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.

Tuesday, June 25, 2019

Effects of MDMA(Ecstasy or Molly) on neuroplasticity, amyloid burden and phospho-tau expression in APPswe/PS1dE9 mice

Your doctor can figure out if your short term use of it is justified. Does your doctor even know about its use for PTSD?

Ecstasy Was Just Labelled a 'Breakthrough Therapy' For PTSD by The FDA August 2017

The latest here:

Effects of MDMA(Ecstasy or Molly) on neuroplasticity, amyloid burden and phospho-tau expression in APPswe/PS1dE9 mice 

Show all authors
Sonia Abad, Carla Ramon-Duaso, Raúl López-Arnau, ...
First Published June 20, 2019 Research Article



Abstract


Background:

3,4-Methylenedioxymethamphetamine (MDMA) is still one of the most consumed drugs by adolescents. Its abuse is related with cognitive impairment, which seems due to maladaptive plasticity and neural stress. In turn, new hypotheses suggest that Alzheimer’s disease (AD) may be promoted by neural stressors.

Aims and methods:

To test if there is an increase in vulnerability to AD after chronic MDMA consumption, we investigated the effects of this drug on recognition memory and its neurotoxic and neuroplastic effects in a transgenic mouse model of presymptomatic familiar AD (APP/PS1 dE9, Tg).

Results:

MDMA-treated animals showed recognition memory deficits, regardless of genotype, which were accompanied by changes in plasticity markers. Tg mice showed an impaired expression of Arc compared with wild-type animals, but exposure to MDMA induced an increase in the expression of this factor of the same percentage in both genotypes. However, the expression of c-fos, BDNF and p-CREB was not significantly altered by MDMA treatment in Tg mice. Although Tg mice had higher free choline levels than wild-type mice (about 123%), MDMA did not modify these levels in any case, ruling out any specific effect of this drug on the acetylcholine pathway. MDMA treatment significantly increased the presence of cortical amyloid plaques, as well as Aβ40, Aβ42 and secreted APPβ levels in Tg mice. These plaques were accompanied by increased tau phosphorylation (S199), which does not seem to occur via the canonic pathway involving AKT, CDK5 or GSK3β.

Conclusions:

The present results support previous evidences that MDMA can contribute to the amyloid cascade.
Keywords MDMA, Alzheimer’s disease, mouse model, amyloid plaques, memory

Article available in:

Related Articles

Citing Articles: 0
Posted by at
Labels: , , , , , ,

No comments:

Post a Comment

Subscribe to: Post Comments (Atom)