Deans' stroke musings: Assessment of tenecteplase target-associated pathogenic mechanisms underlying depression in acute ischemic stroke patients: insights from artificial intelligence-driven multi-omics analysis and in vitro validation

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.

Monday, June 29, 2026

Assessment of tenecteplase target-associated pathogenic mechanisms underlying depression in acute ischemic stroke patients: insights from artificial intelligence-driven multi-omics analysis and in vitro validation

You ARE that blitheringly stupid you think administration of clot busters causes depression! WOW! Depression is caused by not having 100% recovery protocols! Get the hell out of stroke and let smarter persons solve stroke!

Assessment of tenecteplase target-associated pathogenic mechanisms underlying depression in acute ischemic stroke patients: insights from artificial intelligence-driven multi-omics analysis and in vitro validation

Qi Wang
X
Xihua Sun
Q
Qiang Fu
J
Jiaqi Lv
L
Li Dong
Qi Yan *

Neurology Department, FAW General Hospital of Jilin Province, Changchun, Jilin, China

Abstract

Background:

As a first-line treatment for acute ischemic stroke (AIS), tenecteplase (TNK) can cause adverse effects, such as depression, in AIS patients.

Objective:

This study aims to elucidate the TNK target-related pathogenic mechanisms underlying major depressive disorder (MDD) in AIS patients.

Methods:

By analyzing six public peripheral blood bulk datasets from AIS and MDD patients using integrative bioinformatics methods (limma, non-negative matrix factorization (NMF), and machine learning), we identified TNK target-associated molecular subgroups and diagnostic models for MDD and AIS patients, respectively. Next, a hub gene involved in the pathogenesis of both MDD and AIS was identified, and its corresponding molecular characteristics were analyzed in the peripheral blood bulk profiles of MDD and AIS patients. In addition, to gain a deeper understanding of the molecular implications of the hub gene involved in the pathogenesis of MDD in AIS, we performed disease ontology (DO) analysis and virtual cell knockout (KO) of the hub gene using public AIS mouse brain single-cell datasets. Furthermore, a deep learning pipeline (DrugReflector) model and molecular docking were used to identify MDD-preventive therapeutic agents for AIS patients based on MDD and AIS public blood bulk data. Finally, the expression pattern of the hub gene was also evaluated in MDD and AIS cell models.

Results:

Myeloperoxidase (MPO) can be considered an upregulated TNK target-associated gene involved in the pathogenesis of MDD in AIS patients, and BRD-K11973162 can be considered an MDD-preventive therapeutic candidate for AIS patients after TNK treatment.

Conclusion:

Our study is the first to identify MDD-associated diagnostic and therapeutic candidates for AIS patients after TNK treatment, providing a novel strategy for their clinical management.