Use the labels in the right column to find what you want. Or you can go thru them one by one, there are only 32,248 posts. Searching is done in the search box in upper left corner. I blog on anything to do with stroke. DO NOT DO ANYTHING SUGGESTED HERE AS I AM NOT MEDICALLY TRAINED, YOUR DOCTOR IS, LISTEN TO THEM. BUT I BET THEY DON'T KNOW HOW TO GET YOU 100% RECOVERED. I DON'T EITHER BUT HAVE PLENTY OF QUESTIONS FOR YOUR DOCTOR TO ANSWER.
Changing stroke rehab and research worldwide now.Time is Brain!trillions and trillions of neuronsthatDIEeach day because there areNOeffective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.
What this blog is for:
My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.
The dry, puckering sensation felt after eating cocoa, berries, or red wine may do more than affect taste-it could also stimulate the brain, according ... Read more
How long will it take your incompetent? doctor and hospital to get this tested in stroke survivors?
Do you
prefer your doctor, hospital and board of director's incompetence NOT
KNOWING? OR NOT DOING? Your choice; let them be incompetent or demand
action!
Traumatic brain injury (TBI) is a critical neurological condition, with neuronal damage being its fundamental pathological basis. However, molecular targets for the prevention and treatment of neuronal injury remain to be further explored. Parkin is an important molecule closely associated with neurodegenerative diseases, yet relatively few studies have investigated its relationship with TBI. In this study, we first established and validated both the controlled cortical impact (CCI) and traumatic neuronal injury (TNI) models. Using these models, we revealed that TBI led to the upregulation of Parkin expression, with a peak occurring 24 h post-injury. Furthermore, at the in vitro level, lentivirus-mediated modulation of Parkin expression revealed that Parkin overexpression alleviated TNI-induced neurotoxicity, apoptosis, oxidative stress, and mitochondrial dysfunction, whereas Parkin knockdown exacerbated neuronal damage. At the mechanistic level, the study demonstrated that Parkin promoted mitochondrial biogenesis and fission while inhibiting mitochondrial fusion and attenuated the impairment of mitophagy after TBI. In other words, Parkin exerts a neuroprotective role through regulating mitochondrial quality control. We further employed adeno-associated viruses and Parkin knockout mice to modulate Parkin expression in vivo. The results showed that Parkin attenuated CCI-induced brain damage, edema, and behavioral deficits, whereas Parkin knockout exacerbated brain injury and functional impairments. Finally, we designed and synthesized a recombinant Parkin protein and preliminarily validated its protective effects at the cellular level. In summary, this study provides new insights for the therapeutic targets against TBI.
Graphical abstract
TBI induces the upregulation of Parkin. Parkin exerts neuroprotective roles through increasing mitochondrial biogenesis and fission, decreasing fusion and alleviating mitophagy dysfunction. Recombinant protein re-Parkin shows promising therapeutic values.
Traumatic brain injury (TBI) is a form of mechanical damage caused by external forces, and its high incidence and disability rates, which impose a substantial economic and social burden [1]. In terms of disease progression, TBI is primarily divided into two types: primary brain injury and secondary brain damage. Primary brain injury is influenced mainly by the external mechanical forces and is addressed by medical professionals through standardized early-stage surgical interventions. Secondary brain damage, on the other hand, involves mechanisms such as inflammatory activation, neuronal excitotoxicity, oxidative stress, and mitochondrial dysfunction [2]. The exact pathological mechanisms underlying these processes remain incompletely understood and constitute a major focus of TBI research. Neuronal damage serves as a critical pathological basis for secondary damage; therefore, studies on the changes in the expression of important genes involved after injury and the downstream effects of these changes are urgently needed.
Parkin was initially identified as a causative gene in juvenile Parkinsonism and functions fundamentally as an E3 ubiquitin ligase [3]. In addition to being involved in the PINK1-Parkin mitophagy pathway, Parkin plays diverse roles. It is also critically important for regulating mitochondrial function, programmed cell death, gene expression, intracellular metabolism, and other processes [4]. Parkin is closely associated with acute brain injury. Previous studies have shown that Parkin can influence the outcome of ischemic brain injury by regulating mitophagy [5]. However, little is known about the relationship between Parkin and TBI, and the role and mechanisms of Parkin in TBI remain to be elucidated.
Mitochondria are crucial organelles responsible for the energy supply of cells, and healthy mitochondria are essential for maintaining homeostasis. Owing to the need to sustain excitability and conduct action potentials, a sufficient energy supply is critical for neurons. Therefore, the functional state of mitochondria plays an undeniably important role in neurons. In recent years, mitochondrial quality control (MQC) has been increasingly recognized as a key regulator of mitochondrial function [6]. MQC refers to the dynamic balancing process that includes mitochondrial biogenesis, mitochondrial fusion and fission, mitophagy, and mitochondrial transport. The relationship between MQC and TBI remains unclear, and the regulatory mechanisms of MQC require further investigation.
I'm doing a 12 cup pot
of coffee a day with full fat milk to lessen my chances of dementia and Parkinsons. Tell me
EXACTLY
how much coffee to drink for that and I'll change. Yep, that is a lot
more than the 400mg. suggested limit, I don't care! Preventing dementia
and Parkinsons is vastly more important than whatever problems it can
cause!
Of course, your fuckingly incompetent? doctor did
nothing with this from 2 years ago! And still hasn't created a 24 hour
coffee station
This line is great: The findings indicate that even the Espresso Martini cocktail contains the espresso's beneficial compounds - and can contribute to staving off dementia.
Two to three cups a day linked with less dementia risk -- but not if it's decaf
Have your competent? doctor reconcile this earlier research with the previous statement! There are no excuses that your doctor shouldn't know about the earlier research! No knowledge is fireable! I take no prisoners in removing dead wood in stroke and that probably means firing at least 2/3rds!
Moderate coffee or tea intake was linked with lower dementia risk and better cognitive performance.
The greatest benefit was associated with 2-3 cups of caffeinated coffee or 1-2 cups of tea daily.
Decaf coffee had no relationship with dementia risk or cognitive outcomes.(Really? Don't you read research?)
Moderate daily consumption of caffeinated coffee or tea was tied to reduced dementia risk and better cognitive function over time, a prospective study of health professionals showed.
Over a median follow-up of 36.8 years, health professionals in the highest quartile of coffee drinking had an 18% lower risk of dementia compared with those in the lowest quartile (HR 0.82, 95% CI 0.76-0.89, P<0.001), reported Dong Wang, MD, ScD, of Brigham and Women's Hospital in Boston, and colleagues.
Top coffee drinkers also showed a reduced prevalence of subjective cognitive decline (prevalence ratio 0.85, 95% CI 0.78-0.93, P<0.001) and modestly better cognitive performance, the researchers said in JAMA.
Approximately two to three cups of caffeinated coffee or one to two cups of tea a day were associated with the lowest risk of dementia, Wang and co-authors stated. Similar patterns emerged for subjective cognitive decline, "reinforcing the notion that a daily intake of two to three cups of caffeinated coffee (around 300 mg of caffeine) was associated with optimal cognition," they wrote.
No additional advantages were seen with higher coffee intake. Decaffeinated coffee was not associated with lower dementia risk or better cognitive performance.
"While our results are encouraging, it's important to remember that the effect size is small and there are lots of important ways to protect cognitive function as we age," Wang said in a statement. "Our study suggests that caffeinated coffee or tea consumption can be one piece of that puzzle."
This is not the first study to show relationships between coffee or tea and cognition, but it's one of the largest and longest, with 131,821 participants from the Nurses' Health Study (NHS) and Health Professionals Follow-Up Study (HPFS) and up to 43 years of follow-up.
In 2024, a study of 8,500 U.K. Biobank participants showed that moderate coffee intake predicted less fluid intelligence decline over 8.8 years; drinking four or more cups daily, however, offered no added benefit. High tea consumption, more common in the U.K., also was tied to better cognitive performance.
Both coffee and tea contain bioactive compounds, including polyphenols and caffeine. Coffee has been associated with lower risks of cardiovascular disease mortality and all-cause mortality. Caffeine also may play a protective role in Parkinson's disease.
Wang and colleagues followed 86,606 women in the NHS from 1980-2023 and 45,215 men in the HPFS from 1986-2023, all of whom did not have cancer, Parkinson's disease, or dementia at baseline. Participants filled out food frequency questionnaires every 2 to 4 years.
Mean baseline age was 46.2 years in the NHS and 53.8 years in the HPFS. Over the follow-up period, 11,033 participants had a dementia diagnosis, identified by death records and physician diagnoses.
Secondary outcomes included subjective cognitive decline, assessed by a questionnaire. Objective cognitive function was evaluated in the NHS only, using the Telephone Interview for Cognitive Status (TICS) tool and a global cognition measure that was a mean z score of six cognitive tests.
In the NHS, top coffee and tea drinkers had higher mean TICS scores versus the lowest quartile, but the effect was modest, the researchers noted. Associations between coffee intake and global cognition z scores were not significant.
Results did not significantly differ across subgroups based on body mass index, smoking status, APOE4 genotype, or Alzheimer's disease polygenic risk scores. Associations between caffeine intake and dementia risk were consistent in a 4-year lag analysis.
The study's limitations included potential residual confounding and a lack of detail about tea type or coffee preparation, which may affect caffeine and bioactive compound concentrations. Each cohort included single-sex health professionals, which may limit generalizability to broader populations, the researchers acknowledged.
