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, February 9, 2026

Berberine Alleviates Lipopolysaccharide-Induced Impairments in Neuroplasticity and Spatial Memory by Modulating Microglial Polarization via MAPK Signaling Inhibition

 I guess your doctor has been incompetent in berberine use for many years.
  • berberine (7 posts to November2017)

    • Berberine Alleviates Lipopolysaccharide-Induced Impairments in Neuroplasticity and Spatial Memory by Modulating Microglial Polarization via MAPK Signaling Inhibition



    Abstract

    Neuroinflammation-induced cognitive impairment is characterized by a continued decline in memory, executive functioning, and information-processing abilities. Although berberine (BBR) exhibits anti-inflammatory and neuroprotective properties, its ability to mitigate cognitive deficits by regulating microglial-mediated neuroinflammation remains incompletely understood. To investigate the potential of BBR in mitigating microglial-mediated neuroinflammation and its detrimental effects on neuroplasticity and spatial memory, a mouse model was established through intrahippocampal microinjection of lipopolysaccharide (LPS). The results showed that BBR pretreatment significantly improved cognitive performance, suppressed microglial activation, reduced hippocampal neuronal damage, and increased the density of functional dendritic spines. Mechanistic analysis revealed that BBR treatment inhibited the phosphorylation of key proteins in the MAPK signaling pathway within microglia. These findings suggest that BBR is a promising therapeutic agent for mitigating neuroinflammation-induced cognitive impairment and provide significant evidence for its potential application in treating inflammation-related cognitive deficits.

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