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.

Tuesday, May 19, 2026

From Stress to Neurodegeneration: A New Look at the Pathogenesis of Parkinson’s Disease

 

All stroke patients are under massive stress because your incompetent? doctor doesn't have 100% RECOVERY PROTOCOLS. Your doctor has known since medical school that stroke recovery is a complete shitshow and done nothing to fix that! With your risk of Parkinsons post stroke that just adds more stress. 

From Stress to Neurodegeneration: A New Look at the Pathogenesis of Parkinson’s Disease


by 1,*, 2,*, 1,3, 1 and 1
1
Institute of Translational Biomedicine, St. Petersburg State University, Universitetskaya Nab. 7/9, 199034 St. Petersburg, Russia
2
School of Engineering, Johns Hopkins University, Baltimore, MD 21218, USA
3
Center for Transgenesis and Genome Editing, St. Petersburg State University, Universitetskaya Nab. 7/9, 199034 St. Petersburg, Russia
*
Authors to whom correspondence should be addressed.
Biomedicines 2026, 14(5), 1130; https://doi.org/10.3390/biomedicines14051130
Submission received: 10 April 2026 / Revised: 14 May 2026 / Accepted: 14 May 2026 / Published: 16 May 2026
(This article belongs to the Special Issue Advances in Parkinson’s Disease Research)

Abstract

The relationship between stress and Parkinson’s disease is regarded as complex and multifaceted, although a direct causal link has not yet been conclusively proven. One prevailing hypothesis is based on the activation of the hypothalamic–pituitary–adrenal (HPA) axis and the consequent elevation of glucocorticoid levels. Prolonged exposure to these hormones may exacerbate oxidative stress, thereby rendering the dopaminergic neurons within the brain’s subcortical structures more susceptible to degeneration. Furthermore, stress may intensify neuroinflammation through the activation of microglia—a mechanism that could constitute a significant factor in the pathogenesis of Parkinson’s disease. Another important concept concerns the direct interaction of stressors with the dopaminergic system. Physiological and psychological stress can alter dopaminergic transmission by affecting both the synthesis and release of dopamine, as well as the sensitivity of dopamine receptors. Severe or chronic stress may contribute to the disruption of dopaminergic mechanisms and accelerate the onset of clinical symptoms in predisposed individuals. Furthermore, many researchers draw attention to the role of stress-induced aggregation of α-synuclein—a key protein implicated in the pathogenesis of Parkinson’s disease. Clinical data suggest a highly probable link between post-traumatic stress disorder and an increased risk of developing Parkinson’s disease, although these findings remain inconclusive. It is possible that stress acts not as a primary cause, but rather as a modifying factor that interacts with genetic predisposition, accelerating or triggering neurodegenerative processes. The aim of our narrative review was to examine these concepts and discuss possible directions for future research into the interaction between stress and Parkinson’s disease.

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