Deans' stroke musings: The Role of Phosphorylated-Tau 181 in Enhancing Neuroplasticity After Ischemic Stroke

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.

Thursday, June 5, 2025

The Role of Phosphorylated-Tau 181 in Enhancing Neuroplasticity After Ischemic Stroke

Interesting, good for stroke recovery, bad for Alzheimer's. Your competent? doctor will need to ensure your levels are correct at each point in your stroke recovery. I bet your incompetent? doctor can't do that!

The Role of Phosphorylated-Tau 181 in Enhancing Neuroplasticity After Ischemic Stroke

Lasta Arshinta, Ketut Widyastuti*, I Putu Eka Widyadharma

Neurology Department, Faculty of Medicine, Universitas Udayana,

Ngoerah General Hospital, Denpasar, Indonesia

*Corresponding author details: Ketut Widyastuti; kt_widyastuti@unud.ac.id

ABSTRACT

Ischemic stroke is a predominant cause of neurological impairment globally. Notwithstanding progress in acute treatment, the long-term functional recovery of individuals continues to be constrained. Recent research has concentrated on the function of neurodegenerative biomarkers, particularly phosphorylated tau 181 (p-tau 181), in influencing neuroplasticity following ischemic stroke. This study seeks to investigate the function of p-tau 181 in augmenting neuroplasticity following ischemic stroke. This investigation was performed by literature analysis and examination of experimental data from animal models and human subjects. The findings indicated that p-tau 181 levels were markedly elevated during the subacute phase post-stroke and correlated with the reconfiguration of brain circuits facilitating the recovery of motor and cognitive functioning. The mechanisms involved encompass enhanced synaptic connection, the induction of neurogenesis, and augmented myelination. While p-tau 181 is frequently linked to the neurodegenerative mechanisms of Alzheimer's disease, in the setting of stroke, the transient elevation of p-tau 181 seems to serve an adaptive function to facilitate recovery. These findings create new prospects for the advancement of biomarker-driven therapy techniques to enhance post-stroke recovery. Nonetheless, additional investigation is required to comprehend the physiological and pathological thresholds of p-tau 181 and its possible long-term implications.

Keywords: phosphorylated-tau 181; neuroplasticity; ischemic stroke.