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.

Saturday, February 21, 2026

Perampanel Regulates Neuroinflammation and Ferroptosis via Activating FSP1 Following Brain Ischemia

 Your competent? doctor is already quite familiar with this, right? And is completely ready to ensure human testing gets done, right!

  • Perampanel (2 posts to June 2022)
  • Ferroptosis (10 posts to July 2012)

    • Your doctor, if competent at all, should have already known about ferroptosis from this research from September 2017.  And should have initiated stroke treatment interventions from it. But I bet incompetence prevailed! No excuses are allowed, call that president and have these incompetent doctors fired!

    Perampanel Regulates Neuroinflammation and Ferroptosis via Activating FSP1 Following Brain Ischemia

    Authors Lv JM, Pan YJ, Wang X, Zhang MM, Li W, Liu J, Wang T

    Received 4 June 2025

    Accepted for publication 3 October 2025

    Published 17 October 2025 Volume 2025:18 Pages 14423—14437

    DOI https://doi.org/10.2147/JIR.S544785

    Checked for plagiarism Yes

    Review by Single anonymous peer review

    Peer reviewer comments 4

    Editor who approved publication: Prof. Dr. Dharmappa Krishnappa

    Jian-Meng Lv, Ya-Juan Pan, Xuan Wang, Mei-Mei Zhang, Wei Li, Juan Liu, Tao Wang

    Department of Neurology, Shaanxi Provincial People’s Hospital, Xi’an, Shaanxi, 710068, People’s Republic of China

    Correspondence: Tao Wang, Department of Neurology, Shaanxi Provincial People’s Hospital, 256 Youyi West Road, Xi’an, Shaanxi, 710068, People’s Republic of China, Email wangtao_sxrm@163.com

    Purpose: Ischemic stroke remains a leading cause of global disability and mortality, with neuroinflammation and ferroptosis emerging as critical contributors to secondary neuronal damage. Perampanel, a non-competitive α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor antagonist, exhibits neuroprotective properties in neurological disorders, yet its mechanisms in ischemic stroke remain incompletely understood. This study investigated the therapeutic potential of post-injury perampanel administration in both in vivo and in vitro models, focusing on neuroinflammation, ferroptosis, and the role of ferroptosis suppressor protein 1 (FSP1).
    Methods: Rats received intraperitoneal perampanel (1.5 mg/kg) 10– 15 minutes post-reperfusion for 3 days and exposed to middle cerebral artery occlusion (MCAO) for 60 minutes. Neurological function, neuronal survival, and markers of neuroinflammation and ferroptosis were assessed via immunostaining, Western blot, and behavioral tests. The in vitro ischemia model was mimicked by oxygen glucose deprivation (OGD) in primary cultured cortical neurons.
    Results: Perampanel significantly attenuated MCAO-induced neuronal loss (NeuN+ cells) and improved motor coordination in rotating pole tests. It suppressed microglial (Iba-1+) and astrocytic (GFAP+) activation, indicating its anti-inflammatory effects. Mechanistically, perampanel reversed the MCAO-driven downregulation of ferroptosis markers FTH-1 and GPX-4, while enhancing neuronal FSP1 expression. Crucially, the FSP1 inhibitor icFSP1 abolished perampanel-mediated neuroprotection, neuronal preservation, and ferroptosis suppression, supporting the FSP1-dependent mechanisms. In in vitro conditions, perampanel exerted protective effects in a dose- and time-dependent manner. The results of immunostaining and Western blot showed that perampanel attenuated neuronal ferroptosis via activation of FSP1.
    Conclusion: These findings demonstrate that perampanel mitigates post-ischemic brain injury by inhibiting neuroinflammation and neuronal ferroptosis via FSP1 activation. This study highlights FSP1 as a novel therapeutic target and positions perampanel as a promising candidate for ischemic stroke treatment, leveraging its established safety profile and clinical availability.
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