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.

Friday, July 10, 2026

Transthyretin at the crossroads of neurodegeneration: a silent guardian in Parkinson’s disease

 Will your competent? doctor be doing something with this because of your risk of Parkinsons post stroke? Oh NO, NOTHING DOING! So, INCOMPETENCE REIGNS AGAIN! Your doctor is becoming an expert at incompetence and your board of directors is so incompetent they can't recognize it in their hospital! 

Transthyretin at the crossroads of neurodegeneration: a silent guardian in Parkinson’s disease

Abstract

Parkinson’s disease (PD) is a progressive neurodegenerative disease characterised by disruption of brain homeostasis and degeneration of dopaminergic neurons in the substantia nigra. PD is characterised by motor symptoms, like tremor, rigidity, bradykinesia, and postural instability, as well as non-motor symptoms like cognitive impairment, mood disorders, sleep disturbances, and autonomic abnormalities that significantly affect quality of life. The molecular pathogenesis of PD involves Oxidative stress, neuroinflammation, mitochondrial dysfunction, α-synuclein (α-syn) misfolding and aggregation, insufficient autophagy-lysosomal clearance, and synaptic degeneration, leading to progressive neuronal loss. Transthyretin (TTR), a tetrameric transport protein that is primarily produced in the liver and choroid plexus, is well-known for carrying thyroxine and retinol-binding protein. Experimental studies have shown that TTR can protect neurons by binding misfolded proteins, such as α-syn, decreasing toxic aggregation, regulating oxidative stress responses, and affecting selective autophagic degradation. PD-related changes in TTR expression in brain tissue and cerebrospinal fluid provide strong evidence of TTR’s significance as a molecular biomarker and a physiological regulator in the pathogenesis of the disease. This review highlights TTR involvement in neuroinflammation, oxidative stress, and α-syn aggregation, and discusses emerging evidence supporting TTR stabilizers as potential biomarkers and therapeutic targets for modulating disease progression in PD.

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