Deans' stroke musings: A chronic low dose of Δ9-tetrahydrocannabinol (THC) restores cognitive function in old mice

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.

Wednesday, October 25, 2017

A chronic low dose of Δ9-tetrahydrocannabinol (THC) restores cognitive function in old mice

I bet this dose is not even enough to get you high. It is good to be a mouse. Nothing will occur for testing this in humans in the US until we get some intelligence in our federal legislature. I may have to retire in a more progressive country like North Korea, Russia, Canada, Mexico, Costa Rica, Ecuador, Italy, Jamaica, Netherlands, Peru, Portugal, Spain and look up the rest on your own.
https://www.nature.com/articles/nm.4311

Nature Medicine 23, 782–787 (2017)
doi:10.1038/nm.4311
Download Citation
- Cognitive ageing
- Epigenetics in the nervous system

Received:: 27 July 2015
Accepted:: 07 February 2017
Published online:: 08 May 2017

Abstract

The balance between detrimental, pro-aging, often stochastic processes and counteracting homeostatic mechanisms largely determines the progression of aging. There is substantial evidence suggesting that the endocannabinoid system (ECS) is part of the latter system because it modulates the physiological processes underlying aging^1,2. The activity of the ECS declines during aging, as CB1 receptor expression and coupling to G proteins are reduced in the brain tissues of older animals^3,4,5 and the levels of the major endocannabinoid 2-arachidonoylglycerol (2-AG) are lower⁶. However, a direct link between endocannabinoid tone and aging symptoms has not been demonstrated. Here we show that a low dose of Δ⁹-tetrahydrocannabinol (THC) reversed the age-related decline in cognitive performance of mice aged 12 and 18 months. This behavioral effect was accompanied by enhanced expression of synaptic marker proteins and increased hippocampal spine density. THC treatment restored hippocampal gene transcription patterns such that the expression profiles of THC-treated mice aged 12 months closely resembled those of THC-free animals aged 2 months. The transcriptional effects of THC were critically dependent on glutamatergic CB1 receptors and histone acetylation, as their inhibition blocked the beneficial effects of THC. Thus, restoration of CB1 signaling in old individuals could be an effective strategy to treat age-related cognitive impairments.