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.

Sunday, May 2, 2021

Cannabidiol confers neuroprotection in rats in a model of transient global cerebral ischemia: impact of hippocampal synaptic neuroplasticity

Sounds promising. Now we just need our stroke doctors and hospitals to get research done in humans and protocols created. 

 Cannabidiol confers neuroprotection in rats in amodel of transient global cerebral ischemia: impact of hippocampal synaptic neuroplasticity

Erika Meyer
State University of Maringá Centre of Health Sciences: Universidade Estadual de Maringa Centro de
Ciencias da Saude
Jéssica Mendes Bonato
State University of Maringa Centre for Humanities Letters and Arts: Universidade Estadual de Maringa
Centro de Ciencias Humanas Letras e Artes
Marco Aurélio Mori
State University of Maringá Centre of Health Sciences: Universidade Estadual de Maringa Centro de
Ciencias da Saude
Bianca Andretto Mattos
State University of Maring�: Universidade Estadual de Maringa
Francisco Silveira Guimarães
USP FMRP: Universidade de Sao Paulo Faculdade de Medicina de Ribeirao Preto
Humberto Milani
State University of Maring�: Universidade Estadual de Maringa
Alline Cristina de Campos
USP FMRP: Universidade de Sao Paulo Faculdade de Medicina de Ribeirao Preto
Rubia M W Oliveira (  rubiaweffort@gmail.com )
University of Sao Paulo https://orcid.org/0000-0002-6181-1881
Research Article
Keywords: Cannabidiol, transient global cerebral ischemia, memory, hippocampus, neuroplasticity
DOI: https://doi.org/10.21203/rs.3.rs-447933/v1
License:   This work is licensed under a Creative Commons Attribution 4.0 International License.
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Abstract

Evidence for the clinical use of neuroprotective drugs for the treatment of cerebral ischemia (CI) is still
greatly limited. Spatial/temporal disorientation and cognitive dysfunction are among the most prominent
long-term sequelae of CI. Cannabidiol (CBD) is a non-psychotomimetic constituent of Cannabis sativa
that exerts neuroprotective effects against experimental CI. The present study investigated possible
neuroprotective mechanisms of action of CBD on spatial memory impairments that are caused by
transient global cerebral ischemia (TGCI) in rats. Hippocampal synaptic plasticity is a fundamental
mechanism of learning and memory. Thus, we also evaluated the impact of CBD on neuroplastic
changes in the hippocampus after TGCI. Wistar rats were trained to learn an eight-arm aversive radial
maze (AvRM) task and underwent either sham or TGCI surgery. The animals received vehicle or 10 mg/kg
CBD (i.p.) 30 min before surgery, 3 h after surgery, and then once daily for 14 days. On days 7 and 14, we
performed a retention memory test. Another group of rats that received the same pharmacological
treatment was tested in the object location test (OLT). Brains were removed and processed to assess
neuronal degeneration, synaptic protein levels, and dendritic remodeling in the hippocampus. 
Titles of sections follow:

3.1.1. Cannabidiol prevented the amnestic effect of

ischemia

3.1.2. Cannabidiol alleviated TGCI-induced spatial memory

impairments without affecting general motor activity

3.2.1. Cannabidiol attenuated TGCI-induced

neurodegeneration

3.2.2. Cannabidiol changed neuroplasticity markers in the

hippocampus of rats that were subjected to TGCI

3.2.3. Cannabidiol prevented ischemia-induced dendritic

spine loss

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