Use the labels in the right column to find what you want. Or you can go thru them one by one, there are only 32,247 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.
Tuesday, February 10, 2026
Parkin protects against traumatic brain injury through regulating mitochondrial quality control
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.
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