroke rehabilitation

 

I can't find any pictures or video on this so no clue how it might work.

ReGear: an upper and lower limb simultaneous system for stroke rehabilitation

Abstract

Rehabilitation robotics is a rapidly advancing field that improves the treatment methods for several neurological injuries, including motor recovery for post-stroke patients. However, most of the structures consider upper and lower limb exercises separated. This paper concerns the development of a novel robotics structure called “ReGear” designed for a combined process of providing rehabilitation and helping post-stroke patients perform simple training sessions of both paretic limbs, simultaneously. The main goals of this structure are to assist motor recovery and improve the coordination of both affected limbs. Initially, a mathematical model of the proposed device is developed based on the geometrical relations and desired angular motion. Therefore, a tridimensional model is constructed and applied to computational simulations. Afterward, a prototype is built, including a microcontroller and a DC motor coupled with a rotary encoder. An assist-as-needed control design is applied to the system, which is connected to an electronic game developed to enhance the experience during the training sessions. The clinical trial tests were performed on healthy and post-stroke subjects, applying surface electromyography to correlate the muscular activity of both limbs with the system and game response. The experimental results demonstrate good responsiveness of ReGear and preliminary evidence that it can provide active–passive motion training for patients recovering from a stroke.

This is a preview of subscription content, access via your institution.

Availability of data and material

All data collected, and software applied in this research are provided to preserve data transparency.

 

Plasticity in the sensorimotor cortex induced by Music-supported therapy in stroke patients: a TMS study

 Did your doctors and hospital create protocols on music therapy when this came out 8 years ago? Or are they still completely incompetent having done nothing? If they have done nothing you don't have a functioning stroke hospital.

Plasticity in the sensorimotor cortex induced by Music-supported therapy in stroke patients: a TMS study

Front. Hum. Neurosci., 03 September 2013 | https://doi.org/10.3389/fnhum.2013.00494

  • 1Cognition and Brain Plasticity Group, Bellvitge Biomedical Research Institute - IDIBELL, Barcelona, Spain
  • 2Neurology Section, Hospital Universitari de Bellvitge, Bellvitge Biomedical Research Institute - IDIBELL, Barcelona, Spain
  • 3Institute of Music Physiology and Musicians' Medicine, Hannover University of Music, Drama and Media, Hannover, Germany
  • 4Department of Neurology, University of Lübeck, Lübeck, Germany
  • 5Department of Basic Psychology, University of Barcelona, Barcelona, Spain
  • 6Catalan Institution for Research and Advanced Studies, ICREA, Barcelona, Spain

Playing a musical instrument demands the engagement of different neural systems. Recent studies about the musician's brain and musical training highlight that this activity requires the close interaction between motor and somatosensory systems. Moreover, neuroplastic changes have been reported in motor-related areas after short and long-term musical training. Because of its capacity to promote neuroplastic changes, music has been used in the context of stroke neurorehabilitation. The majority of patients suffering from a stroke have motor impairments, preventing them to live independently. Thus, there is an increasing demand for effective restorative interventions for neurological deficits. Music-supported Therapy (MST) has been recently developed to restore motor deficits. We report data of a selected sample of stroke patients who have been enrolled in a MST program (1 month intense music learning). Prior to and after the therapy, patients were evaluated with different behavioral motor tests. Transcranial Magnetic Stimulation (TMS) was applied to evaluate changes in the sensorimotor representations underlying the motor gains observed. Several parameters of excitability of the motor cortex were assessed as well as the cortical somatotopic representation of a muscle in the affected hand. Our results revealed that participants obtained significant motor improvements in the paretic hand and those changes were accompanied by changes in the excitability of the motor cortex. Thus, MST leads to neuroplastic changes in the motor cortex of stroke patients which may explain its efficacy.

Introduction

Stroke represents a major cause of death and the most important cause of acquired disability in adults of developed countries (World Health Organization, 2003). In stroke survivors, motor deficits are present in a majority of patients (Rathore et al., 2002), leading to limitations in the participation of activities of daily living and preventing patients to live independently. For this reason, restoration of motor deficits is the target of many different therapies (Langhorne et al., 2011).

Usually, the rehabilitation process of motor impairments comprises different stages. At the beginning, motor function is assessed through domain-specific measures in order to set goals with the patient. Subsequently, therapeutic interventions are provided and, finally, reassessment is performed to ensure that motor improvements have been achieved (Warlow et al., 2008). In practice, this process is not always evidence-based but many times guided by the practitioner's expertise. Thus, there is a necessity to investigate effective motor rehabilitation therapies to provide evidence for clinicians (Taub et al., 2002; Cramer et al., 2011; Langhorne et al., 2011).

Besides their clinical efficacy, rehabilitation techniques may be validated by evidence for neuroplasticity which is defined as the capacity of the central nervous system to reorganize its structure, function and connections in response to internal and external constraints and goals during learning, development or after injury (Kolb and Whishaw, 1998; Cramer et al., 2011). Neuroplasticity may be induced due to therapy as behavior can lead to a reorganization of representational maps (Nudo et al., 1996; Muellbacher et al., 2002) as well as intra- and interhemispheric changes and balance (Chollet et al., 1991; Murase et al., 2004; Grefkes et al., 2008).

One of the most studied rehabilitation techniques is the Constraint-Induced Therapy (CIT) (Taub et al., 1993), which comprises the forced use of the paretic extremity for many hours a day by restricting movement of the healthy extremity in combination with shaping techniques. Studies in subacute and chronic patients have shown improvements in motor function that are accompanied with cortical reorganization of motor regions evidenced by Transcranial Magnetic Stimulation (TMS) (Taub et al., 1993; Liepert et al., 1998). For example, Liepert et al. (2000) reported an expansion of the contralateral cortical area responsible for arm movements after the application of CIT. It has been suggested that the success of this therapy may rely on repetitive massed practice of movements performed with the affected extremity overcoming its learned non-use. Notice that learning processes feature prominently not only in neurorehabilitation (Krakauer, 2006) but also in the development of the motor deficits themselves. For example, patients with a motor deficit of the right hand will learn to perform movements predominantly with the (usually non-dominant) left hand. At the same time, this may lead to additional learned non-use of the right hand. It is important to develop new therapeutic strategies to overcome the learned non-use of the affected side, paying special attention on how to perform specific movements. A way to achieve this goal could be through techniques where there is a specific training for patients in activities that could represent the acquisition of new motor skills that could promote brain plasticity (Dayan and Cohen, 2011). During motor skill learning, massive practice of movements can reduce kinematic and dynamic execution errors (Krakauer et al., 1999; Doyon and Benali, 2005). On the other hand, motor skill training will be more effective if task variability is introduced in the training program. These variations could be related to sensorial cues involved in the training (multimodality) which leads to dynamic sensorimotor readjustments and, consequently, internal motor control models can be created and generalized to other situations (Conditt et al., 1997). In this regard, it has been demonstrated that neuroplasticity could be observed at cortical and subcortical levels due to motor skill learning (Karni et al., 1995; Nudo et al., 1996; Willingham, 1998; Draganski et al., 2004; Dayan and Cohen, 2011; Penhune and Steele, 2012).

One example of a skill involving movements of the hand is musical instrument playing. The presence of music during motor learning posits unique and complex demands for the central nervous system (Zatorre et al., 2007), as playing an instrument requires the integration of multimodal information (auditory, visual, and sensorimotor information) (Pantev and Herholz, 2011). During music performance there are feedback and feedforward interactions between the auditory and premotor areas of the cortex. As in other motor skills, motor, premotor, supplementary motor area (SMA), the cerebellum and the basal ganglia are involved in musical motor performance (Lotze et al., 2003; Meister et al., 2004). In addition, the sound of the instrument processed by the auditory cortex can be used to readjust movements leading to interactions between the auditory and motor systems (Zatorre et al., 2007). Compared to other sensorimotor activities, music learning involves the integrated activity of motor and auditory systems. Furthermore, because of the consequent and consistent auditory feedback (Zatorre, 2003), correction of errors in timing, strength and position of the movement is possible. Studies with functional Magnetic Resonance Imaging (fMRI) exploring professional musicians and non-musicians have demonstrated that musical training leads to structural and functional changes in motor regions of the brain, especially those involving auditory and sensorimotor cerebral networks (Gaser and Schlaug, 2003; Bengtsson et al., 2005; Bangert et al., 2006; Baumann et al., 2007; Hyde et al., 2009; Herholz and Zatorre, 2012; Steele et al., 2013). For instance, in healthy subjects, motor cortex was explored with TMS when participants were trained to play the piano showing an enlargement of the cortical representation of the hand after the training (Pascual-Leone et al., 1995). Therefore, learning to play the piano is an example of a music making activity that requires repetitive massed practice and entails variations in the training task (i.e., movement sequences), involving complex coordination. Moreover, playing the piano engages different regions of the brain and could be associated with structural and functional brain changes. Beyond the plasticity in motor regions associated to music making, studies investigating the effects of music listening as a rehabilitative intervention have revealed improvements in cognition and emotional factors (Särkämö et al., 2008; Särkämö and Soto, 2012). These findings add value to the interventions based on motor learning using music making because their possible impact in other cognitive and emotional domains aside from the expected motor improvements.

Recently, Schneider et al.(2007, 2010) have developed Music-supported therapy (MST) to restore motor function after stroke. In this therapy, patients are trained to play a MIDI piano and/or an electronic drum set that produces piano tones, involving fine and gross movements, respectively. MST has been tested in stroke patients showing improvements in the execution of movements revealed by an increase in the scores of behavioral motor tests after the application of MST (Schneider et al., 2007, 2010; Altenmüller et al., 2009). A recent study about a single chronic stroke patient showed that MST can lead to improvements in motor function after 2 years since stroke. Gains in motor function were accompanied by changes in motor cortex excitability (evaluated using motor mapping TMS) with an expansion of the cortical representation of the hand and by activation changes in fMRI (Rojo et al., 2011; Rodríguez-Fornells et al., 2012). In addition, Amengual et al. (2013) have reported evidence from a group of chronic patients that have been treated with MST. Patients improved their motor function as well as an increase of the excitability of the motor system was encountered. Moreover, gains in motor performance were correlated with changes in the cortical representation of a muscle of the paretic hand.

In the present study, MST was administered to stroke patients with hemiparesis of the upperlimb to restore their motor function. Thus, the aim of the present study is to investigate improvements in motor function in subacute stroke patients and whether this restoration is accompanied by neuroplastic changes in the sensorimotor cortex.

More at link.

 

Dementia signs are in the blood, researchers say

 

With your good chance of getting dementia this test should be prescribed by your doctor to establish a baseline for you. And then if found implement THOSE EXACT DEMENTIA PREVENTION PROTOCOLS  your doctor should have competently already set up.

Your risk of dementia, has your doctor told you of 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 

The latest here:

Dementia signs are in the blood, researchers say

 

Researchers have reportedly found warning signs that could indicate impending dementia in the blood

In a new study published Monday in the scientific journal "EMBO Molecular Medicine," scientists from the German Center for Neurodegenerative Diseases (DZNE) and the University Medical Center Göttingen said that certain levels of microRNAs could be harbingers of the condition.

MicroRNAs are molecules that regulate and influence the production of proteins and are a central process in metabolism.


Combining the analysis of human data and mechanistic studies in model systems, the study's authors said they identified identify a circulating 3-microRNA signature that reflects key processes associated with the ability of a cell or system of cells to detect perturbation and generate a compensatory response to restore baseline function.

The group analyzed both young and healthy humans with already diagnosed patients in addition to animal and cellular disease models to identify the signature – which also informs about the mechanism by which a pathological condition occurs in the brain and they wrote that targeting the 3-microRNA signature using RNA therapies could enhance disease phenotypes in animal models.

"When symptoms of dementia become noticeable, the brain is already massively damaged. The diagnosis is currently far too late to even have a chance of effective treatment. If dementia is detected early, the chances of positively influencing the course of the disease increase, " André Fischer, research group leader, spokesperson at the DZNE site in Göttingen and professor at the UMG's clinic for psychiatry and psychotherapy, said in a press release. "We need tests that ideally respond when dementia has not yet broken out and reliably assess the risk of a later disease. So they warn early on. We are confident that our current study results will pave the way for such tests. "

In healthy individuals, levels of microRNAs correlated with mental fitness and individuals with a lower blood count performed better in cognition testing.

In mice, the researchers found the value rose even before the animals began to exhibit cognitive decline, regardless of the subject's age or because they had developed symptoms similar to those with Alzheimer's dementia.

Patients with mild cognitive impairment were found to have an increased blood level of the three microRNAs and 90% developed Alzheimer's disease within two years.

Lastly, the study found that – on mice and cell cultures – the three microRNAs influence inflammatory processes in the brain and "neuroplasticity," including the ability of nerve cells to connect to one another.

"In our view, they are not only markers, but also have an active impact on pathological processes. This makes them potential targets for therapy," Fischer said. "Indeed, we see in mice that learning ability improves when these microRNAs are blocked with drugs. We’ve observed this in mice with age-related mental deficits, as well as in mice with brain damage similar to that occurring in Alzheimer’s disease."

While the study suggests that the microRNA signature could be used as a "point-of-care" screening approach to detect individuals at risk for developing Alzheimer's disease – as well as highlights the potential of RNA therapies to treat it – the technique is not yet suitable for practical use.

In further studies, Fischer said that the group aims to validate the biomarker clinically.

In the U.S., of those at least 65 years of age, there were an estimated 5 million adults with dementia in 2014 and there are projected to be nearly 14 million by 2060.

The World Health Organization (WHO) reports that there are currently more than 55 million people with dementia across the globe and nearly 10 million new cases every year.

Age, family history, poor heart health, race and ethnicity and traumatic brain injuries can all increase the risk for dementia, according to the U.S. Centers for Disease Control and Prevention (CDC).

Repurposed drug reverses signs of Alzheimer's in mice, human cells

You'll want your doctors and stroke hospital to be closely following this so as soon as it is proven protocols are written and implemented in your hospital. If your hospital doesn't have a dedicated research analyst whose only job is to follow and implement research then you don't have a functioning stroke hospital. You'll have to ask your doctor if this works for non-APOE4-related Alzheimer’s disease.

Hell your doctor should have been using bumetanide for 9 years already.

Your risk of dementia, has your doctor told you of 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 

The latest here:

 

Repurposed drug reverses signs of Alzheimer's in mice, human cells

The Scientist|October 13, 2021

Bumetanide, a drug already approved to treat swelling associated with conditions such as heart failure, improved performance on cognitive tests and reduced the buildup of amyloid plaques in mice with an Alzheimer’s-like condition, researchers report. Furthermore, in cultured human neurons derived from stem cells, bumetanide reversed gene expression changes associated with Alzheimer’s, and the electronic health records of millions of patients point to a link between the drug and reduced odds of being diagnosed with the disease.

On the basis of these results, published this week (October 10) in Nature Aging, Gladstone Institutes neurobiologist and study coauthor Yadong Huang tells STAT that he and his team are now pursuing a clinical trial to test the drug in human patients with at least one copy of the APOE4 variant, a well-known risk factor for the disease.

Bumetanide blocks ion channels in the cell membrane, thereby altering salt balances and reducing water retention, but how this mechanism might affect neural function is not known. “The mechanism of the drug is well-known, but what the authors haven’t addressed is how that mechanism is related to what they think might happen if they were to give this drug to Alzheimer’s patients,” Johns Hopkins University neurologist Shilpa Kadam, who was not involved in the study, tells STAT.


While bumetanide did shrink amyloid plaques in a mouse model of Alzheimer’s, the drug is not thought to target these protein aggregations directly as many experimental Alzheimer’s drugs have. Many such drugs have failed, and one that was recently approved, Biogen’s Aduhelm, has been mired in controversy, with some questioning its efficacy and the legitimacy of its regulatory review.

The new study supports a growing body of evidence that amyloid plaques are but one piece of the puzzle. In Alzheimer’s patients with at least one copy of APOE4, nearly 2,000 genes showed altered expression compared with healthy controls, Huang and his colleagues found. These included genes involved with circadian rhythms, morphine addiction, and the neurotransmitter GABA.

“There are many cellular and molecular changes in Alzheimer’s disease patients besides plaques, but we usually don’t talk about them,” Huang tells STAT. He adds that “patients may have different underlying cellular mechanisms that lead to their neurodegeneration,” and thus may require different treatments. “More and more people are accepting this concept, but it’s definitely still an emerging idea.”

Jeffrey Cummings, director of the Chambers-Grundy Center for Transformative Neuroscience at the University of Nevada Las Vegas, tells STATthat the new study reveals “a repertoire of pathways that have not been adequately investigated,” but notes that bumetanide can cause dehydration and electrolyte imbalances. “This drug’s relationship to Alzheimer’s disease is not quite proven and its side effect profile is undesirable in older people,” he says.

To read more, click here

 

Turkeys

 Don't see these too often, but about 12 were running around in a pack. Deer are much more common. Getting the zoom on on my smartphone is very challenging one-handed, which is why the pictures are awful.



 


Mushroom consumption may lower risk of depression

 There are now multiple reasons for mushroom consumption but I bet your doctor still will not instruct the hospital dietician to create a diet protocol on this.

Mushrooms are full of antioxidants that may have antiaging potential  November 2017 

Can Lion's Mane Mushroom Improve Brain Function? September 2021

 

But what about magic mushrooms? Do you get three for one?

Psilocybin: Magic mushrooms have been found to boost neurogenesis.(Aug. 2013) Science isn’t really sure why.

The latest here: 

Mushroom consumption may lower risk of depression

ScienceDaily Top Health|October 12, 2021

Mushrooms have been making headlines due to their many health advantages. Not only do they lower one's risk of cancer and premature death, but new research led by Penn State College of Medicine also reveals that these superfoods may benefit a person's mental health.

Penn State researchers used data on diet and mental health collected from more than 24,000 U.S. adults between 2005 and 2016. They found that people who ate mushrooms had lower odds of having depression.

According to the researchers, mushrooms contain ergothioneine, an antioxidant that may protect against cell and tissue damage in the body. Studies have shown that antioxidants help prevent several mental illnesses, such as schizophrenia, bipolar disorder and depression.


"Mushrooms are the highest dietary source of the amino acid ergothioneine — an anti-inflammatory which cannot be synthesized by humans," said lead researcher Djibril Ba, who recently graduated from the epidemiology doctoral program at the College of Medicine. "Having high levels of this may lower the risk of oxidative stress, which could also reduce the symptoms of depression."

White button mushrooms, which are the most commonly consumed mushroom variety in the U.S., contain potassium, which is believed to lower anxiety. In addition, certain other species of edible mushrooms, especially Hericium erinaceus, also known as Lion's Mane, may stimulate the expression of neurotrophic factors such as nerve growth factor synthesis, which could have an impact on preventing neuropsychiatric disorders including depression.

According to the researchers, college-educated, non-Hispanic white women were more likely to eat mushrooms. The average age of surveyed participants was 45, and the majority (66%) were non-Hispanic white people. The investigators observed a significant association between mushroom consumption and lower odds of depression after accounting for socio-demographics, major risk factors, self-reported diseases, medications and other dietary factors. They said, however, that there was no clear additional benefit with relatively high mushroom intake.

"The study adds to the growing list of possible health benefits of eating mushrooms," said Joshua Muscat, a Penn State Cancer Institute researcher and professor of public health sciences.

The team conducted a secondary analysis to see if the risk of depression could be lowered by replacing a serving of red or processed meat with a serving of mushrooms each day. However, findings show that this substitution was not associated with lower odds of depression.

Prior to this research, there have been few studies to examine the association between mushroom consumption and depression, and the majority have been clinical trials with fewer than 100 participants. The researchers said this study highlights the potential clinical and public health importance of mushroom consumption as a means of reducing depression and preventing other diseases.


The researchers noted some limitations that could be addressed in future studies. The data did not provide details on the types of mushrooms. As a result, the researchers could not determine the effects of specific types of mushrooms on depression. Food codes issued by the U.S. Department of Agriculture were used to determine mushroom intake; therefore, some entries may have been misclassified or inaccurately recorded.

John Richie and Xiang Gao from Penn State Cancer Institute; Laila Al-Shaar and Vernon Chinchilli from Penn State College of Medicine; and Robert Beelman from Penn State College of Agricultural Sciences also contributed to this research. The researchers declare no conflicts of interest or specific funding support.

To read more, click here

 

Endurance exercise more beneficial to your health than resistance exercise

It is completely and totally your doctor's responsibility to get you recovered enough to do endurance exercise. I can't do two wheel biking so had to switch to a three wheel recumbent. Haven't tried running yet but will with the help of the Tommye-K. Mayer book 'Teaching Me to Run'.

Endurance exercise more beneficial to your health than resistance exercise

 

Endurance exercise such as biking or running is more beneficial to human health than resistance exercise such as weightlifting, according to the findings of a new study. The study is published in the Journal of Applied Physiologyand has been chosen as an APSselect article for October.

Mitochondria are often referred to as the powerhouse of cells. Increased mitochondrial activity, which occurs after exercise, can help improve overall metabolic health. Good metabolic health translates to ideal levels of blood sugar, cholesterol, blood pressure and waist circumference. On the other hand, poor metabolic health means your risk for heart disease, diabetes and stroke increases. That’s why robust physical activity—in this case, endurance training—is encouraged.

Researchers from Karolinska University Hospital and Linköping University in Sweden determined endurance exercises stimulate circulating levels of certain mitochondrial-derived peptides, which could lead to increased longevity and metabolic health. They did not find similar beneficial results from resistance exercise.


“This stresses it’s our own responsibility to be active and keep moving,” said co-researcher Ferdinand von Walden, MD, PhD, of the Karolinska Institute in Sweden. “This is one small piece that adds to the importance of being a physically active individual, so stay active.”

To read more, click here

Post-stroke fatigue is associated with resting state posterior hypoactivity and prefrontal hyperactivity

So what? There will be no followup research to solve this fatigue problem. Your doctors and stroke hospital will completely fail, as always, to initiate research into this.

Post-stroke fatigue is associated with resting state posterior hypoactivity and prefrontal hyperactivity

Georgia Cotter1, Mohamed Salah Khlif2, Laura Birdhttps://orcid.org/0000-0001-7073-725X2, Mark E Howard1,3,4,5, Amy Brodtmann2, and Natalia Egorova-Brumleyhttps://orcid.org/0000-0002-9244-29001,2
Background
Fatigue is associated with poor functional outcomes and increased mortality following stroke. Survivors identify fatigue as one of their key unmet needs. Despite the growing body of research into post-stroke fatigue, the specific neural mechanisms remain largely unknown.
Aim
This observational study aimed to identify resting state brain activity markers of post-stroke fatigue.
Method
Sixty-three stroke survivors (22 women; age 30–89 years; mean 67.5 ± 13.4 years) from the Cognition And Neocortical Volume After Stroke study, a cohort study examining cognition, mood, and brain volume in stroke survivors following ischemic stroke, underwent brain imaging three months post-stroke, including a 7-minute resting state functional magnetic resonance imaging. We calculated the fractional amplitude of low-frequency fluctuations, which is measured at the whole-brain level and can detect altered spontaneous neural activity of specific regions.
Results
Forty-five participants reported experiencing post-stroke fatigue as measured by an item on the Patient Health Questionnaire-9. Fatigued compared to non-fatigued participants demonstrated significantly lower resting-state activity in the calcarine cortex (p < 0.001, cluster-corrected pFDR = 0.009, k = 63) and lingual gyrus (p < 0.001, cluster-corrected pFDR = 0.025, k = 42) and significantly higher activity in the medial prefrontal cortex (p < 0.001, cluster-corrected pFDR = 0.03, k = 45).
Conclusions
Post-stroke fatigue is associated with posterior hypoactivity and prefrontal hyperactivity reflecting dysfunction within large-scale brain systems such as fronto-striatal-thalamic and frontal-occipital networks. These systems in turn might reflect a relationship between post-stroke fatigue and abnormalities in executive and visual functioning. This whole-brain resting-state study provides new targets for further investigation of post-stroke fatigue beyond the lesion approach.
Keywords
Calcarine/lingual gyrus, fractional amplitude of low-frequency fluctuations, medial prefrontal cortex, post-stroke fatigue, resting state functional magnetic resonance imaging, stroke subtypes
1Melbourne School of Psychological Sciences, University of Melbourne, Melbourne, Australia
2Dementia Theme, the Florey Institute of Neuroscience and Mental Health, Melbourne, Australia
3Turner Institute for Brain and Mental Health, School of Psychological Sciences, Monash University, Clayton, Australia
4Institute for Breathing and Sleep, Melbourne, Australia
5Victorian Respiratory Support Service, Austin Health, Heidelberg, Australia
*These authors are joint senior authors.
Corresponding author(s):
Natalia Egorova-Brumley, Melbourne School of Psychological Sciences, Redmond Barry Building, The University of Melbourne, Melbourne, VIC 3010, Australia. Email: natalia.egorova@unimelb.edu.au

Introduction

Post-stroke fatigue (PSF) is a common sequela of ischemic or hemorrhagic stroke and is reported by stroke survivors as one of their most disruptive symptoms. It is associated with poor functional outcomes and reduced quality of life, a reduction in the likelihood of returning to work, and increased mortality.1 Prevalence rates of PSF vary from 29% to 92% of stroke survivors,2 far exceeding the 10–23% prevalence of fatigue in the general population.3
Prior studies aiming to identify the neural mechanisms of PSF have focused on associations with stroke types and lesion locations.4 No associations have been found with the kind of stroke (ischemic or hemorrhagic), stroke severity, stroke side, or infarct volume.4 In contrast, some work in the field suggested that stroke subtype (e.g., lacunar, partial, or total anterior or posterior circulation) could be associated with PSF.5,6
Posterior circulation infarctions (POCIs), which account for roughly 20% of ischemic strokes, have been linked to higher levels of fatigue than other stroke subtypes,5,6 albeit not universally supported.7 With regard to lesion locations, many studies did not find any links with PSF,8–10 or reported heterogeneous findings. PSF was linked to right-sided lesions,11 caudate and putamen,12 and most consistently to posterior circulation lesions, including the brainstem, cerebellum, midbrain, and thalamus,6 reinforcing the association between PSF and POCI.
To date, few researchers have utilized functional magnetic resonance imaging (MRI) to explore the neural correlates of PSF. An association between high fatigue and perceived effort in stroke and a greater activation in the pre-supplementary motor area and the ipsilateral inferior frontal gyrus has been reported,14 as well as functional connectivity in the fronto-striato-thalamic (FST) network15 predictive of the response to the alertness-promoting treatment modafinil for PSF.16 The FST circuitry has been implicated in fatigue in other conditions, including in multiple sclerosis,17 traumatic brain injury,18 Parkinson’s disease,19 and chronic fatigue syndrome (CFS).20
We aimed to identify the neural correlates of PSF in terms of stroke subtype, lesion locations, and resting-state brain functioning at the whole-brain level. Specifically, we measured the fractional amplitude of low-frequency fluctuations (fALFF), computed as the relative contribution of the low-frequency band (0.01–0.08 Hz) to the entire detectable frequency range (0–0.25 Hz). fALFF indexes local spontaneous neuronal activity and thus is suitable to probe the neural basis of PSF. We hypothesized that there would be an association between PSF and posterior circulation ischemic stroke, posterior lesion locations, as well as a difference in the resting-state neural activity between stroke survivors with and without PSF in the FST network.
 
More at link,

13th World Stroke Congress

I have SEEN NOTHING FROM THE WSO that even remotely suggests they know anything about getting to 100% recovery.

At #WSC2021 we believe in providing everyone with the opportunity to access the latest #stroke science! That is why nurses, students & young researchers can enjoy our advanced virtual educational experience for as little as €35: worldstrokecongress.org/register/ #neurotwitter #neurology


 

In Neurodegenerative Diseases, Brain Immune Cells Have a Ravenous Appetite for Sugar

 So what is the takeaway from this news?  Should we be going directly to a keto diet at the first sign of MCI?

Don't listen to me, I'm not medically trained. Demand your doctor  definitively answer this question, no heming or hawing.

Your doctor should have been working on micro-glia for two years already

Inflammation within the Neurovascular Unit: Focus on Microglia for Stroke Injury and Recovery July 2019

Or are you allowing nothing to be done to solve stroke by your doctors?

In Neurodegenerative Diseases, Brain Immune Cells Have a Ravenous Appetite for Sugar

Summary: In the early stages of neurodegenerative diseases, microglia consume glucose to a greater extent than previously believed. The findings may serve as a new biomarker for a range of neurodegenerative disorders.

Source: DZNE

At the beginning of neurodegenerative disease, the immune cells of the brain – the “microglia” – take up glucose, a sugar molecule, to a much greater extent than hitherto assumed.

Studies by the DZNE, the LMU München and the LMU Klinikum München, published in the journal Science Translational Medicine, come to this conclusion.

These results are of great significance for the interpretation of brain scans depicting the distribution of glucose in the brain. Furthermore, such image-based data could potentially serve as a biomarker to non-invasively capture the response of microglia to therapeutic interventions in people with dementia.

In humans, the brain is one of the organs with the highest energy consumption, which can change with age and also due to disease – e. g. as a result of Alzheimer’s disease.

“Energy metabolism can be recorded indirectly via the distribution of glucose in the brain. Glucose is an energy carrier. It is therefore assumed that where glucose accumulates in the brain, energy demand and consequently brain activity is particularly high,” says Dr. Matthias Brendel, deputy director of the Department of Nuclear Medicine at LMU Klinikum München.

The measuring technique commonly used for this purpose is a special variant of positron emission tomography (PET), known as “FDG-PET” in technical jargon. Examined individuals are administered an aqueous solution containing radioactive glucose that distributes in the brain. Radiation emitted by the sugar molecules is then measured by a scanner and visualized.

“However, the spatial resolution is insufficient to determine in which cells the glucose accumulates. Ultimately, you get a mixed signal that stems not only from neurons, but also from microglia and other cell types found in the brain,” says Brendel.

Cellular Precision

“The textbook view is that the signal from FDG-PET comes mainly from neurons, because they are considered the largest consumers of energy in the brain,” says Christian Haass, research group leader at DZNE and professor of biochemistry at LMU Munich.

“We wanted to put this concept to the test and found that the signal actually comes predominantly from the microglia. This applies at least in the early stages of neurodegenerative disease, when nerve damage is not yet so advanced. In this case, we see that the microglia take up large amounts of sugar. This appears to be necessary to allow them for an acute, highly energy-consuming immune response. This can be directed, for example, against disease-related protein aggregates. Only in the later course of the disease does the PET signal appear to be dominated by neurons.”

This shows a brain
In humans, the brain is one of the organs with the highest energy consumption, which can change with age and also due to disease. Image is in the public domain

The findings of the Munich researchers are based on laboratory investigations as well as PET studies in about 30 patients with dementia – either Alzheimer’s disease or so-called four-repeat tauopathy. The findings are supported, for instance, by studies on mice whose microglia were either largely removed from the brain or, so to speak, deactivated. In addition, a newly developed technique was used that allowed cells derived from the brains of mice to be sorted according to cell type and their sugar uptake to be measured separately.

 

Wednesday, October 13, 2021

Sertraline for Functional Recovery After Acute Ischemic Stroke: A Prospective Observational Study

 

Will your stroke doctors and hospital be competent enough to get research going in humans that definitely answers the question?

Sertraline for Functional Recovery After Acute Ischemic Stroke: A Prospective Observational Study

Isabella Stuckart*, Timo Siepmann, Christian Hartmann, Lars-Peder Pallesen, Annahita Sedghi, Jessica Barlinn, Heinz Reichmann, Volker Puetz and Kristian Barlinn
  • Department of Neurology, University Hospital Carl Gustav Carus, Technische Universitaet Dresden, Dresden, Germany

Background: Neuroprotective and neurorestorative effects have been postulated for selective serotonin-reuptake inhibitors (SSRI). We hypothesized that sertraline, which is characterized by less severe adverse effects and more stable pharmacokinetics than classic SSRI, is associated with improved functional recovery in acute ischemic stroke patients with motor deficits.

Methods: Prospective observational study of consecutive acute ischemic stroke patients who received sertraline for clinically suspected post-stroke depression (PSD) or at high risk for PSD. Eligibility comprised acute motor deficit caused by ischemic stroke (≥2 points on NIHSS motor items) and functional independence pre-stroke (mRS ≤1). Decision to initiate treatment with SSRI during hospital stay was at the discretion of the treating stroke physician. Patients not receiving sertraline served as control group. Favorable functional recovery defined as mRS ≤2 was prospectively assessed at 3 months. Multivariable logistic regression analysis was used to explore the effects of sertraline on 3-months functional recovery. Secondary outcomes were frequency of any and incident PSD (defined by BDI ≥10) at 3 months.

Results: During the study period (03/2017–12/2018), 114 patients were assigned to sertraline (n = 72, 62.6%) or control group (n = 42, 37.4%). At study entry, patients in sertraline group were more severely neurologically affected than patients in the control group (NIHSS: 8 [IQR, 5–11] vs. 5 [IQR, 4–7]; p = 0.002). Also, motor NIHSS scores were more pronounced in sertraline than in control group (4 [IQR 2–7] vs. 2 [IQR 2–4], p = 0.001). After adjusting for age and baseline NIHSS, multivariable regression analysis revealed a significant association between sertraline intake and favorable functional outcome at 3 months (OR 3.10, 95% CI 1.02–9.41; p = 0.045). There was no difference between both groups regarding the frequency of any depression at 3 months (26/53 [49.1%] vs. 14/28 [50.0%] patients, p = 0.643, BDI ≥10). However, fewer incident depressions were observed in sertraline group patients compared to patients in control group (0/53 [0%] vs. 5/28 [17.9%] patients, p = 0.004).

Conclusions: In this non-randomized comparison, early treatment with sertraline tended to favor functional recovery in patients with acute ischemic stroke. While exploratory in nature, this hypothesis needs further investigation in a clinical trial.

 

Vascular interventions may not reduce dementia incidence

So nothing yet on how to successfully prevent dementia.

Vascular interventions may not reduce dementia incidence

Interventions that targeted vascular risk factors in a real-world setting did not appear to reduce dementia incidence in old age, according to study results in a research letter published in JAMA Neurology.

Researchers evaluated these interventions in the pragmatic multidomain Prevention of Dementia by Intensive Vascular Care (preDIVA) trial.

infographic showing percentage of participants who developed dementia
Infographic data derived from: Hoevenaar-Blom MP, et al. JAMA Neurol. 2021;doi:10.1001/jamaneurol.2021.3542.

“PreDIVA is the first and only trial aiming at real-world evidence of dementia prevention, in contrast to short-term trials with intermediate outcomes, such as cognitive decline,” Marieke P. Hoevenaar-Blom, PhD, of the department of public and occupational health, Amsterdam UMC, University of Amsterdam, the Netherlands, told Healio Neurology. “After 6 to 8 years of multidomain intervention, there was no significant effect on dementia. Because dementia takes years to develop, it was important to investigate whether an effect would occur after a longer follow-up period.

“However, follow-up after more than 10 years, comprising over 30,000 person-years, failed to provide evidence of dementia prevention,” Hoevenaar-Blom added.

Epidemiological studies have shown an association between modifiable risk factors and up to 40% of dementia cases; however, no consistent evidence has shown preventive or delaying effects on dementia related to multidomain interventions that target these risk factors.

In the current research letter, Hoevenaar-Blom and colleagues reported the results of the preDIVA trial following an extended observational follow-up period of up to 12 years after baseline. A total of 3,526 participants aged 70 to 78 years without dementia participated in the trial after being recruited from the general population between 2006 and 2009. Of these participants, 4% scored less than 24 points on the Mini-Mental State Examination. The researchers randomly assigned participants to either a practice nurse-administered multidomain intervention that focused on vascular risk factors, such as smoking, unhealthy diet, physical inactivity, overweight, hypertension, dyslipidemia and diabetes, or usual care during the 6- to 8-year period.

During a maximum of 4 years of observational follow-up, Hoevenaar-Blom and colleagues assessed dementia status among all participants who survived without dementia in the trial phase, which resulted in a median follow-up of 10.3 years since random assignment. They labeled as having no dementia surviving participants who scored greater than 30 on the Telephone Interview of Cognitive Statue and who did not have a formal dementia diagnosis. Further, the researchers searched the general practitioners’ electronic health records for information on possible dementia in all other cases.

Hoevenaar-Blom and colleagues identified 176 participants diagnosed with dementia during observational extension, as well as 233 participants diagnosed with dementia during the trial phase. A total of 217 of 1,871 intervention participants (11.6%) developed dementia compared with 192 of 1,620 control participants (11.9%) (HR = 0.99; 95% CI, 0.89-1.1) since baseline. The researchers reported no statistically significant interactions for sex, age, cardiovascular history, apolipoprotein e4 genotype, hypertension or hypercholesterolemia in intention-to-treat and per-protocol subgroup analyses. A total of 561 participants (29.7%) died in the intervention group compared with 487 (29.8%) in the control group (HR = 0.97; 95% CI, 0.92-1.04). They found similar results for the intervention effect on dementia, according to results of Fine-Gray models that factored in the competing risk for death.

“For clinical practice, prevention of dementia is not an easy task in older people already having access to good preventive health care,” Hoevenaar-Blom said. “For researchers, we showed that pragmatic trials are feasible that are sufficiently powered, with long-term follow-up and with dementia as the primary outcome. Future research is warranted in populations at higher risk, at younger ages or in countries with less developed preventive health care.”